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Plomin Blueprint

Robert Plomin. Blueprint. Allen Lane, London. 2018

Plomin has written the book that summarizes his career, the one that he previously avoided writing because of what he describes as his own cowardice. Harsh judgement, but investigators into the genetics of intelligence are given a rough ride in contemporary academia, where genetics generates a hostility not meted out to sociological explanations. Over his long and highly productive career Plomin thought it prudent to publish in scientific journals, rather than to go public with all his views, which would invite even more criticism than he was already getting from doing his scholarly work. So, this is his “coming out” book.

The analogy of a blueprint, of course, makes more sense to my generation than it probably does to more recent ones. No engineering analogy will fit the intricacies of biology, but the implication is clear: DNA is what makes stuff happen, given only some basic environmental circumstances habitually found on this planet. The genetic code is causal.

A blueprint is a plan. It is obviously not the same as the finished three-dimensional structure – we don’t look like a double helix. DNA isn’t all that matters but it matters more than anything else put together in terms of the stable psychological traits that make us who we are. (Prologue, ix)

I agree with the sentiment. I merely note that people now often say of organizations and products and cultural creations that “they have the DNA of their predecessors”. DNA is now a meme.

So, what does Plomin say, now that no reticence is required?

1 Plomin has written a clear and non-technical account which ought to be accessible to a wide audience. For example, pages 24 and 25 explain variance, covariance and correlation in simple terms, with two illustrative scatter plots, and subsequent pages show how correlations found in identical and fraternal twins are used to estimate heritability. Plain language is hard to write. This book reads well, and ought to reach a wider public. Even for those who have been reading his papers for the last decade, there are new things to learn from seeing the whole story in one place.

One natural casualty of writing for a general audience is that the text is reference-free. Some scholars may be hurt not to see their names in print, but it is the findings that matter. There is no author index, but a full 59 pages of supporting notes. These differ in their nature and intensity: some list relevant publications, others explain ideas and misconceptions in far more detail. Readers will differ in whether they read the notes, and if so, at what stage. I mostly left them to the end of each chapter, so as to let the narrative flow while scribbling in my own questions in the margins.

2 Plomin has given an enlightening account of his research career, culminating in the long-term Twins Early Development Study, which has become a front runner in the DNA revolution. Research is a life-consuming business. Some researchers give up their weekends, most don’t. TEDS has more than 12,000 twins, and has generated 55 million items of data, described in over 300 published papers and 30 PhDs. Respect.

3 Plomin shows that there is strong evidence that, as a rule of thumb, most human characteristics are 50% heritable. He concludes his second chapter saying: “Inherited DNA differences are by far the most important systematic force in making us who we are”.

4 Plomin makes big inroads into that great big squashy thing “the environment” by showing that important aspects of it are heritable. At first this sounds nonsensical, but I think Plomin wins through. For example, at first glance it would appear that because some mothers read to their children and others do not, the former habit is the key to children’s language development. Whole programs have been devoted to this supposition, including well meaning projects giving books to families, because it has been found that number of books in the house predicts children’s scholastic achievements. On the contrary, Plomin shows, “parents who like to read have children who like to read”.

Plomin first found this when studying stressful life events (relationship problems, financial status and illness) which seemed to be truly external to the individuals concerned. Identical twins were twice as similar as fraternal twins on these measures (correlations of .30 and .15 respectively). These apparently completely environmental events were almost a third due to genetics.

ORDER IT NOW

Identical twins are more concordant for divorce (55%) than fraternal twins (16%). Divorce does not rain down unbidden from the sky: it happens more frequently to those who are joyful, engaged with life, emotional and impulsive. So there. In 20,000 adopted individuals the likelihood of divorce was higher if their real mother, who played no part in their upbringing, later got divorced, than if their adoptive mothers later got divorced. After controlling for genetics, Plomin says, no environmental causes of divorce have been identified.

Divorce doesn’t just happen by chance. We make or break our relationships. We are not just passive bystanders at the whim of events “out there”. Pg 39.

TV has been associated with many unfavourable outcomes, perhaps unfairly. Interestingly, parents and their children are more similar (.30) than adoptive parents and their adopted children (.15) in the time they devote to this freely chosen activity. In fact, heritable components are found in many traits which had been classified as “external” such as chaotic family environments, being bullied, neighbourhood safety, being exposed to drugs, and quality of marriage. Plomin calls this “the nature of nurture”. Smart, but confusing. I said in 2013 that they were “self-made environments” or “personally created niches”. Our genetics influences us in the way we build our nests.

Plomin explains:

Some children have more accidents than others: the number of children’s scrapes and bruises shows genetic influence. For adults, automobile accidents are not always accidental either, of course. Automobile crashes are often caused by reckless driving – driving too fast, taking chances or driving under the influence of alcohol and other drugs. Pg 48.

Years ago I had hoped that the Home Observation for Measurement of Environment would provide detailed indications of which aspects of the environment were worth manipulating so as to boost children’s intelligence. Families showed the expected .5 correlation with HOME, adopted children half that. All the good parenting is revealed to be half of it due to genetic causes. Brighter parents have brighter children. Although it looks as if encouragement is doing the trick, it is at most half of the cause of the children being bright. Plomin concludes:

Genetic differences in children’s aptitudes and appetites affect the extent to which they take advantage of educational opportunities. [] This is a general model for thinking about how we use the environment to get what our DNA blueprint whispers that it wants. Pg 51

5 Plomin reveals the counter-intuitive finding that DNA matters more as time goes by. Heritability estimates for intelligence rise as we age, possibly because the niches we create help boost our intellectual skills over our lifetimes. Eventually, we become more like our parents.

6 Abnormal behaviour is the far end of the normal spectrum, a finding which is closer to the psychologist’s dimensional model than the psychiatrist’s categorization model.

7 Genetic effects are general rather than specific. Importantly, parental psychopathology predicts that children of such parents are more likely to have psychological problems, but not the same diagnosis as the parent. There are strong genetic links between generalized anxiety disorder and major depressive disorder. Perhaps the different presentations are due to unspecified environmental factors. Many studies confirm three genetic clusters of psychiatric disorders:

A) internalizing disorders like anxiety and depression;
B) externalizing disorders like conduct disorders and aggressiveness in childhood, and antisocial behaviour, and alcohol and drug problems in adulthood;
C) Psychotic disorders such as schizophrenia, bipolar disorder and major depression.

Psychiatry is going to have to be re-written. Symptoms are not everything when treating disorders: the genetic underpinnings matter.

The other genetic finding relates to intelligence. Most genetic effects are general across cognitive abilities. Vocabulary, spatial ability and abstract reasoning yield genetic correlations greater than .5 and there is a greater than 50% chance that a DNA difference associated with one cognitive ability will also be associated with other cognitive abilities. Some genetic effects are specific to each cognitive ability, but most genetic effects are general to all cognitive abilities. “g” has a biological reality.

Interestingly, the genetic correlation between the capacity to read real word and non-words is .9 showing that these apparently different skills have the same biological substrate. In general, notions of cognitive modularity are not supported at all. In fact, since genetic influence is caused by many genes of small effect, and these effects affect many traits, it seems likely that generalist genes result in generalist brains. The multi-purpose brain has led to humans surviving ancient threats, and it was not tuned to the specific problems of written English, but can cope with these challenges by using tried and tested general problem-solving abilities.

8 Children in the same family are different because, for example, siblings correlate only .4 for intelligence, an average 13 IQ point of difference, compared to 17 IQ points for pairs chosen at random in the general population. What adoption shows is that environmental influences shared by family members do not make a difference. This is an astounding finding for any psychologist brought up in the standard model of seeing the family as the origin of individual and group differences. It leads to the petulant enquiry: Does that mean that everything I did as a parent was wasted? No. Parenting is important, but does not lead to permanent differences in children. They are already different, for genetic reasons. The lack of shared family effects even holds true of altruism, caring and kindness, the very things that parents might be able to inculcate in their children. Plomin summarises his futile search for non-shared environmental influences thus:

Non-shared environmental influences are unsystematic, idiosyncratic, serendipitous events without lasting effects. The systematic, stable and long-lasting source of who we are is DNA. Page 80.

9 Parents matter but they don’t make a difference. “Put crudely, nice parents have nice children because they are all nice genetically.” Parenting is often a response to children’s genetic propensities, not a cause of them. “The most important thing parents give their child is their genes.” Parents should help their children become what they are.

10 Schools matter but they don’t make a difference. Well, about 2% of a difference. Scholastic performance at age 16 is largely predicted by school performance at age 11.

11 Life experiences matter but they don’t make a difference, particularly as we get older. Life experiences matter a lot to us, but don’t change us the way we imagine they do. We differ in our propensities to experience life events. We don’t all climb mountains and hang glide down again. The heritability of life events is about 25% which allows much in the way of environmental variation, though little of it will be systematic. Falsifying these claims is easy: just demonstrate that parenting, schooling and life experiences make a difference after controlling for genetic influence.

This reminds me of a question I put to Stephen Pinker after David Lubinski had interviewed him about his career at ISIR 2017: were his accounts of intellectual influences and turning points in his life consistent with what we knew about genetics? Pinker didn’t blink. He took one of his cherished memories aged 13 years, of him reading an article in the New York Times about Chomsky’s work on transformational grammar and thinking “that is what I will study” and said of it: “Yes, you are right. What may have been more important than reading that article was having parents who took out a subscription to the New York Times.”

Perhaps all our biographies will have to be rewritten. I find I am very reluctant to give up my treasured narrative of my life, ascribing as I do some important effects to both family and education that seem to make sense to me, though perhaps they only serve as alibis. Any immigrant has to wonder how life would have turned out if they had stayed at home. Does life really have turning points, or are they only unfoldings? Arthur Koestler said somewhere that to think of human beings as no more than flotsam battered by waves of historical inevitability was are demeaning as viewing them as constructions propped up by genes. In all these confections the essential features of being human seem lost, subsumed into vexatious particulars, and stripped of agency and dignity. We are torn between our predicaments and our proclivities.

12 Plomin then goes on to make some even bolder claims:

Rather than blaming other people and ourselves for being depressed, slow to learn or overweight, we should recognize and respect the huge impact of genetics on individual differences. Genetics, not lack of willpower, makes some people more prone to problems such as depression, learning disabilities and obesity. Genetics also make it harder for some people to mitigate their problems. Success and failure – and credit and blame – in overcoming problems should be calibrated relative to genetic strengths and weaknesses.

Going even further out on a limb, I’d argue that understanding the importance of genetics and the random nature of environmental influences could lead to greater acceptance and even enjoyment of who we are genetically. Rather than striving for an ideal self that sits on an impossibly tall pedestal, it might be worth trying to look for your genetic self and to feel comfortable in your own skin.

Plomin immediately corrects himself

I do not mean to imply that people should not try to work on any of their shortcomings or not try to improve certain aspects of themselves.

Sorry mate, too late. I am getting comfortable with my DNA, and you can get your own breakfast. (Just wait till all Plomin’s remarks fall into the hands of US criminal lawyers).

As Jensen pointed out, the idea that once the genetic basis of behaviour is understood we will all accept this result in the same way is silly. If my prospects are poorer because of the genes I was given, why should I not be compensated for this unfairness? Plomin understand this dilemma, and at his point (page 92) the book goes on a little excursion about opportunity and meritocracy. I wouldn’t have done this (so many others will plunge into this deep pool of policy implications) but it is relevant from a public point of view, and has interesting twists to it.

13 Here is Plomin’s argument on equal opportunity and meritocracy. While equal opportunity means that people are treated similarly and given equal access to schooling, health and the law, meritocracy only comes in when selection takes place, say in employment. People being “equal” does not mean they are identical: the essence of democracy is that people are treated fairly despite their differences.

From a genetic point of view, equality of opportunity does not translate to equality of outcome. One of the most extraordinary implications of genetics is that heritability of outcomes is an index of equality of opportunity: if environments were all-powerful and varied unfairly that would wash out the heritability effect and set it to zero. The high heritability of school achievement of 60% in the UK suggests that the system is uniformly good, or at least uniformly OK. Half the remaining variance, 20%, might be due to individual school quality, but this seems to wash out by the time children go to university.

Also, as already discussed, many apparently systematic environmental effects reflect actual genetic differences.

The socioeconomic status of parents is a measure of their educational and occupational outcomes, which are both substantially heritable. This means that the correlation between parents’ socioeconomic status and their children’s outcomes is actually about parent-offspring resemblance in education and occupation.

Parent-offspring resemblance is an index of heritability, and heritability is an index of equal opportunity. So, parent-offspring resemblance for education and occupation indicates social mobility rather than social inertia.

Genetic differences in children’s aptitudes and appetites affect the extent to which they take advantage of educational opportunities. This is why equal opportunities cannot be imposed on children to create equal outcomes. [] To a large extent, opportunities are taken, not given.

When Norway expanded its educational provisions after World War II the first twin study found that the heritability of educational attainment increased and the impact of shared environment decreased, and the same pattern was found subsequently in other countries that increased the equality of schooling. Recent evidence in the US suggests that heritability estimates are decreasing, possibly because of increased educational inequality.

In the UK, children at selective secondary schools do a whole grade better than unselective state schools in their exams at 16 years, something they assure fee-paying parents is due to the quality of their teaching. Perhaps so. When Plomin controlled for the factors used to select students the difference shrinks to 1%, consistent with selection being meritocratic. Equally, when you look at university acceptances, the advantage of selective schools disappears when you control for selection factors: students would have been just as likely to be accepted by the best universities if they had not gone to a selective school. Indeed, given that those schools are seen as conferring an unfair advantage, it would be craftier to apply from an unselective State school. In the UK, private education is not worth the money.

Even “progress” measures, designed to show how much value schools add, are not a pure measure of student progress, because correcting for school achievement at the age of eleven does not correct for other heritable contributions to performance on the GCSE test (taken at 16) such as intelligence, personality and mental health.

Plomin also argues that shared environmental influence on occupational status is negligible, so the systematic effects of on job status and income can be attributed to genetics. Job selection is noisy, but not an effect of systematic bias.

He feels the fear of genetic castes is mistaken, because heritability is 60% not 100% so there is regression to the mean, with a shuffling down and shuffling up of intellects, and the more numerous middle ground will be the main source of high ability students. Perhaps so, but groups who consistently select high ability husbands and wives will regress to that higher group mean, not the population mean. It is possible to create cognitive elites by following strict rules for at least 16 generations.

Plomin concludes Part 1 of the book on page 105 saying “no specific policies necessarily follow from genetic findings, because policies depend on values.”

14 The shorter second part explains the DNA revolution. As one might expect, it is a clear and expert account and worth printing on its own. The basics of DNA are explained in Chapter 10: “dumb molecules, which are the same in each of our trillions of cells, produce life in all its amazing complexity”. These molecules are in a rope ladder held together by 3 billion weak, easily broken rungs, twisted into a double helix so that it forms a spiral, consisting of a 4 letter alphabet which creates 64 DNA words. 99% of the 3 billion rungs are identical for all human beings but 30 million rungs differ. Each difference in rungs is a SNP (snip) and we each have 4 million personal snips. The UK population has about 10 million SNPs. Chapter 11 is about the development of genome-wide association studies. Chapter 12 is a very substantial one about genetic prediction. Chapter 12 is Plomin’s real coming out: he reveals his polygenic scores for all to see. Naturally, this is a teaching opportunity, explaining the insights and the limitations of such measures. Figs 6 and 7 are worth showing again and again, if only to explain polygenic scores and their overlaps, and the fact that they provide probabilistic estimates, not certainties.

This is an explosive book. It leaves the environmentalist position looking threadbare. Whilst the DNA story is advancing and capturing new ground in the form of self-created environmental niches, the other environmental component is in retreat, reduced to saying that really bad environments would change the picture. Indeed they would, but the global story is of an improving world, with higher standards of living, of increasing access to education and health, and of more prosperity. As good environments become widespread the variance accounted for by genetics will only increase.

What can environmentalists turn to? I think their best bet is to find some good and solid long-term effects of adoption, since adoption is the most intense environmentalist intervention. Absent that, they will be left with a scorched earth policy, destroying everything they can in the hope of halting the spread of new ideas. In fact, the ideas in question are pretty old, known to most farm workers and every race horse breeder.

Deliberately absent from the discussion is any mention of genetic group differences. Questioned in an interview about this omission Plomin said “That’s the third rail” and questioning moved to other matters. Wise.

This is also a sobering book. It changes our views of ourselves and, shorn of any reassuring nostrums, invites us to understand our limitations, and to work within them. Genetics deals us a hand to play, and we must play it as best we can.

 
• Category: Science • Tags: Genetics, Heredity, Robert Plomin 
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  1. Polymath says:

    I don’t have much to take issue with here, but one example stood out as glaringly off: the role of genetics in obesity may mean that who becomes obese in a given society is largely genetically determined, but genetics completely fails to explain the enormous rise in obesity in the last two generations. To say that it is “mostly genetic” seriously misses the point, and suggests that there may be other phenomena than obesity where the article’s takeaway message that environmental factors don’t make much difference is too complacent.

  2. There is one assumption that is key for the standard conclusions (namely Wilson effect, aka increasing heritability with age, and minimal environmental effect) to hold, namely that effects can be segregated into purely genetic and purely environmental.

    Let the sensitivity to environmental contamination, e.g. uptake, be genetically variable, and the heritability (twin studies) lose their force in regards to lack of environmental effect.

    Notice that such an effect is qualitatively different from genetic correlation with environment. If one merely has genetic correlation with environment, the standard conclusions would remain viable.

    As many of the allegedly genetic effects are correlated with IQ, either the same genes must be responsible for both, or the environmental variable responsible for both has a genetically variable sensitivity. Lead, which is a continual concern in the age during which the bulk of these studies were conducted, is extremely likely to be genetically variable in uptake. Note also that in several countries, after phase-out of leaded petrol, lead poisoning remains a problem due to backyard recycling of car batteries, e.g. Jamaica and Brazil, as is described in the lead poisoning literature.

    Genetically variable sensitivity to environment may also explain (and predict) a large, though temporally varying component of parent child correlation. The prediction component should be particularly troubling in environmental studies, as such studies usually subtract parental effects to correct for genetic effects, on the simple additive environmental versus genetic model, i.e. ignoring genetic variation in sensitivity. Thus most such sensitivity models are likely underestimated, and if they segregate their study populations for dose, may find hormesis artefacts.

    Thus most of the found genetic effects may be due to poor mathematical formulation. Thus the importance of scientific realism in derivation.

    • Replies: @Johan Meyer
  3. @Polymath

    All variance apportionments depend on the circumstances and time frame in which the data were collected. Over a short time period genetics account for a large part of the variance. Over a period of decades then secular trends are far more relevant. So, global increases in obesity cannot have been caused by genes (the change has been far too fast) but it still the case that some people have got more obese than others, and their genetics is a major cause of this.

  4. @Johan Meyer

    A test can be conducted to detect the effect of lead on heritability. As prenatal uptake is governed by maternal genes rather than one’s own genes, a good check is to see whether maternal correlation is greater than paternal correlation, although assortive mating may still guarantee a healthy paternal correlation. Also, mixed ancestry mothers might show less correlation with children than monoethnic mothers, and children whose parents are of different ancestry may show more maternal correlation than paternal relative to non-mixed, even when paternity is shown genetically.

  5. @Polymath

    Genetics + prosperity & crappy corporate food offerings?

    • Replies: @dearieme
  6. res says:
    @James Thompson

    I agree with your comment, but still think Polymath makes an important point. One of my big hopes for increased genetic knowledge is offering the ability to fine tune the environment for individuals. Rather than someone being doomed to obesity by genes, knowing their particular vulnerabilities may allow easier prevention.

    A simple example of this is lactose intolerance (in adulthood). The genetics of that seem pretty straightforward (though there are different variants in different populations). I understand there can be environmental effects as well (e.g. the body produces more/less lactase depending on lactose consumption over time), but I think that is actually a good argument for looking at the underlying genetics. For example:
    1. Even though drinking milk after a long period of non-consumption may cause initial problems you can tell if someone is likely to adapt eventually.
    2. Even though someone may have consumed milk with no problem for years, their genetics may indicate a problem is worth watching for as they grow older.

    I think Polymath’s point is good to emphasize for multiple reasons.
    - It makes clear we do not believe in genetic determinism. (that strawman needs to die)
    - It offers positive examples about the utility of genetic knowledge in helping individuals.
    - It removes some of the helplessness (real or feigned) from those who think/say they can’t do anything about X because of their genes.

    P.S. Wikipedia gives a good overview of lactose intolerance: https://en.wikipedia.org/wiki/Lactose_intolerance

    • Replies: @Emil O. W. Kirkegaard
  7. Factorize says:

    Surprisingly there is no mention of the UK’s strong leadership in DNA research. The UKBB certainly springs to mind as does the research that discovered the double helix. For various reasons other nations are far far behind. If I had to award the GWAS medals, it would be a UK sweep. Perhaps there is a gene for DNA research?

    • Replies: @James Thompson
  8. dearieme says:
    @Fidelios Automata

    Decades of government propaganda recommending eschewing fats and proteins, and tucking into carbohydrates?

  9. dearieme says:

    P.S. Doc, that was a fascinating summary. Thank you.

  10. @res

    I outlined a general approach to utilizing family data to find plausible cases of environmental causality here: https://osf.io/8v4xa/ Unfortunately, no one else with coding skills is seemingly interested in implementing it in a large dataset, so it remains a project proposal for now. The genomic variant of this idea has already been tested and found to hold https://www.biorxiv.org/content/early/2018/03/30/291062

    • Replies: @res
    , @Johan Meyer
  11. I agree – and I’ve worked here and there with obese people. Maybe Plomin is a tad too straightforward/ impatient here.

  12. “People being “equal” does not mean they are identical: the essence of democracy is that people are treated fairly despite their differences.”

    Dear Doctor (Jagger /Richards// Sweet Virginia) Thompson, this is so dense and clear – this sentence of yours is ready for future rememberings (Ernst Bloch).

    • Replies: @James Thompson
  13. res says:
    @Emil O. W. Kirkegaard

    Very interesting. We should talk. I’m pretty busy for the next two weeks, but after that I will try to revisit this. I am mostly using R for data analysis these days. Does that work for you? Have you had any luck with your data requests?

    • Replies: @Emil O. W. Kirkegaard
  14. I once wrote – commenting on something Steve Sailer posted – that twin studies were mostly worthless and were the most overrated subfield in the social sciences..

    I still think that, but that is because twin studies are so often exploited by people with poor logic skills —
    and if anyone who has spent a research lifetime on twin studies, including weekends, was offended, I apologize. The 90 percent, or 95 percent or more, of logically unsound twin studies really make the rest of the studies seem unconvincing.

    (the following part of this comment explains why I think genetic discoveries are not going to be as successful at convincing people who were wrong that they were wrong as one might think) ….I am not sure how much limit there is to our capabilities, by genetics. Let’s assume von Neumann was a magnitude better aligned, by genes, to understanding the type of equations that best described the world the way it was mathematically described in the nineteenth century, than Einstein (if you don’t know what von Neumann’s capabilities were, do a little research….they were at least one in a billion) … but Einstein is the icon, because he was surrounded by the likes of Mach and Poincare and poor von Neumann grew up with self-measuring proud people who tracked their own triumphs against the triumphs of others, measured one against the other by the metric of who had the most interesting article in the local Hungarian elite math periodical in the most recent month (and it was elite, don’t get me wrong – these guys made the MIT freshman math club look like a junior high team of scrubs) rather than tracking their triumphs against the complexity of the world. Dying young in his 50s, von Neumann wasted exponentially more time than Einstein (with respect to the more interesting questions) on interesting but less than central (for the time) challenges, and so – the result is – for every one tribute to von Neumann from hoi polloi there are ten thousand to Einstein. But the genes of von Neumann, my best guess is, were exponentially better aligned for the great work of deep physical insight ….. but it did not quite work out …. the way one would have expected …..

    And we all know that Mozart and Beethoven lived for music, had hearts full of music, and we all know that they were born in a place and time (MittelEuropa, early middle to late middle 1700s) in which maybe a hundred musical prodigies a year were born, whereas we now live in a global classical music world with a thousand or two thousand prodigies being born every year,and yet nobody expects a single great symphony from any of them. Same genes, different opportunities.

    My best guess is that in any field that is limited to those with one in ten thousand genetic luck (that is a number I got from Steve Hsu, whose estimate is that one in ten thousand babies are born with the genes to usefully work on modern theoretical physics in academia or as independent researchers) nurture (Einstein growing up in Vienna where Mach was talked about in coffee houses versus von Neumann growing up in Budapest where math was viewed as an elite competitive sport ….) is responsible for 10 times the variance that nature is.

    My best guess is that in any field that is limited to those with one in ten thousand genetic luck, nurture is responsible for 10 times the variance in the extremely difficult successful achievements that the people with that one in ten thousand luck eventually obtain.

    And if the most beloved children of the deity (most beloved with respect to intellectual gifts, not necessarily with respect to anything else), a deity who supports knowledge and science, can, at their advanced level, easily outrun their genetic inheritance by tenfold or a hundredfold ….

    then it will be difficult to convince the more commonly gifted people that anything less than a clear hundredfold advantage – in leadership, in the ability to run the afternoon shift at the Pizza Hut, in the ability to vote with an informed view of the issues – is more significant than the general feeling that we are all more or less equal.

    A basic and honest and widely acknowledged understanding of genetics is not going to happen in my lifetime. I will live and die in a world where almost nobody cares enough about other people to understand genetics.

  15. @middle aged vet . . .

    “easily outrun their genetic inheritance” was not what I wanted to say, three paragraphs from the end …

    “easily outrun their competitors with a similar genetic inheritance”.

    That is what I wanted to say.

    Otherwise, except for the fact that I wanted to ramble on about what Aquinas considered to be the difference between human ratiocination and the angelic approach to understanding, and I didn’t, I think there are no typos or omissions in my 2:22 AM comment.

  16. @Emil O. W. Kirkegaard

    Your model has two objectionable components, namely avoiding explicit formulation in terms of random variables and lack of consideration for genetically variable sensitivity to environment. A reformulation is possible to detect genetically variable sensitivity based on e.g. neighborhood, so if you want, I could try to send it by year’s end. Also, if you want coding for your formulation, I could have a look.

    • Replies: @Emil O. W. Kirkegaard
  17. @res

    I only use R for data analysis, so that would be perfect. I currently have loads of data and too few analysts. Unfortunately, good analysts are not easy to come by! Applying for datasets for this should be no problem, but there are public datasets one can utilize to begin with. It doesn’t have to be MZ twins, one can estimate the within MZ pair estimate if one has multiple other family relations, e.g. halfsibs + sibs. See e.g. Sariaslan’s paper I commented on here: http://emilkirkegaard.dk/en/?p=6235

  18. @Johan Meyer

    Johan,

    I find your posts to be mostly uninterpretable. I had an engineer friend of mine who is familiar with the behavioral genetics literature read your posts in the other thread. He was able unable to make much sense of what you are saying. My best guess what what you are proposing is a GxE model with genetically varying susceptibility to environmental insults (e.g. lead exposure). This model has a very low prior because interactions in general have low prior, and because previous research on GxE fails to find much of anything. Here’s two recent examples:

    - https://www.repository.cam.ac.uk/handle/1810/264528
    - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5628077/

    The onus is on critics to show substantial GxE effects in the real world. It is not enough to be able to come up with some hypothetical alternative scenario. Behavioral genetics methods have been very well validated for >100 years using a very large variety of methods. It is this collective body of evidence one has to take on if one wants to be taken seriously.

  19. @Factorize

    The UK does science very well. Take no-one’s word for it.

  20. @Dieter Kief

    Thanks, but I was quoting Plomin.

    • Replies: @Dieter Kief
  21. @middle aged vet . . .

    The twins are fine. James Shields got it right in 1962. Critics carped, so it was all done again on larger samples by Thomas Bouchard and others. Critics carped again, so it was all done again with very much larger samples and better measures of achievement by Robert Plomin. Enough.

    The 1 in 10,000 criterion comes from Galton, who judged that the benchmark of eminence.

    Agree that von Neumann was very bright but that his contributions did not have the impact of Einstein’s, not by a country mile.

    I think that your point about “nurture” being important for the actual achievements of the intellectually eminent is very hard to test. In fact, looking at what you argue, I think you mean that cohorts are faced with different opportunities, partly dependent on what previous bright people have already sorted out. Some low hanging fruit has been picked. Nothing directly to do with nurture. Sometimes things come together at particular moments.

    Testable prediction might be to look at who manages to find a great use for graphene.

  22. Anon[100] • Disclaimer says:

    I do not mean to imply that people should not try to work on any of their shortcomings or not try to improve certain aspects of themselves.

    Such as going on the James Thompson “Eat Less Diet” for “Intelligent Health” because “Diet is an IQ Test”?

    But of course. Genetics is what is, not what could be. And what could be is the two-thirds of the population with a BMI north of 25 going on the Eat Less Diet, and obtaining normal weight.

    Of course Plomin, though not Thompson, knows in his heart that the ability to work on shortcomings is just as genetically determined as weight. If you’re past a certain age, and you’ve never successfully lost and kept off weight, it’s not going to happen for you.

    • Replies: @notanon
  23. @James Thompson

    Oh – : – I was indeed quite excited when I read your insightful article for the first time. Brilliant Plomin-quote you chose, thanks – and not only for that!

  24. You ask for an area of life were parental influence has an impact and so does environment. I think a very obvious one is in family formation and fertility rates. The population in “pre-modern” times generally seemed to average about 6 children per woman today in “developed” countries it’s almost always less than 2, sub replacement. You can see extreme environment effects amongst Amish and highly religious groupings, I think the idea that what sets these people apart is purely a genetic difference is kind of hard to believe. It’s clearly an environmental effect which people not raised in their environment don’t share, highly religious groupings like Amish or Huitterites have between 6-10 children on average.

    I’m not stating genetics plays no role in this, within these groupings they do have a % of their children leave their communities so those with more “non-conformist” genes will leave and over time they will become increasingly genetically suited to their steady state environments. However the key indicator that there’s a key environmental factor is that their “high” fertility rates today were the norm for the general population in the not too distant past. So why in the general population has this practice become all but unknown whilst is the norm still for them? It seems clearly to be their religious teachings and the influence of their communities and their own expectations about how to live.

    • Replies: @notanon
    , @Anon
  25. JackOH says:

    Dr. Thompson, I’m a big admirer of your contributions here. I’ve read your recommendation here of Plomin’s book, also the reviews on Amazon’s UK site.

    I’m half-hooked. Is Blueprint as you say it is, something for the educated but non-expert reader?

    Is there any second title you’d suggest on the same subject for readers who are looking for something authoritative, but have neither the time nor expertise for wider reading?

  26. @middle aged vet . . .

    And we all know that Mozart and Beethoven lived for music, had hearts full of music, and we all know that they were born in a place and time (MittelEuropa, early middle to late middle 1700s) in which maybe a hundred musical prodigies a year were born, whereas we now live in a global classical music world with a thousand or two thousand prodigies being born every year,and yet nobody expects a single great symphony from any of them. Same genes, different opportunities.

    Not SAME genes, exactly, because most of musical prodigies are not composers. Composition require a lot of creativity while capacity to replicate it not necessarily. Openess to experience in very open environment maybe will be very distractive for people who ”score” higher in this psychological trait, a over-saturation of environmental stimuli, depressing the willpower to concentrate in specific activities. Many very talented artists migrated from classical areas to modern ones because they are novel-seeking too. Another nongenetic reasons we no longer have modern greater classical composers is that this area already reached its full potential; many potentially genius-classical composers choose different professions because today leftist ideology is prevalent in contemporary classical music.

    Yes, creative achievements are unique for their respective space and time.

  27. Inuits, fareast, africans [from sub to over-nutrition], latin americans also has experienced exponential increase on obesity rates. The pattern seems trans-cultural.

    https://www.washingtonpost.com/news/animalia/wp/2016/04/25/they-did-it-without-liposuction-weight-loss-secrets-from-zoo-animals/?noredirect=on&utm_term=.21706fe07613

    • Replies: @dearieme
  28. dearieme says:
    @Santoculto

    “The pattern seems trans-cultural.” Oh well, either it’s because food is much cheaper everywhere or because of some yet-to-be-identified infection. Or both.

  29. @Emil O. W. Kirkegaard

    I read your references—one looking at gene environment interaction for type 2 diabetes, the other for “stressful situations” (ill-defined, and unlikely to have àny effects—low prior). A comment on the diabetes matter is appropriate. Once one has type 2 diabetes, one may retain some glycemic control via diet, but the threshold for losing glycemic control is reduced after losing control once.

    I would have to look at the literature that is being reviewed to see if and how they estimate the rate of avoiding a first loss of glycemic control, as that would, one the basis of a distribution in daily intake, be unlikely to have substantial variation with population mean intake, if the probability is nearly unity (the probability should have a sigmoid rather than linear relationship with intake). If the study does not include a valid proxy for the probability of at least one upset per susceptible person, it may reject, or poorly support, a gene environment interaction based on the invalid proxy used.

    Lead uptake arguably has a high prior probability of such interactions, based on consistent ethnic disparities in elevated blood lead. A twin correlation study could have been attempted during a consistent poisoning period (presently Brazil or Jamaica) on blood lead level, or e.g. using deliberate poisoning of elderly twin volunteers. The alternative hypothesis is consistent racism, which is unlikely, as it would involve consistently failing to harm ethnic groups that have been targets of discrimination campaigns in the past (e.g. Chinese and Japanese).

    As for the issues that I raised on the previous thread, I am making an explicit formulation and intend to send it, perhaps by May.

  30. @Emil O. W. Kirkegaard

    In case there is any confusion in regards to the matter of regression to genetic setpoint, my argument can work purely without genetically variable sensitivity, as it arises purely from an additive model of variation, in the sense that gene x provides additional growth \Delta L_x(m) at age m, as may in principle be found in a regression of growth on genes. Then one takes the genetic and environmental contributions in growth as random variables, and calculates the correlation coefficient, using entirely uncontroversial methods from random variables. I leave the rest to May.

  31. @Emil O. W. Kirkegaard

    Did the engineer in question take any e.g. graduate level coursework in random variables?

  32. JLK says:

    Most of this is old hat to those who have followed Charles Murray and his fellow apostates.

    The next frontier is using sociobiology to study how inherited brain structure influences political and philosophical predispositions. And how forcing contrary dogma down the throat of certain groups can cause cognitive dissonance and be psychologically damaging.

    Oh for the day when the paleos will be a protected class who can claim that the New York Times or academia is a hostile work environment, and can extract monetary damages using legal cases for psychological battery.

  33. @James Thompson

    “All variance apportionments depend on the circumstances and time frame in which the data were collected. Over a short time period genetics account for a large part of the variance. Over a period of decades then secular trends are far more relevant.”

    Doesn’t that last sentence invalidate this one ?

    “After controlling for genetics, Plomin says, no environmental causes of divorce have been identified.”

    Because the native British haven’t changed that much genetically in the last 60 years, yet divorce rates have soared. And the reasons are obvious – the incentives (“environment”) have changed dramatically. 60 years back divorce was hard to obtain, there was no ‘no-fault’ divorce, and the “at-fault” spouse was unlikely to get the house, kids and a chunk of income out of it, but was likely to get the cold shoulder from their respectable neighbours.

    I had a debate with Jayman on this subject – say you had identical 16thC Balkan teenage twins, Christians, only one happened to be out in the woods when the Ottoman official came round selecting likely candidates for the Janissaries. Ten years on they might still have closely correlated intelligence, diligence, ways of scratching their nose etc – but one would be a peaceful (for the Balkans) Orthodox villager and father, perhaps on the village council, while the other was a celibate, Muslim, elite trained killer – an SAS-style figure.

    • Replies: @James Thompson
  34. @Emil O. W. Kirkegaard

    One more thing. The derivation to which I referred in the previous thread to produce the Wilson effect is a small variation on the derivation of the Falconer equations in a certain letter, but including a random variable account of the effect of monochorionic placenta. I do wish to do it carefully though.

    If you reject that derivation, are the Falconer equations to be accepted simply ex cathedra, or is there another random variable derivation?

  35. This bozo’s whole argument is what rhetoricians call “begging the question.”

    Look it up, geniuses.

  36. plomin’s whole career is a fraud as demonstrated by james lee and herr doktor doktor professor steve shoe. that he’s still trying to sell his snake oil means he’s a criminal.

    james lee said (i paraphrase): rare variants can never be identified as having small effect, precisely because they are rare and there aren’t enough people on earth to demonstrate their effect, therefore, my study is definitive. in the narrow range of environments of the US and blighty h^2 for educational attainment is 10% and 6% when corrected for stratification.

    steve shoe: i professor shoe have been shown to be delusional, so i’m doubling down on my delusional-ness.

    GAME OVER!

  37. res says:
    @James Thompson

    Agree that von Neumann was very bright but that his contributions did not have the impact of Einstein’s, not by a country mile.

    I don’t know what metric you are using, but von Neumann’s contributions were nothing to sneeze at. I am partial to his game theory and computer work. https://www.britannica.com/biography/John-von-Neumann

    From Murray’s Human Accomplishment we see von Neumman listed under Technology (Index = 26) and Mathematics (Index = 19)

    Murray specifically calls out (1946 USA)

    Arthur Burks, John von Neumann, and Herman Goldstine’s “Preliminary Discussion of the Logical Design of an Electronic Computing Instrument” provides the conceptual foundation for computer development in the coming decades.

    Einstein is at another level, with a Physics Index of 100 and a Combined Sciences Index of 48 (and about a half dozen specific accomplishments listed), but I’m not sure “country mile” is appropriate.

    • Replies: @James Thompson
  38. Anon[350] • Disclaimer says:
    @Polymath

    genetics completely fails to explain the enormous rise in obesity in the last two generations

    FYI, this is all discussed in the book.

  39. as a great admirer of this type of work and somebody who has great respect for many of the important insights discovered by these researchers, i still have to object that some of plomin’s claims as summarized here are pure baloney.

    plomin may qualify some of these statements so that they make more sense in the book. otherwise assertions such that schools don’t matter are pure nonsense. the idea that key life events don’t matter makes even less sense. i could go into more detail, but i doubt anybody wants to read a long point by point response to the plomin pronouncements made here. maybe dr thompson or emil kirkegaard would be interested, off line. instead i’ll just throw this monkey wrench:

    if environment doesn’t matter much, why the HUMONGOUS swing in fertility rate? carrying capacity was about replacement level for most of human history according to greg clark. 2 kids per set of parents was about what you got. then, europeans figured out lots of stuff, and fertility levels among europeans skyrocketed. 3 kids, 4 kids, or more, is what you got. then, europeans figured out too much stuff, and fertility levels crashed to BELOW REPLACEMENT.

    how can a self reproducing system deliberately go from 3 or 4 surviving offspring per generation, down to 1, in just 100 years, if environment doesn’t matter? the genes didn’t change THAT much in one century. so, what happened?

    lots of what plomin is talking about here is complete nonsense. john calhoun was more accurate with his mouse experiments. boomers definitely had a more conducive environment than millenials, and the numbers show it, across the board. environment is having more effect on them than genetics.

    • Replies: @notanon
  40. @dearieme

    I rread somewhere [in the rainbrown] that humans has been evolved to move constantly to remain athletic. What’s more intersting is these people who gain kg, are sons or grandsons of normal-weighted parents/relatives and have overweight kids.

    • Replies: @dearieme
  41. @YetAnotherAnon

    I don’t think the statements are invalidated, but agree we need to specify time frames and the variables in question more precisely.
    As you say, divorce has become easier. Previously (prior to 1950?) it was so difficult to divorce that you would have had to measure “married but living apart” or even “married, living together, but in other relationships” all of which would be hard to quantify. Now that it is easy it is a better variable for revealing genetic differences.
    Similarly with obesity. Prior to 1830 food was sometimes scarce and restricted in quality for the poor. By 1920 things were better, and after 1980 even better, with more variety and much lower real costs. An 800 gram loaf of bread can be earned in 5 minutes on the average wage. So, weights increase.

  42. Bruno says:
    @Polymath

    I have just received the book but not opened it yet.

    I understand that there are macro environmental effects (time and place) – That are obvious for stature – that are quite outside of the score of the individual reach.

    So the thesis would be weight is 50% genetics, 20% due to the country and time where you live and the rest is mostly random. That don’t give people much hope for a positive action. That would explain why most diets are useless for most in medium term (5 years without relapse)

  43. So genes are most important in life outcomes where the environments (in which the population you’re studying exist) are relatively equal. And the more equal the environments, the more important the genes.

    (I wouldn’t diss private schools – while the education may not be that much better, though it is definitely better, the peer group is the thing if you have an easily influenced child. If you can find a state school where the “cool kids” and the sporty ones still think its OK to study and get good grades, you’ve hit the educational sweet spot.)

    PS – it wasn’t THAT difficult to divorce then (happened in my working class family), but it was very definitely fault-based and came with a lot of negative social feedback – enough that the guilty party would usually move elsewhere.

  44. MissLucy says:

    There’s really nothing new here. The Bell Curve, The g Factor: The Science of Mental Ability, and other books have already discussed all these topics.

  45. Ben Gunn says:

    What about Barbara McLintock’s Nobel for proving environmental factors?

    She identified two new dominant and interacting genetic loci that she named Dissociation (Ds) and Activator (Ac). She found that the Dissociation did not just dissociate or cause the chromosome to break, it also had a variety of effects on neighboring genes when the Activator was also present, which included making certain stable mutations unstable. In early 1948, she made the surprising discovery that both Dissociation and Activator could transpose, or change position, on the chromosome.[43][44][45][46] – Wikipedia

    • Replies: @Peripatetic commenter
  46. @res

    I do not sneeze at Von Neumann’s achievements! I simply meant that they had not had widespread impact in a cultural sense. All his contemporaries were amazed that he was not better known.

    • Replies: @res
  47. Thank you, Dr. Thompson, (I think) or at least Dr. Plomin should thank you. Yours is the first review that has made me want to buy and read the book with the expectation of finding more than a rehash of the nature/nurture debate.

  48. dearieme says:
    @Santoculto

    I used to cycle everywhere but I still became fat – not as fat as an American perhaps but distinctly – ahem – burly. Now I can’t cycle; nevertheless I have lost weight. It might, I suppose, be that I am suffering from an undiagnosed cancer, but maybe it’s because I have changed my diet, especially at breakfast, away from carbohydrates and towards meat, fish, eggs, and cheese.

    • Replies: @Santoculto
  49. Anon[340] • Disclaimer says:

    Apparently Robert Plomin is a now being smeared as a white nationalist, according to RationalWiki: https://rationalwiki.org/wiki/Robert_Plomin

    • Replies: @res
  50. Agent76 says:

    This is a great view on how we develop.

    Nov 14, 2011 Conception to birth — visualized

    Image-maker Alexander Tsiaras shares a powerful medical visualization, showing human development from conception to birth and beyond.

  51. res says:
    @James Thompson

    Ah, in a cultural sense. Agreed with that.

    Claude Shannon is another good example. I think he is even less known than von Neumann (e.g. does not even appear in Murray’s book), but did some important work. https://en.wikipedia.org/wiki/Claude_Shannon

    • Replies: @James Thompson
  52. res says:
    @Anon

    This is interesting.

    he is a practitioner of racial inexplicitness, the tactic of advancing racist policies without directly mentioning race.

    Thoughtcrime! I wonder how they define “racist policies”?

    From the page of the user who created that hatchet job. Can this serve as the goodthinker’s credo?

    We critics of biological determinism are like members of a fire brigade, constantly being called out in the middle of the night to put out the latest conflagration, always responding to immediate emergencies, but never with the leisure to draw up plans for a truly fireproof building. Now it is IQ and race, now criminal genes, now the biological inferiority of women, now the genetic fixity of human nature. All these deterministic fires need to be doused with the cold water of reason before the entire intellectual neighborhood is in flames.

    - Richard Lewontin, Steven Rose, and Leon J. Kamin, Not in Our Genes

    At least they identify the strawman right up front: biological determinism. I must be a goodthinker since I don’t believe in that either.

  53. LondonBob says:
    @Polymath

    They do something to the food, when I moved to Russia I lost a stone within a month or two. The food manufacturers need to be looked in to.

    • Replies: @AnonFromTN
    , @Sam J.
  54. notanon says:
    @Polymath

    some of the environment effects may also be genetic but indirectly

    for example say you have a population who are genetically better adapted to processing fat than processing carbohydrates due to their ancestral diet but then due to environmental factors they switch from a moderate fat, moderate carb diet to a low fat and high carb diet.

    another example might be a connection between depression and lack of sunlight – say a farmer with those genes isn’t effected because he is outdoors a lot and one of his sons follows suit and also isn’t affected but a second son gets a job in an office with long hours with only artificial light or a job working nights and as a result has recurring problems with depression.

  55. Many things make us what we are. DNA is one of them, but not the only one.
    That’s true for all social animals, not just humans. Some might remember debacle in South Africa, when they tried to transport elephants to a new place and found that young males pushed from the herd by the matriarch become aggressive, destructive, and don’t even do the right thing with females. Finally, they figured that you need some older males to teach young males correct behavior.

  56. @LondonBob

    The same thing would happen if you move to continental Europe. I think it’s simple: if you eat real good food, you feel satiated for a long time. In contrast, if you eat crap like fast food, you feel full right after the meal (with enormous number of calories), and then want to eat again in an hour or so.

    • Replies: @LondonBob
  57. notanon says:
    @Anon

    If you’re past a certain age, and you’ve never successfully lost and kept off weight, it’s not going to happen for you.

    it might if *what* they eat is as important for their individual genetics as how much.

  58. notanon says:
    @Sanguinius

    It seems clearly to be their religious teachings and the influence of their communities and their own expectations about how to live.

    no birth control is an environmental factor

    it seems genetic desire for children may have been quietly selected *against* during the centuries women didn’t have a choice.

  59. That something is inherited does not mean that it is “genetic.” All cells in the body have the same DNA, but cell differentiation occurs. Therefore DNA is not the cause of cell differentiation. So any trait that can be traced back to differences on the cellular level is not in the DNA.

  60. notanon says:
    @prime noticer

    if environment doesn’t matter much, why the HUMONGOUS swing in fertility rate?

    birth control

    in an environment where (since farming)
    - women had little choice over sex
    - little control over pregnancy
    - high child mortality
    - high childbirth mortality
    it seems to me *lack* of desire for sex and children might be selected for to compensate until it balanced the risks at the point of replacement level reproduction.

    so then when you change those factors the genetic desire for children is no longer in balance?

    maybe its possible to model those factors in some way to estimate the reproductive “g” factor?

    (it would be interesting if late-weaning HGs had a different balance point?)

  61. @res

    Interesting. Shannon was a big name in my psychology course, and I assumed everyone knew about him and his impact on communication theory. Perhaps it was simply that his work was highly relevant to psychology and, even more important, within my span of comprehension. Perhaps the attraction of Einstein is that people can imagine they understand him, and that they know his formula, if not the units in which it is formulated.

    • Replies: @res
  62. res says:
    @James Thompson

    I did not know Shannon’s work was so relevant to psychology. Could you expand on that a bit?

    I think you are right about that being part of Einstein’s popularity. I think some other parts are:
    - Catchy story about “just a patent clerk.”
    - His appearance works with the mad scientist stereotype.
    - The Einstein–Szilárd letter: https://en.wikipedia.org/wiki/Einstein%E2%80%93Szil%C3%A1rd_letter

  63. @Polymath

    Everyone is making this very simple concept – genotype by environment interaction – far more complicated than it needs to be.

    Here’s the best and simplest example:

    1) If no one smokes (or lives in Beijing) lung cancer will be extremely rare.

    2) If everyone smokes like a chimney, many people will get lung cancer but many will not. This is primarily due to genetics.

    So lung cancer can be genetic or environmental, but in a society where some people smoke and some do not it’s both genetic and/or environmental. BTW: my grandmother smoked every day since she was 14 and sailed past 90 in good health. She only died when her appendix burst in her mid-90s and she ignored it.

    Same thing for obesity. If we all ran around like hunter gatherers eating nothing but wild game meat (including the organs) and wild fruits and vegetables, and occasionally went a day without eating, pretty much everyone would be thin. Humans, in our ‘natural’ environment, are naturally thin. Even the Eskimos – the fattest hunter-gatherers – were lean by American standards.

    Just like smoking. You introduce the Western diet and some people have the genetics to handle it while others do not. Also, some groups – those that have a long history of agriculture – will handle it better than others. That’s why Chinese and French people are less likely to become morbidly obese on the Western Diet compared to Plains Indians. (To be fair, the Western Diet still makes plenty of French and Chinese fat).

    I’m a typical Caucasian – neither fat nor thin on the typical Western diet. However, I’ve learned that if I want to stay relatively lean past 40 I need to do intermittent fasting – usually a 7/17 daily schedule. (I tried Paleo, and it works, but I just don’t have the willpower to stick to it long term).

    • Replies: @Santoculto
  64. notanon says:

    one thing to bear in mind is some people have a craving to fix things and as a result don’t like genetic determinism so it’s worth mentioning to those people

    1) the fine details of genetic effects e.g. relating to diet, sunlight, allergies etc may fix some problems so more research will likely yield more benefit than making that research taboo

    2) the environment selects for genes so average IQ can be changed, propensity to stab people can be changed, time preference can be changed, pit bulls can be turned into sheep dogs etc but only through selective breeding over multiple generations and voluntary selective breeding can be encouraged by telling the truth or manipulated through public policy (for example by locking up stabby people for longer to handicap their reproduction).

    3) elites *will* be doing this so if liberals don’t want a caste society carved in genetic stone they will have to accept and adopt egalitarian eugenic policies i.e. lifting up the bottom half of the population and not just the top.

  65. Are we not certigying the obvious? Any dog breeder, or owner, can tell you that intelligence and personality are very largely genetic.

    “Success and failure – and credit and blame – in overcoming problems should be calibrated relative to genetic strengths and weaknesses.” This is very good news for racial apologists. Before, they said that a black rapist did it because of his childhood, oppression, and so on. Now there is rock-solid scientific evidence that he was largely predestined genettically, with a bad childhood for an increaded discount. If a genetic analysis shows that he is fifty percent predestined to offend, does he get half a normal sentence? It sounds like a Get out of jail free card. And do we do jury selection by geneitc heritability of vengefulness against empaty?

    • Replies: @JLK
    , @Anon
    , @utu
  66. JLK says:
    @Frederick V. Reed

    You are correct that it raises a lot of policy questions. Better to make policy based on the facts than on myths, though.

  67. Anon[884] • Disclaimer says:
    @middle aged vet . . .

    Yours is one fascinating post.

    The variables are infinite. It could also be that Von Neumann, even if he was set in the same place and time as Einstein, would still have focused his mind on less “central” issues.
    I believe a 1-in-a-million mind tends to disregard what looks “central” to the others (= seek personal fame) more than a 1-in-a-hundred-thousand mind.
    There are also things that a 1-in-a-million mind may be unable to grasp, whilst a 1-in-one-hundred-thiusand may.
    Mental rarity is multi-dimensional. I am a subscriber to the theory of G (general intelligence) but its truth doesn’t imply there isn’t an unkown number of unknown and unknowable other factors at play.

    I also believe, moving on to the Bach/Beethoven/Mozart/and quite some other ones issue, that today the opportunities in that sense are way more. Today an Internet connection and a service like Spotify or Google Music or iTunes gives the potentially musical genius the chance to hear and learn of everything done in music.

    So it’s not opportunities. And I don’t know what it is.

    As for the “general willingness to declare everybody equal”, this is a more-than-one-layer thing.
    Social objectives (going from the bare wish to not be assaulted by one’s neighbours) compel to show one’s belief in equality (or equivalence) of skill.
    Then, the averagely strong-minded person will spare themselves a lot of cognitive load believing, on a conscious level, that they believe what they in truth feign to.

    And then there is the subconscious or unconscious, where, of course to different degrees of clarity, everyone knows “the truth” about inter-individual, and intergroup, differences in cognitive skills and other attributes.
    Genetics would, in any event, fall short of explaining everything.

  68. Anon[884] • Disclaimer says:
    @Frederick V. Reed

    The obvious is always what can’t be said — hence there is some merit in certifying it, I’d say.

    As to get-out-of-jail free cards, you reason as if people were to be imprisoned for the sake of administering punishment to them. It seems to me that in our time they are imprisoned to prevent them from committing other outlaw actions (outlaw actions being the sort of crimes a wide enough majority of people have evolved past committing, thus want to be outlawed. Offences a high enough number of people still want to commit are safe from being outlawed, of course, as are they from being labeled crimes).

  69. @dearieme

    Well, remember that there are somatotypes isn’t*

  70. @Anonymous Jew

    I thought the fundamental difference is not be thin or fat but musculous or flaccid because somatotypes.

  71. still no explanation on how in only 50 years a growing and self reproducing system got set on a course to extinction within the next couple generations?

    what changed in the genes in only 50 years to make europeans go from a growing population expanding across the entire planet, to a rapidly shrinking group outnumbered everywhere and about to disappear?

    what say you, plomin? little to no effect from environment? somebody activated the self destruct gene?

    or could it be that rapidly shrinking living space, steadily increasing economic cost of child birth, turning half of all european women into fat asses covered in tattoos and with purple hair, and most european women being coached and instructed into seeing relationships as combat instead of as partnerships, could be…the explanation? and NOTHING AT ALL to do with genes?

    yeah. environment still a HUGE factor.

    at this point probably better to look at biology as the field with more explanatory power. bacteria, viruses, cancer cells, growing in a petri dish, fed with oxygen and glucose, and observing their colony sizes over time, versus other competing colony sizes.

  72. @James Thompson

    I agree that genetics accounts for the greatest part of environmental influences.

    My people ( Eastern Europeans) peasants before 1800 and now still subject to those genes. Obesity can be overcome but one has to fight the farmer gene in very strong terms. Easy access to large quantities of food will destroy the weak of spirit. Vigilance must be a 24 hour a day job. The donuts and Whoppers/Quarter pounders are always there in out environment.

    In our age we need to invent ways to keep up the good fight.

    • Replies: @utu
    , @Anonymous Jew
  73. @Ben Gunn

    You appear to be talking about plant genetics.

  74. utu says:
    @Johan Meyer

    The Wilson effect might be driven more by DZ twins divergence with age rather than by MZ twins convergence with age in the Falconer’s formula: H^2=2(r_mz – r_dz). It is not that the correlation r_mz is increasing but r_dz is decreasing.

    I do not believe in the explanation for the Wilson effect that genes express themselves more with age . I think it is the opposite. It is rather the effect of cultural indoctrination because the choice offered by culture are much narrower in adulthood than in childhood. The culture imposes the corset not genes. Lower heritability in young age has more to do with noise in IQ testing. Children can’t repeat the same task as well as adults so IQ test of adults will be less noisy and that will increase correlation.

    • Replies: @Johan Meyer
    , @phil
  75. utu says:

    30 million rungs differ. Each difference in rungs is a SNP (snip) and we each have 4 million personal snips. The UK population has about 10 million SNPs.

    If “4 million personal snips” and “UK population has about 10 million SNPs” what is the lowest number of SNPs two people must or do share?

    • Replies: @James Thompson
  76. utu says:
    @Frederick V. Reed

    It sounds like a Get out of jail free card.

    No, it does not. You do not repair faulty machine for ever, you send them to a scrap yard. In the world of IQism we are all machines. Though penalties, moralizing, guilt tripping and shaming may still work for some machines just like putting software patches in some computer. Machines are better when running the software not believing they are machines. You will see what will happen when the IQists will finally succeeded convince Afro-Americans they are inferior machines. Machines who run the software believing they are machines are more deadly to other machines. The IQsts run software believing they are superior machines.

    • Replies: @HallParvey
  77. utu says:
    @europeasant

    Vigilance must be a 24 hour a day job.

    How do you sleep?

    • Replies: @europeasant
  78. Sparkon says:

    Aspartame, Splenda and other artificial sweeteners in our food and beverages not only impair the body’s ability to digest food properly, but also suppress the satiety signal so that no matter how much one eats, the hunger never goes away, and some folks just keep on eating.

    These poor souls must be eating all the time to accumulate the truly astonishing layers of fat I see these days on some of the morbidly obese, who cannot even ambulate on their own two feet at the grocery store, and instead must rely on motorized fatty wagons carts to get around the aisles to do their shopping.

    I suspect many academics don’t like simple answers because they can’t get a grant for that, nor can they drag out their research for years, but for people simply wanting to lose weight, I suggest first lose the diet soda.

    There are many scientific studies showing correlation between aspartame consumption and weight gain, both in lab rats and in run-of-the mill humans, and obesity is not the only possible repercussion from drinking diet soda.

    But mouse experiments now suggest that when aspartame breaks down in the gut, it may disrupt processes that are vital for neutralising harmful toxins from the bacteria that live there. By interfering with a crucial enzyme, these toxins seem to build up, irritating the gut lining and causing the kinds of low-level inflammation that can ultimately cause chronic diseases.

    “Our results are providing a mechanism for why aspartame may not always work to keep people thin, or even cause problems like obesity, heart disease, diabetes and metabolic syndrome,” says Richard Hodin at Massachusetts General Hospital in Boston.

    New Scientist: Why diet drinks with aspartame may actually help make you fatter

    • Replies: @AnonFromTN
    , @HallParvey
  79. @James Thompson

    I agree with you about twin studies, I saw a few where the authors bungled simple logic, and I was rude, and than I apologized after I heard about twin studies that did not bungle simple logic. There is a lot to be learned from twin studies.

    Galton may have said the one in ten thousand thing first, but the first place I heard it was at Steve Hsu’s weblog.

    And yes, I did mean exactly this – there are hundreds of musical young people who could, probably, today, rewrite most — or at least some — of Mozart’s best works, for example, but who can’t, because the beautiful music has been written. (the fruit has been harvested … true …. maybe sad but true …. but, sad or not (and maybe not))…. true ….

    I don’t feel sorry for them, though, the young musical one in ten thousand geniuses of today —- who would not want to be someone like Mozart, with a seven or eight decade life expectancy, in the 21st century —- even if being the person most genetically similar to Mozart today merely means you get to go to school on full musical scholarship, that you get to attract everyone of the opposite sex who is attracted to musical genius, and that you get to avoid all those diseases that killed people so young, back in Mozart’s day?

    Even I, no musical genius, have had the great fortune to listen to most of the great works of Mozart in many different decades. One wonders, sometimes, if Mozart, before he was born, would have chosen (a) being Mozart for just 37 years or (b) being someone who loves music and who got to listen to the works of Mozart for 70 or 80 years or more …..

    Seriously, I have heard the word “graphene” many times, but I have no idea what it really means. I have no illusions – if there are people in this world who will find a great use for graphene, then I am not one of them —- and, a fortiori, if there are no such people, I am still not one of them.

  80. @utu

    My issue with res and EOWK is that I derived formulae for the MZ and DZ cases in terms of the genetic variance, environmental variance, and genetic-environmental covariance, in a letter that I sent to EOWK amongst others. The correlation formulae take the definition of correlation as the ratio of covariance to variance (products of standard deviations, but the two standard deviations are equal). Consequently, as the genetic variance increases (variance increases with age, and it is a fair guess that in developmental standards, the variance is almost exclusively genetic), the MZ and DZ correlations become closer to full heritability.

    The formulae can be split up (MZ and DZ environmental variances no longer equal) to model the monochorionic placenta effect (a bit simplistic, but not too far off). Then direct genetic causation can account for the Wilson effect in weight (too well—one gets a better growth in MZ correlation than what is found in the experimental Wilson effect data), and a portion of the length data (the Wilson effect is larger than what would be expected on the basis of increasing genetic variation with age). The shared environmental variance of the DZ twins is diluted in the increasing half genetic variance, and it thus reduces. The algebra is trivial, after the derivation is done.

    • Replies: @utu
  81. @utu

    I was aware I had probably summarized too much! Best to read the whole chapter, but pg 113 top paragraph says:

    “You and I have about 4 million SNPs but many of those are present only in a few people, which means that we do not have the same 4 million SNPs. There may be as many as 80 million SNPs in the world. Any particular population – the UK for example – has about 10 million SNPs. The rest of this book focuses on SNPs, because they have played a central role in the DNA revolution”.

    • Replies: @for-the-record
    , @utu
  82. @utu

    You will see what will happen when the IQists will finally succeeded convince Afro-Americans they are inferior machines.

    Shocking as it may seem, perhaps there are other elements to life’s competitions than I.Q.
    And, in the end, the only thing that counts is who shows up for the next generation.

  83. @Sparkon

    You have to be sensible using artificial sweeteners. I use some of those (BTW, Stevia comes from a plant, so in a way it is natural) for my taste buds plus a pinch of real sugar for my glucose receptors in my morning coffee. Works fine.

    In general, there is a conservation law. If you eat more calories than you spend, the difference is accumulated as fat in your body. As most of us don’t have enough time to burn more calories (nature made us pretty efficient, as excess food was never a problem in the wild, so a full hour of exercise rarely burns more than 400 calories; see https://www.mayoclinic.org/healthy-lifestyle/weight-loss/in-depth/exercise/art-20050999), just eat less, and your weight will be in the normal range. You can find that range (in kilograms or medieval pounds, your choice) on the internet (e.g., here: https://www.rush.edu/health-wellness/quick-guides/what-is-a-healthy-weight).

    • Replies: @dearieme
  84. @Sparkon

    I suspect many academics don’t like simple answers because they can’t get a grant for that, nor can they drag out their research for years, but for people simply wanting to lose weight, I suggest first lose the diet soda.

    Bingo.
    This is the primary reason for any disagreement with the findings of this and other original works by people who find heredity to be the cause of most things of importance.

    The female body has evolved to make babies. This process causes the body to prepare, at a certain age, for the happy event by accumulating energy stores, i.e. fat, and is therefore a part of natural processes. Disruption in creating babies, for example, birth control pills, does not interfere with the bodies accumulation of energy stores (fat) in preparation.

    Male bodies, as well as female, accumulate excess fat by sitting. Modern jobs requiring eight hours each day sitting at a desk are an important reason for so much excess fat.

    All that said, there are genuinely large people. Still, strictly hereditary.

  85. @James Thompson

    “There may be as many as 80 million SNPs in the world.”

    How does this relate to the “30 million rungs [that] differ”?

  86. 30 million rungs that can differ in 4 ways. Can, but do not have to differ, so the 80 million actually found is smaller than all the combinations which might be possible.

  87. dearieme says:
    @AnonFromTN

    “the normal range. You can find that range … on the internet”. What do you mean by “normal”?

    • Replies: @AnonFromTN
  88. @dearieme

    That’s the term physicians use, as opposed to overweight and obese. They go by BMI, which should be (according to them) below 24.9.

    • Replies: @dearieme
  89. @europeasant

    See my post above and look up intermittent fasting.

    Sincerely,
    -Anonymous (but thin) Jew, descended from many fat Jews

  90. phil says:
    @utu

    Heritability increases with age for other traits besides intelligence.

    IQ tests are less reliable in the case of young children, but this “noise” is largely gone by age 8, on average.

    Systematic environmental factors may be quite important until the end of adolescence. “Culture” is “narrower” during childhood, and to some extent during adolescence, in the sense that the young person’s interaction with people is dominated by family interactions, especially with parents.

    Plomin is the best there is at highlighting the role genes may play in shaping the environment, including socioeconomic status. Note also his frequent use of studies comparing one-egg twins vs. two-egg twins, whereas studies of identical (one-egg) twins separated near the time of birth (and put up for adoption) are often criticized for downplaying the “restricted range” of adoptive families; adoptive families tend to be middle-to-upper income families.

    Nevertheless, even when lower-income adoptive families have been part of a study of one-egg twins (France), and even when twins are tested for cognitive ability before the end of adolescence (gsce scores in the UK), heritability estimates are typically above 50%.

    The most important environment effects in adulthood concern “non-shared environment,” which is, as Plomin emphasizes, very idiosyncratic.

  91. utu says:
    @James Thompson

    Thanks for the answer.

    Genetic distance between two individuals can be defined as the number of SNPs they do not share. Then for any individual one could calculate the average distance to the rest of the world. Then for the whole world population we could order individuals from those who have the highest distance to the world to the individual with the lowest distance. One could make a histogram. Somewhere out there there is an individual who is the least similar to the rest of us.

  92. utu says:
    @Johan Meyer

    Any derivation of Falconer’s formula requires making several assumptions that can’t be verified whether they are valid or not, so the errors can’t be estimated. The biggest objections to heritability derived from this formula is that MZ twins evoke more similar environment responses than DZ twins. The objections is legitimate and there is no known correction.

    Recently Jay Joseph, well know critic of twin studies wrote a paper on MISTRA.

    https://www.madinamerica.com/wp-content/uploads/2018/11/Twenty-Two-Invalidating-Aspects-of-the-MISTRA-by-Jay-Joseph-Full-Version.pdf

    This is about twins separated at birth. He finds anomalies when looking at MZ and DZ twins.

    • Replies: @Johan Meyer
    , @Johan Meyer
  93. @utu

    “How do you sleep?”

    Very well, thank you.

  94. dearieme says:
    @AnonFromTN

    Fair enough, but when I once asked a doctor whether he used “normal” to mean ‘common’ or ‘usual’, or instead to mean ‘desirable’, he just goggled. It had never crossed his mind that the term is ambiguous.

    As for “normal” BMI, it’s a fraud. You have to explain why the “normal range” was once 20 – 27.5 and then – shazam! – it was suddenly 18.5 – 25. You have to explain why there can possibly be a desirable range that is the same irrespective of age, sex, and race.

    In particular, you have to explain why people in late middle age and older (i.e. the people most at risk of death) live longer if they are overweight or mildly obese. “Normals” do worse, and the underweight do much worse.

    BMI supports fake science. It’s very easy to believe that there are extremes of fatness that are life-threatening. But to believe any good will come of trying to bully non-fat people into feeling guilty about their weight is dangerous tripe – a pagan cult of healthism that ignores the mortality statistics.

    • Replies: @AnonFromTN
  95. @dearieme

    You make a valid point: the fact that the “norms” change shows that they are arbitrary. However, purely biological perspective suggests that nature did not design us for being overweight or obese: excessive weight increases the probability of having diabetes, high blood pressure, heart problems, and so on. Just seeing seriously obese people walk tells you that being obese is not normal. But you are right: there are no magic numbers, every correlation describes a continuum, rather than a threshold thing. Not to mention that “normal” weight, just like “normal” blood pressure, is different for every individual. I’d say if you feel comfortable going about your usual activities, your weight is OK for you, no matter what the “norm” tables say.

    • Replies: @Peripatetic commenter
  96. utu says:
    @phil

    (one-egg) twins separated near the time of birth

    Because of change of adoption philosophy and policies separated at birth twins are hard to come by. In general the study of twins is limited because samples are small. So I wonder why we do not see studies of parent children correlations from which one easily obtains the narrow sense heritability using the Breeder’s equation? The narrow sense heritability is Breeder’s equation’s slope. I could imagine one could make arbitrarily large samples and measure correlations at different children ages. The few studies I saw report 0.35-0.44 correlations for IQ and about half of it for children given for adoption. Could the narrow sense heritability tell us something?

    • Replies: @AnonFromTN
    , @phil
  97. @utu

    Every scientist knows that correlations do not prove cause-and-effect relationship. To make it simple: the fact that I see the same red Honda when I drive to work does not mean that it is there because I drive to work.

    • Replies: @utu
  98. phil says:
    @utu

    Studies that separate out narrow-sense from broader-sense heritability are well-worth doing in their own right.

  99. Art says:

    First a very interesting article — Thanks!

    Hmm – are the anti-social behaviors of lying, dishonesty, and greed – genetic traits? Is the capacity to ignore an obvious intellectual truth a genetic trait? Can an environmental social order be generated that promotes these negative genetic traits? (Hmm – how long does it last?)

    Is integrity a genetic trait?

    Clearly, the beauty and simplicity of intellectual truths are valued by the human mind. Can this integrity trait be cultivated by humanity? Can integrity, push and push humanity into an ever lasting forever?

    Isn’t this gene already being cultivated and fostered by Christian Western culture?

    Think Peace — Art

    • Replies: @phil
    , @Santoculto
  100. phil says:
    @Art

    But what if Christianity was a hoax, or at the very least, a colossal misunderstanding?

  101. @AnonFromTN

    Up until very recently obesity was not a problem for the majority of people.

    Selection thus could not select against obesity so our genes have few defenses against it.

  102. @phil

    Doesn’t really matter. Each culture has cultural items that are illogical or simply wrong.

    Their value is that most people born into that culture adhere to them and over long periods of time they develop genetic support for accepting/believing them.

  103. @utu

    Some DZ IQ correlations were published:

    https://www.ncbi.nlm.nih.gov/m/pubmed/1864898/

    Are these from another group? Is there evidence to suggest great variation in DZ IQ correlations? While I find the self-selected environment concept intellectually deficient, genetic susceptibility to environment will produce a mathematically similar result.

    The group that he attacks at least acknowledges that the ACE heritability model implies an algebraic connection between the genetic fraction of variance and heritability per their model. Taken literally, EOWK and res’s objection to my model for producing a Wilson effect, constitutes a rejection of such a relationship, hence my dumbfoundment.

    That is, whatever the reality of the accusations of research misconduct that you link, I am much closer in my interpretation of twin studies to them than are res and EOWK, if I am to take the latter two’s argument against my Wilson effect model at face value.

    • Replies: @utu
  104. @phil

    Note also his frequent use of studies comparing one-egg twins vs. two-egg twins, whereas studies of identical (one-egg) twins separated near the time of birth (and put up for adoption) are often criticized for downplaying the “restricted range” of adoptive families; adoptive families tend to be middle-to-upper income families.

    However, all that would tend to indicate is, based on the data, being adopted by smart parents cannot improve your IQ above what your genes specify, while the jury is still out on whether being adopted by dumb parents would reduce your IQ below what your genes specify.

    • Replies: @phil
  105. Art says:
    @phil

    Art: Isn’t this (integrity) gene already being cultivated and fostered by Christian Western culture?

    Phil: But what if Christianity was a hoax, or at the very least, a colossal misunderstanding?

    IT makes no difference if Jesus lived or not – it is the empathic story that lives on in Christian Western culture that matters.

    I personally believe that he did live – but if not – I’m still better off for the story.

    The honesty and integrity fostered by Christian Western culture has slowly increased humanity’s lot.

    Think Peace — Art

    • Replies: @Santoculto
  106. phil says:

    The Church did act aggressively to limit cousin marriages. In 1075 Pope Gregory VII declared that the Church owed its allegiance to God and not Kings. There were competing courts and legal systems. Gradually, conflicts were resolved more and more via abstract rules rather than armed conflict or threats of excommunication. King John signed the Magna Carta in 1215, thus limiting his power and recognizing individual rights. A legal framework for capitalism was evolving. Out of its surplus earnings the Medici family in Florence funded artists and scientists.

    The Church definitely played an important role.

    But an endless number of the paintings concerned a crucifixion. A guy from the Middle East who was nailed to a cross.

    When is Ron Unz going to do an article exposing that story?

    • Replies: @AnonFromTN
  107. utu says:
    @Johan Meyer

    I do not know what you are talking about.

    • Replies: @Johan Meyer
  108. @Art

    Belief in witches is part of christian genetic background*

  109. @Art

    You have very little knowledge about your own history…
    Expected from whitey…

  110. LondonBob says:
    @AnonFromTN

    I eat a healthy diet though, there was no change in lifestyle and eating habits.

  111. “A blueprint is a plan. It is obviously not the same as the finished three-dimensional structure – we don’t look like a double helix. DNA isn’t all that matters but it matters more than anything else put together in terms of the stable psychological traits that make us who we are. ”

    True for things uniquely biological (and even then there are variances anomalies because even the best laid plans of DNA can get way laid by environment).

    As to impact guarantees to other aspects of living:

    personality, intelligence, emotions., attitudes, wealth, etc. — the case is very dodgy to say the least.

    • Replies: @notanon
  112. utu says:
    @AnonFromTN

    Every scientist knows that correlations do not prove cause-and-effect relationship.

    Unfortunately not every scientist knows how resist repeating trite cliches.

    One does not have to establish casualty to build predictive models. Correlation between twins just states that traits of one twin are a good predictors of traits in the second twin. Why is it so is entirely different story.

    In the case of the Falconer’s formula when deriving it one uses the following assumption that there is some variable X which MZ twins share and DZ twins share only 1/2 of it. The derived formula expresses the variance due to X in terms of correction between MZ twins and correlation between DZ twins.

    This leads to a possibility that one could construct a predictive mode of IQ based on variable X that would explain H^2 percent of variance. So far predictors built on DNA were able to predict no more than 1/7th-1/8th of what Falconer’s formula promised.

  113. @utu

    The definition of heritability is the fraction of variance that is genetic. I derived the MZ and DZ twin correlations, on the assumption that their means and standard deviations of both the environmental and genetic components are the same for MZ and DZ twins. When using the Falconer heritability equation, using my derivation, one obtains heritability (wide sense) as the fraction of variance that is either genetic or covariance of genetic and environment. Thus my derivation accords with the usage of the group, that the paper to which you link attacks. To wit, I am doubtful, allowing for the existence of the effects that they (your author or authors) claim, that it would radically alter the understanding—at best, if the twin correlations given in your link are in fact what they found, it could be an effect of small sample size, or ironically, a consequence of the deprivation (selection for large environment) that they identify with the twins reared apart.

    Once one allows that heritability (hence difference between MZ and DZ twin correlations) increases as the genetic variance fraction increases, it becomes obvious that there are two ways to achieve the Wilson effect (increasing heritability with age), namely by decreasing the environmental variance (regression to genetic setpoint) or increasing genetic variance (age-relevant or growth-proportional standard deviation). My argument boils down to the that the second is as possible as the first.

    Only after that need one notice that genetic variation in environmental effect (e.g. uptake) works almost as well as direct genetic variation in increasing the genetic variance relative to non-genetically correlated variance—which might be necessary to make regression to genetic setpoint unnecessary in the length case, but not in the weight case (where increasing apparent genetic variance is already more than adequate to produce the Wilson effect). Of course, the regression to genetic setpoint versus increasing genetic variance should be an empirical question. All that is needed prior to empirical work is mathematical clarity.

    • Replies: @utu
  114. utu says:
    @Johan Meyer

    “The definition of heritability is the fraction of variance that is genetic.” – this definition is imprecise. A precise definition is as the variance of an univariate function of genes that minimizes the rms of residuals. The residuals however are not necessarily free of gene dependence. In other words the variance due to genes and variance due to environment not necessarily add up to 100%.

    Falconer’s formula is what it is. It calculates something. When this something is plotted against the age of twins we see monotonic increasing function. I saw some data that suggests that the increase is more due to reduction of r_DZ than increase of r_MZ which means that with age DZ twins get less alike while similarity between MZ twins stabilizes sooner.

    Perhaps you should show your formulas instead of talking about them. Link?

    • Replies: @Johan Meyer
  115. dearieme says:
    @Roderick Spode

    Thank you for the links.

    It was an easy guess to make, given that I’m half persuaded that the epidemic of heart attacks in men in middle-age and early old age was indeed an epidemic, with a micro-organism as the cause. I say “was” because it’s practically over. And the decline has little or nothing to do with diet, statins, or stopping smoking – the decline started too early and too steeply for those to matter much.

    In Britain the long increase in longevity seems to have stopped, and perhaps even reversed just a little. Maybe it’s just noise on the signal, or maybe it’s a consequence of giving people statins for decades. Who knows?

    • Replies: @YetAnotherAnon
  116. @utu

    I have not uploaded the document and supporting data, due to concerns given the current violent and ad hominem opposition to HBD. If one of the original recipients wishes to send you a copy, that would be nice *cough cough*. At any rate, a simplified (and intermediate) result is (below more):

    [MORE]

    $$\mathrm{r_{mz}}=\frac{\sigma_\mathrm{IQ_{gene}}^2+\sigma_\mathrm{IQ_{env}}^2\,\mathrm{R}_\mathrm{IQ_{env}\,twin}+2\sigma_\mathrm{IQ_{env}}\sigma_\mathrm{IQ_{gene}}\,\mathrm{R}_\mathrm{gene,env}}{\sigma_\mathrm{IQ_{gene}}^2+\sigma_\mathrm{IQ_{env}}^2+2\sigma_\mathrm{IQ_{gene}}\sigma_\mathrm{IQ_{env}}\,\mathrm{R}_\mathrm{gene,env}}$$

    $$\mathrm{r_{dz}}=\frac{\frac{1}{2}\sigma_\mathrm{IQ_{gene}}^2+\sigma_\mathrm{IQ_{env}}^2\,\mathrm{R}_\mathrm{IQ_{env}\,twin}+2\sigma_\mathrm{IQ_{env}}\sigma_\mathrm{IQ_{gene}}\,\mathrm{R}_\mathrm{gene,env}}{\sigma_\mathrm{IQ_{gene}}^2+\sigma_\mathrm{IQ_{env}}^2+2\sigma_\mathrm{IQ_{gene}}\sigma_\mathrm{IQ_{env}}\,\mathrm{R}_\mathrm{gene,env}}$$

    where $\mathrm{R}_\mathrm{IQ_{env}\,twin}$ is the intratwin pair correlation in environment (yes, this may differ for mz and dz twins, but the difference is not expected to radically alter the estimate of heritability), and $\mathrm{R}_\mathrm{gene,env}$ is the gene-environment correlation. I am agnostic on this latter quantity being meaningfully different from zero, and my suspicion is that much of $\sigma_\mathrm{IQ_{gene}}^2$ is really genetic variance in uptake or dose response multiplied by mean dose squared (normally means do not enter correlation calculations, but in this case it would).

    Note that the heritability is

    $$H^2&=2(\mathrm{r_{mz}}-\mathrm{r_{dz}})\\
    &=\frac{\sigma_\mathrm{IQ_{gene}}^2}{\sigma_\mathrm{IQ_{gene}}^2+\sigma_\mathrm{IQ_{env}}^2+2\sigma_\mathrm{IQ_{gene}}\sigma_\mathrm{IQ_{env}}\,\mathrm{R}_\mathrm{gene,env}}$$

    or precisely the genetic fraction of total variance. Some assumptions enter this derivation, but they do not alter the heritability conclusion, as the total variance does include the gene-environment covariance.

    Also, the above formulas may contain errors, as the computer on which my files were was stolen, so I have to reenter from the pdf…

    • Replies: @utu
  117. utu says:
    @Johan Meyer

    Clearly you have a problem in the communication department. If you really wanted to share you idea you would make an effort to make it readable. End of conversation. Get lost.

  118. “One does not have to establish casualty to build predictive models.’

    No one can build predictive models along a steady set of variables. However, Correlation means just that — a steady set of variables — not a single cause, but perhaps a a cause inter-related among an array of variables.

    In this specificity is key because the claim is aimed supporting IQ, etc to one particular genetic make-up — skin color.

    So correlations would be insufficient to make the cause and effect claim x causes y. Poverty does n ot cause crime, but one can make some predictive analysis related to crime to specific neighborhoods that involve certain variables that indicate crime and poverty are related — that is not the same thing as cause and effect.

  119. Sam J. says:
    @LondonBob

    That is really interesting. It may be the particular type of gut bacteria that is expressed in US foods. Link in original post.

  120. Sam J. says:
    @Polymath

    It may well be that gut bacteria is the reason for all the “excessive” obesity. Look at these links showing the great differences if specific types of gut bacteria predominate. BIG DIFFERENCE!

    https://www.orlandosentinel.com/news/space/go-for-launch/la-sci-sn-gut-bacteria-aging-20181115-story.html

    http://stan-heretic.blogspot.com/2018/09/lactobacillus-reuteri-and-anti-aging.html

  121. notanon says:
    @phil

    what if Christianity was a hoax

    from a genetic selection point of view it wouldn’t matter

    as long as a society conferred reproductive benefits to those adopting “Christian” behavior then people who were already best adapted to that behavior would be selected for and those traits would spread.

    the unfortunate irony is a society like this would need to apply harsh sanctions on behavior that didn’t fit the ideal and this selection for “niceness” would eventually lead to the population being too “nice” to apply those harsh sanctions and so the “Christianizing” process would unravel and start to reverse.

    • Replies: @dearieme
    , @Santoculto
  122. notanon says:
    @EliteCommInc.

    personality, intelligence, emotions., attitudes, wealth, etc. — the case is very dodgy to say the least.

    dog breeding has proved all this for millennia

    the blank slate is what needs proving

    until cultural Marxists (or the people they fooled) can take 100 random pitbulls and return 100 working sheepdogs without selective breeding their entire argument is nonsense.

  123. dearieme says:
    @notanon

    If Christians were actually to read the ruddy Bible, and understand some of Jesus’s reported remarks about family, they might produce rather few offspring.

    • Replies: @notanon
  124. @notanon

    ”christianism is so nice”

    someone with no knowledge in whitey history.

    • Replies: @notanon
  125. notanon says:
    @Santoculto

    population stage A (very nasty)
    -> 2000 years of a “christianization” process with harsh sanctions (mostly nasty)
    population stage B (not nasty enough)

    • Replies: @Santoculto
  126. notanon says:
    @dearieme

    when i say Christianity i mean the set of cultural values with reproductive cost/benefit promoted by various Christian groups over the centuries which may or may not have anything to do with the bible itself (and much of which may have been pre-Christian in origin).

    i’m using “Christianity” as the label for the European version of culture based selection pressure.

  127. phil says:
    @Peripatetic commenter

    There is always more research to be done. In the French adoption research, being adopted by lower-income parents did have a negative impact, although not as much of an impact as genetic factors.
    Thus, there were substantial shared environmental effects, but the testing occurred at age 14, and typically the shared environmental effects are washed out by the time adolescence ends.

    And if being adopted by smart, higher-income parents were to have a lasting effect, why do biologically-unrelated children raised in the same adoptive family NOT have IQ scores that are correlated by the time they reach adulthood?

  128. Factorize says:

    Looks like 2019 will be the year of IQ uplift!

    Widespread media coverage has finally arrived!
    New Scientist, BBC etc.
    I suppose they wanted to wait closer until the time that they could actually show superbabies. Well superbabies should start arriving next April.

    The official birthday should be near April 8th, 2019. This would be 37 weeks since the Nature article appeared online. One concern would be the question of the phase transition barrier. What happens to the babies born on April 7th?

    This is a truly dramatic moment for humanity. All the more so as it is completely unstoppable. Parents-to-be could easily step around any restrictions placed on their right to reproductive freedom. Strategic mate choice will greatly amplify IQ Uplift. A point that is oddly absent from the learned publications commenting on the story

    • Replies: @YetAnotherAnon
  129. @notanon

    2000 years!!! So fast!!!!

    two world wars + imperalism + …. [elites which don't care about their own worker classes] = not nasty enough.

  130. @phil

    There is an Israeli joke about it.
    A guy comes to rabbi and says:
    - Dear Rabbi, I have one son, such a great boy, I had high hopes for him, but he abandoned our religion and converted to Christianity.
    Rabbi answers:
    - That’s a great misfortune. I don’t even know what to tell you and how to console you. Ask God.
    The guy asks God:
    - Dear God, I have one son, such a great boy, I had high hopes for him, but he abandoned our religion and converted to Christianity.
    The God answers:
    - I don’t know whether it would console you, but two thousand years ago exactly the same thing happened to me.

  131. Factorize says:

    Now that mainstream media has picked up on the Superbaby story, shouldn’t unz.com have a headline thread dedicated to IQ Uplift? The Genetic Singularity is no longer far off on the horizon. To knowledgeable readers it should be obvious that profound change is rapidly approaching. It is, therefore, important that informed discussion begin on this topic. Much of the current coverage does not present the story realistically. When the genie lets out a Singularity event out of the bottle, it is time for serious and
    thoughtful dialogue: Time for unz.com!

    • Replies: @AnonFromTN
  132. @Factorize

    There is hype about super-baby. However, let’s remember history: 99 times out of a hundred the hype remains just that, hype. Most likely that’s yet another snake oil.

    • Replies: @Factorize
  133. Factorize says:
    @AnonFromTN

    AnonFromTN, thank you for replying.

    The shift in tone that I am noticing with the current reporting has caught my attention. Some of these articles slip in “genes are involved in IQ” without any great emphasis. The entire conversation is transforming. The premise that Superbabies are now in process by storks is no longer even considered worthy of argument.

    Yet, the connection between IQ and genetics was fought for almost a century. It would not be entirely inaccurate to suggest that the fight at times descended to harsh words being spoken. Now it is readily acknowledged without qualification.

    We are only 4 months away from the era of genetic enhancement, denying reality any longer would clearly be dangerous for all of us. Delusion is simply not adaptive behavior considering that the children that are approaching most certainly will be of profound intellectual ability. The currently accepted lifestyle of humans needs to be abruptly curtailed. A legal upgrade needs to occur rapidly.
    How should the community now respond to a mother who chose to drink while pregnant? How could we cope with a world in which 200 IQ children with the potential to vaporize our solar system might have fetal alcohol symptoms? These questions should no longer be regarded as hypothetical.

    Fortunately global media are finally demonstrating a minimum standard of faithfully informing the public about this issue that they are legally obliged to provide. An informed conversation needs to begin as there is a great deal to discuss.

    Those who are carefully following this story unfold, typically do not regard it as snake oil. Sometimes people have seen so much snake oil, that they no longer recognize the genuine article.

    • Replies: @AnonFromTN
  134. @Factorize

    I see no reason to worry unnecessarily. Thing is, even if we assume that some babies with potential for IQ 200 are born (which is a big if), what makes you think that this event would have serious effect on human affairs? There are humans with that kind of IQ already. If there is more really smart people, there would be fewer takers for banking and business jobs, as they are extremely boring, not to mention that there is no glory or intellectual satisfaction in fooling the fools. If more smart people take up research, the humanity would benefit. If they take drugs instead, we’d remain exactly where we are. So, what’s the big deal?

  135. Factorize says:

    AnonFromTN, we are so blessed!

    This is without question THE moment of the genesis of a new human super-species. It is the start of an entirely new era of human existence. We are extremely fortunate that we will be a witness to this.

    It is all the more fortunate that the mainstream community is now being informed. The time for argument is over. IQ uplift is going mainstream! Further, the genetics of IQ is massively polygenic. This is true for all humans. IQ uplift is going mainstream and global!

    A global scale effort to optimize human genetics will introduce a powerful network force.
    Intelligence like so many other technological wonders is fully potentiated only when it is networked. Those who believe that they would be so much better off if they had it all for themselves, only have to unplug their internet connection to experience the impoverishment of a network of one. Once the entire mating pool of humanity dedicates itself to maximal IQ enhancement, the Genetic Singularity will truly be in full swing.

    It is not reasonable to expect that increasing IQ will be of little consequence. In the past even increasing IQ by a single point had demonstrable effects on humans civilization. The rise of cities,
    creation of language etc., all required an intelligence upgrade to occur. We can barely imagine what
    innovations will soon arrive after IQ is enhanced.

    Why wait? It has taken over a decade to scale up to an IQ GWAS of 1 million people. Why not scale up to a 10 million GWAS….. today? There are at least 10 million gene chip files out there. People could upload their files and then play video games to determine their IQ. I am sure there is enough supercomputer CPU out there to handle the job. There is no great reason to wait years and years when we could claim our dividend tomorrow.

    • Replies: @Santoculto
    , @EliteCommInc.
  136. An interesting treatment on why female IQ variance must be lower than male IQ variance:

    http://precedings.nature.com/documents/3238/version/1

    Read the PDF. It’s fully available.

    • Replies: @JLK
  137. JLK says:
    @Peripatetic commenter

    I theorized the same thing (two X chromosomes having an averaging effect) as to why females have a lower standard deviation than males for IQ back in the early 2000s.

    Jensen, A. R., & Reynolds, C. R. (1983) found that females have a 13.55 standard deviation versus males that have a 14.54 standard deviation.

    It has a profound effect on the male/female ratio on the extreme ends of the curve. For example, Judit Polgar is the only woman in the top 100 rated chess players of all time (a group estimated to be in the 170-180 IQ range).

    The Unz meritocracy article didn’t get into male-female ratios at the top tier Ivy League schools, but there’s no question that some type of affirmative action must be in play for women to have equal representation.

  138. @JLK

    And yet others suggest that the male mean is 4 or 5 points higher than the female mean.

    https://paulcooijmans.com/intelligence/sex_differences.html

    And then there is this:

    http://iqcomparisonsite.com/SexDifferences.aspx

    • Replies: @James Thompson
  139. utu says:
    @JLK

    females have a 13.55 standard deviation versus males that have a 14.54 standard deviation

    This suggests that the X and Y chromosomes are responsible for 14.1% of genetic IQ part of variance while remaining 22 autosomes are responsible for 86% which is 3.9% per autosome. Which means that X and Y have 3.5 times more impact on IQ that each remaining autosome on average.

  140. This suggests that the X and Y chromosomes are responsible for 14.1% of genetic IQ part of variance while remaining 22 autosomes are responsible for 86% which is 3.9% per autosome.

    Mostly the X chromosome. There are only about 50-60 genes on the Y chromosome as opposed to ~1,000 on the X:

    The Y chromosome likely contains 50 to 60 genes that provide instructions for making proteins. Because only males have the Y chromosome, the genes on this chromosome tend to be involved in male sex determination and development. Sex is determined by the SRY gene, which is responsible for the development of a fetus into a male. Other genes on the Y chromosome are important for male fertility.

    https://ghr.nlm.nih.gov/chromosome/Y

  141. Sean says:

    Deliberately absent from the discussion is any mention of genetic group differences. Questioned in an interview about this omission Plomin said “That’s the third rail” and questioning moved to other matters. Wise.

    Unwise of Plomin to say anything, no matter how oblique, to someone that published a private conversation on a subject that the author chose not to have in his book. Although his book does talk about whether there are specific group differences in heredity between the sexes, so maybe your recollection of what was said is also inexact.

    • Replies: @James Thompson
  142. @Sean

    The interview was on a public broadcast BBC program, not a private conversation. A public matter.

    • Replies: @Sean
  143. Sean says:
    @James Thompson

    Sorry, you are right, I had a Jean-Claude Juncker style breakfast and got a bit mixed.

    I wonder if the unwisdom of Plomin being drawn into using a term like the Third Rail is something he later realized was a hostage to fortune, and hoped would receive no further publicity. He got repeatedly pressed on whether telling their score could make them give up in an inteview I heard a bit of.. He says in the book that he never thought he was particularly clever and he inclines to the idea that conscientious effort is the most important trait. That kind of thing is easier to change than one’s degree cleverness.

    He says (top of p133) most SNP associations with psychological effects are found in the regions of the genome that don’t code for proteins, and thus not with genes in the traditional sense at all.

    • Replies: @dearieme
  144. dearieme says:
    @Sean

    “most SNP associations with psychological effects are found in the regions of the genome that don’t code for proteins”: let me show my ignorance. How does that work, then?

    • Replies: @AnonFromTN
  145. Sean says:

    Nessa Carey has a book on the subject and she says don’t think in terms of linear pathways, but rather (a la the trick question how many squares are there on a chessboard) interlocking processes. She ends it by saying that the research funding is being dropped so we will have a long wait. Pharma investment is in knowledge they can use to make drugs that recoup their costs, and then some.

  146. @dearieme

    Many non-coding regions of the genome, as well as introns in genes, generate large and small non-coding RNAs that regulate the production and translation of messenger RNAs. This might explain why we have so much DNA (more than 90% of which is non-coding), as well as how come we are so different from chimps, even though we differ with them in the coding regions by less than 2%.

    • Replies: @dearieme
  147. dearieme says:
    @AnonFromTN

    Thanks. In my desire to learn a bit more about genetics I once bought Jim Watson’s book “DNA: the Secret of Life”.

    Perhaps because it’s an American book it has a poor index. This struck me as droll; you can make the case that a good index should be the genome of the book.

    • Replies: @AnonFromTN
  148. @dearieme

    Yes, a good index is at least half of the worth of a scientific book. But Watson’s is more about him and the discovery of DNA than about genetics. I don’t know a good book about genetics proper (there must be some, though). If you are more broadly interested in biology, I can recommend Goodman and Gilman “The Pharmacological basis of therapeutics” that we recommend our grad students. It looks a bit scary, but it’s fairly basic (most of our grad students come from no-name colleges, so they don’t know much). If you are looking for something even more generic and mechanistic, there is Lehninger’s “Principles of Biochemistry”. Both books have very good indexes (Europeans would write indices, like Brits) and can serve as reference material.

    • Replies: @utu
  149. utu says:
    @AnonFromTN

    Could you look at the following statements and questions?

    If we have 22,000 genes that on average have 8000 bp they cover 176 million bp out of 3.2 billion bp which is 5.5%.

    We are told there are 10 million SNPs in human population. This is 0.31% of DNA. Two humans can’t differ by more than 0.31% of DNA.

    How many of SNPs are part of genes and how many SNPs are outside of genes?

    How many SNPs one gene can have? Many SNPs would imply very many alleles.

    Are there genes that do not contain SNPs? If so it would imply that there are genes that everybody must have the same version of it. Then it would no longer be interesting. It might be good to know what the gene does but since everybody has it there is no difference in population and how would one test it?

    • Replies: @AnonFromTN
  150. @dearieme

    “In Britain the long increase in longevity seems to have stopped, and perhaps even reversed just a little. Maybe it’s just noise on the signal, or maybe it’s a consequence of giving people statins for decades. Who knows?”

    Could it just be the changing demography? Asian and black people have about twice the diabetes 2 rate of Native Brits, though I don’t know if there are enough of them yet in the dying age groups. They have more heart disease and strokes too.

    https://www.diabetes.co.uk/diabetes-and-ethnicity.html

    • Replies: @dearieme
  151. @Factorize

    “Strategic mate choice will greatly amplify IQ Uplift.”

    Strategic mate choice has been around for a long time, but over the last 50-odd years it’s been fighting a losing battle as more and more intelligent women suppressed their fertility via higher education, and more and more not-so intelligent women increased their fertility thanks to the benefits system.

    • Replies: @Sean
    , @Factorize
    , @notanon
  152. @utu

    Let me state first that I am not a pro in genetics, I am a biochemist studying cell signaling. Yes, the great majority of our DNA is non-coding, but in the last few years the scientists started to collect evidence showing how these non-coding sequences affect us. There must be junk in our genome, too, like Alu repeats. We have many thousands of them covering ~10% of our genome. They might serve a purpose (genomes of all known animals have this kind of repeats), but we are not aware of it.

    From what I know, there must be a lot more SNPs than we are aware of, as people look for SNPs in and around “suspect” genes, not throughout the whole genome (remember the joke about a drunk looking for his car keys under street lamp, not because he dropped them there, but because he can see there). There are genes with virtually no variation among humans (and between species: say, one of our histones (DNA-binding proteins in the nucleus) differs by just two amino acids from its homologue in potato) and there are other genes that have a lot of variation (sometimes called hot spots). For example, parkin (PARK2 gene) responsible for a fair share of familial Parkinson’s disease, has plenty of identified mutations. Just 23 selected alleles (out of many more existing) are described here: https://www.omim.org/entry/602544. Some ostensibly equally important genes have very few SNPs, in some cases exclusively in the non-coding regions. As far as I know, there are no rules about which gene is variable and which is super-stable, we are still collecting the data.

    One thing is clear so far: in terms of genetic diversity humans are on the very low end. That’s because our species is fairly young (maybe 1-2 million years old). Older species (say, fruit fly Drosophila melanogaster) have many times more variation in their alleles.

    • Replies: @Sean
  153. Sean says:
    @YetAnotherAnon

    https://www.psychologytoday.com/gb/blog/the-imprinted-brain/201308/reading-the-mind-in-waisthip-ratios-paradox-resolved

    WHR is an accurate measure of fertility. Women with higher WHR and lower body weight are less fertile than those with the contrary indications. WHR is also a good indicator of health overall: higher WHR indicates increased risk of death in women independently of weight.

    Data from the Third National Health and Nutrition Examination Survey reveal that, controlling for other correlates of cognitive ability, women with lower WHRs and their children had significantly higher cognitive test scores. The data also suggest that teenage mothers with lower WHRs and their children were protected from the cognitive decrements normally associated with teen births. In the words of the researchers, “these findings support the idea that WHR reflects the availability of neurodevelopmental resources and thus offer a new explanation for men’s preference for low WHR.”* Indeed, the findings offer additional evidence for the heritability of intelligence from the mother…The finding that WHR correlates both with fertility and with higher IQ as conventionally measured goes part of the way towards explaining why intelligence may not have been falling in Western societies in the way in which luminaries like Russell and Fisher feared it would

  154. Sean says:
    @AnonFromTN

    Plomin says 20% of noncoding has been conserved by evolution in lower species right up to us so it is doing something vital. However he also says many of the SNP are really rare and huge studies will be needed to find them.

    The same genes produce apparently different mental disorders, transforming diagnosis and the idea that schizophrenia does not follow any clear pattern in families. So mental illness has more diversity than the genes than the genes that cause it

    • Replies: @AnonFromTN
  155. dearieme says:
    @YetAnotherAnon

    Fair question. I suspect that there aren’t enough of them in the relevant age group to explain the effect. The effect, however, is small so maybe you’re right.

    With government stats it’s impossible (I suspect) to know whether they are ever frank about race issues. I suppose They ought to start publishing trends in cause of death. Though cause of death is so uncertain compared to fact of death, I don’t know what the figures would be worth.

    Or maybe we’re seeing the accumulated effect of the dysgenics promoted by prosperity and the welfare state beginning to outweigh the effect of cheap food, clean water, effective sewerage, and vaccines and antibiotics.

    One medical writer I follow wonders whether the problem is polypharmacy – almost everyone in their eighties is taking lots of different pills.

    Personally I’d rather die quickly, cleanly, and painlessly at eighty than linger on unhappy, in pain, and unable to recognise my wife.

    • Replies: @YetAnotherAnon
  156. @Sean

    True enough. To the best of my (limited) knowledge, practically all mental disorders are multi-gene, so that associations of most individual genes with them are in the 0.1-0.2 range. This is usually statistically significant (meaning that those genes do contribute), but it has no predictive value (meaning that the sum total of other genes and environmental factors play a greater role than any individual gene).

  157. @dearieme

    “One medical writer I follow wonders whether the problem is polypharmacy – almost everyone in their eighties is taking lots of different pills. “

    On the other hand men used to die at around 68 in 1945, and around 73 in 1975 – maybe it’s the pills that are keeping them going in their 80s!

    I have a couple of nonagenarian relatives, and they certainly rattle when you shake them – one is on five different pills a day. Both far from gaga – as bright as can be in fact.

    “With government stats it’s impossible (I suspect) to know whether they are ever frank about race issues.”

    Post-MacPherson HMG started monitoring everything by race, but some stuff soon stopped being published. The 2004 homicide stats showed that for every minority killed by a white person, two white people were killed by a minority. They don’t seem to do that table any more.

  158. Sean says:

    Plomin says the polygenic score for major depressive disorder increased eightfold and the prdictive power went from 1 to 4 %. For schizophrenia the polygenic score is already more accurate than family members having it, having being bullied and other indications

    Bulmores book the Inflamed Mind says biggest association for schizophrenia is with an increased inflammatory signalling gene variant. But that is maybe a little different.

    https://www.nih.gov/news-events/news-releases/schizophrenias-strongest-known-genetic-risk-deconstructed

    https://www.nih.gov/sites/default/files/styles/featured_media_breakpoint-medium/public/news-events/news-releases/2016/20160127-graph-chromosome-6.jpg?itok=s1zFC35n&timestamp=1453912024

    Plomin says the polygenic score for schizophrenia may one day be used to predict capacity for creative thinking, and also that people with a high one should never touch cannabis in adolescence

    https://www.psychologytoday.com/gb/articles/201707/the-mad-genius-mystery
    Alexander Grothendieck Isaac Newton, Kurt Goedel, Ludwig Boltzmann, Florence Nightingale, and John Nash all attained mathematical prominence before succumbing to some type of psychopathology, including depression, delusions, and religious mysticism of the sort engendered by psychosis.

    • Replies: @utu
  159. utu says:
    @Sean

    the prdictive power went from 1 to 4 %

    Awesome!

    • Replies: @Sean
  160. Factorize says:
    @YetAnotherAnon

    YetAnotherAnon, thank you for replying.

    I do not understand why ultra-selective mate choice has been so conspicuously absent from the superbabies headlines. The implementation that they are talking about of selecting 1 embryo in 10 has been caclulated to perhaps uplift IQ by possibly 10 points. My feeling is ultramate selection would give much more than that.

    Up till now very smart couples did not have very smart children. Considering the extremely small effect sizes of the variants this is entirely as expected. Regression to the mean has been an inevitable feature of human existence until now. Yet, if careful selection of parents were to be done, then this would no longer be true. One could design children with genotypes that could never regress to the mean because they would be homozygous for high IQ on both strands of their chromosomes. The children of these children could only receive a high IQ strand from their parents. There is no restriction that government could introduce that could reasonably prevent this strategy from being used.

    There are so many implications of this development. One that springs to mind is that there probably needs to be a rush to the large scale cities. If huge mating pools are needed to fully realize the benefits of ultra selection of mates then creating such pools in culturally uniform urban environments might be needed. It surprises me how foreign people can seem if they were not raised in a very similar contexts. This similar context can sometimes even be apparent if they were not raised in the same city. Those from the rural Hinterland will be at an impossibly large disadvantage in this new scenario. There will be a whole range of variables far beyond those typically at play in IQ uplift.

    • Replies: @YetAnotherAnon
  161. Factorize says:

    There are so many foreseeable changes that should result from the emergence of superbabies.

    Delayed childbearing is probably history. The optimal strategy would be as early as possible. Those who did not choose this strategy would quickly fall far far behind in the IQ arms race.

    A truly enormous IQ gap between groups of people should be expected. Surprisingly, there are still places in the world that have minimal access to the first generation of embryo selection that was introduced decades ago. What will happen when clearly different human cognitive sub-species arise? This has been endlessly argued about on this blog. How will we manage when there is no longer anything left to argue about?

    Natural reproduction probably needs to be outlawed. The cognitive disadvantage that natural reproduction would create would be overwhelming. A mass media campaign highlighting the gross features of such procreation would be adaptive.

    • Replies: @Sean
  162. Sean says:
    @utu

    That was for variance of the liability to be diagnosed as having major depressive disorder

    The ceiling is for the score is the heritablity and a lot of things are about 50% heritable

    The polygenic scores for schizophrenia predict 7% of the liability to be diagnosed as having major depressive disorder. Those with the highest tenth of polygenic scores for schizophrenia have 15 times the chance of developing it as those with the lowest tenth.

  163. Sean says:
    @Factorize

    Maybe natural reproduction will become like being anti–vaccination, an elite cause. The elite are a cognitive elite and they keep a genetic IQ advantage through the generations as long as reproduction is kept a natural lottery for everyone. Why would they not try to ban advances that wipe out their advantage or even reverse it>

    • Replies: @Factorize
  164. Factorize says:
    @Sean

    Research has questioned the assumption that the elite are a true cognitive elite.

    It was quite startling to see how much regression to the mean actually occurs in life. In the short term there might be a significant push from those who were dealt a favorable polygenic score though a low SES, to be elevated up the social ladder. There is no great economic efficiency in having those with surprisingly low polygenic scores having higher status than those with surprisingly high polygenic scores.

    Likely the true deciding factor will be that many developing nations will have no choice but to embrace IQ enhancement. China has made it abundantly clear that they intend to aggressively pursue this technology. Given their still incomplete economic ascent it is unlikely that they could choose any other policy. Other elites, who might want to play the game of relatives, would quickly find that all this would bring them would be a hopelessly impoverished backward empire in ongoing decline against those societies that embraced the future. If we were to see this policy path being adopted in developed nations it would be a good time to head for the exits as it would be obvious that such nations had no demographic, economic or political future.

    • Replies: @Sean
  165. Sean says:
    @Factorize

    There are not rigid castes because of regression, but there is enough associative mating to make the elite’s genetic advantages in personality and IQ very real even if it is not sufficient to form a rigid ruling caste. Like Peter Turchin says, elite over production is a recipe for revolution. Even if IQ enhancement was currently available it would take a generation for those uber-humans to mature, and they will be very vulnerable to a revolution caused by elite over-production and affirmative action programs against them ect.

    Bear in mind that China also has a elite whose families would lose their ongoing dominant role, or at least much of their relative advantage, as a result of IQ and other trait genetic enhancement being allowed and resulting in swarms of super-brains from the lower orders of their society.

    I think the big effort will be in AI, that is where the competition will be between states and the sudden leaps will occur, And it will be evolution of a digital timescale vastly exceeding anything genetic enhancement is able to produce, and long before they are adults.

    • Replies: @Factorize
  166. @Factorize

    “One could design children with genotypes that could never regress to the mean because they would be homozygous for high IQ on both strands of their chromosomes. The children of these children could only receive a high IQ strand from their parents. “

    I’m not sure that’s how regression to the mean (or the fusion of the m/f chromosomes) works, though I don’t know enough about it. But I’m pretty sure two 140-IQ people mating can’t guarantee a 140-IQ child, although it’s likely to be well above 100. So you can certainly create a brighter population (with a higher mean to regress to) by breeding for it – that’s what happened to the Ashkenazis if Cochran/Harpending are correct.

    If a population over generations only marry bright people (and are bright themselves) then they’ll end up brighter than the average population – like the Darwin-Wedgewood extended family.

  167. Sean says:

    I’m pretty sure two 140-IQ people mating can’t guarantee a 140-IQ child,

    If they have 15 plus children I think they could expect to get a 140 IQ child. You would want to marry a 140 woman from a family with an excess of boys for the best chance.

  168. Sean says:
    @YetAnotherAnon

    Joshua Wedgwood was quite possibly about as intelligent as Charles Darwin, and it was his natural born craftsman, sales and business genius grandfather Joshua’s vast self made fortune that enabled Charles to think about evolution. Charles married his first cousin (double dip in the old mans money) and I think the general coupling in the familes had more than a little to do with keeping their grandfathers money in it too. Joshua Wedgwood himself had married a relative, it was all to do with money in those days. Joshua was one of eleven children his parents had. Using an argument first proposed by Darwin’s cousin Galton, Ronald Fisher suggested the most intelligent tended to marry heiresses who were necessarily less able to have many children.

    https://pdfs.semanticscholar.org/f82e/c383cdea4a10fced481405398fc69238f4e4.pdf

    Galton in his explanation for the inverse relationship between socioeconomic status and fertility: This was that intelligent and well-motivated young men rise in the social hierarchy and tend to marry heiresses as a way of consolidating their social position. Heiresses tend to come from relatively infertile stocks, because if the stocks had high fertility these women would have had brothers and would not be heiresses. The effect of this was that able men tended to marry infertile women, and so had few children. He cited data in support of his contention that fertility does have some heritability. Fisher proposed that this process has frequently occurred in the history of c ivilizations and explained their decay, and he instanced classical Greece, Rome and Islam as examples. He proposed a universal sociological law asserting that advanced civilizations are characterized by dysgenic fertility, and that this leads to genetic deterioration and ultimately to the decay of civilization.

    Nowadays, women go to university and mix with men socially and so assertive mating is much easier. Too easy perhaps,

    https://www.frontiersin.org/articles/10.3389/fnins.2016.00300/full
    Finally, Plomin and Deary (2015) point out that assortative mating is notably stronger (~0.40) for intelligence than for most other human traits, which maintains additive genetic variation for this trait as well as generating more “extreme” intelligence phenotypes than otherwise expected. Increased autism risk has been attributed by Baron-Cohen et al. (2006) to assortative mating between two individuals high in “systemizing,” and assortative mating is much high among individuals diagnosed with ASD than other disorders (Nordsletten et al.

    • Replies: @Factorize
  169. notanon says:
    @YetAnotherAnon

    and more and more not-so intelligent women increased their fertility thanks to the benefits system

    if the media told the truth about heredity women like that would choose smarter men to have babies with as they’d see it as a pension plan.

  170. Cortes says:

    Conversation with Dot (who books him) and Keller (who carries out the hits):
    “All I know,” he said, “is I had a murderer’s thumb and I grew up to be a murderer.”
    “His Thumb Made Him Do It.”
    Lawrence Block “Hit List” Chapter Nine.

  171. @YetAnotherAnon

    Rigorous assortative mating means that children don’t regress to the population mean but to the mean of that cognitive sub-population. Hence, the possibility of different groups having different intellectual levels, on average.

    • Replies: @res
  172. Factorize says:
    @Sean

    Am I the only one who finds this form of intrafamily mating somewhat unpleasant? Clearly with what is now understood about the polygenic nature of IQ, one should predict that such a reproductive strategy could lead to cognitive enhancement, though with risks. This approach is probably the only successful IQ enhancement strategy that was developed prior to the recent GWAS era.

    The current GWAS results should be able to magnify such enhancement, as it could be easily predicted which of these matings would concentrate more of the IQ increasing SNPs.

    I would need to think carefully about whether or not I could endorse such a strategy. It would lead to enhanced human IQ, though there is a large gross out factor that would need to be overcome.

  173. Factorize says:
    @Sean

    I am not sure whether I agree with the notion of a genetically advantaged elite anymore. While without modern genetic evidence such claims have been largely accepted without question, when the modern genetic evidence is considered such claims are only slightly true. An eternally existing genetically advantaged elite is largely a myth which is maintained by highly selective memories and elite advantages that simply override any meaningful conception of merit. Recent research found that children of high SES families had higher social status even if their EA polygenic scores were 3 SD below the mean while those of some in lower SES were 3 SD above the mean. Such massive divergences from ability and social standing seriously call into question the very meaning of being elite. Even with the base measure of average EA PGS, the children of the elite are virtually indistinguishable from other SES.

    The main driver of social progress is the ongoing inflow of high IQ talent from the middle class. Without this circulation the entire psychometric class structure would rapidly collapse. It should be of some concern that such a process now appears to be underway. It is almost an inevitable consequence of the age of virtual universities. Some of the most globally renowned centres of learning simply do not have the built resources that would make them fun places to learn. Many in fact have substantial deficits in providing students with even a safe learning environment. It is no great wonder why there has been such a rush to onlearning. Such learning does not require a shared physical environment, and thus minimal opportunity for assortative mating to occur. Similar observations would apply to them modern work environments.

    With Asia, there is at least a chance that collective good will be placed before individual good. This is such a strongly held cultural value in Asia that it is difficult to see any other future from emerging. Psychological research has found that this is a deeply wired cultural trait (probably genetically encoded) that will likely guide their future policy choices. For Asians adopting a me before we conception of reality would be seen as a defeat of their entire value system. The pervasive self-projection of Western cultural values unto Asian societies will have no influence on the choices that they will likely make for themselves.

  174. @Johan Meyer

    These known uterine factors don’t account for much variance, it has been tested already. Again, you are arguing with formulas when you should be arguing from data.

    http://emilkirkegaard.dk/en/?p=5873

    • Replies: @res
    , @Johan Meyer
    , @Johan Meyer
  175. res says:
    @James Thompson

    Do you know of any studies looking at that effect in families? Does knowing grandparent IQs as well as parent IQs increase the predictive power for children and/or decrease regression to the population mean?

    • Replies: @James Thompson
  176. res says:
    @Emil O. W. Kirkegaard

    Interesting post. Any thoughts on how it relates to my observations in this comment on the previous post here?

    Is it possible there are uterine effects acting in opposite directions? That could end up canceling in the observations. As you say though, should really be arguing this from the data.

    Two opposite effects which come to mind are:
    - Sharing a similar environment in many ways (temperature, overall chemical environment like stress hormones).
    - Resource competition.

    The latter appears to dominate in the Wilson data discussed at the comment above. Based on that data I think it is hard to argue that chorionic effects don’t appear in childhood (especially early), but the more important question is do they persist into adulthood.

    • Replies: @Emil O. W. Kirkegaard
  177. Factorize says:
    @YetAnotherAnon

    The UCSC Genome Browser provides access to 2,000 phased genomes.
    Using the first run of the 1.1 million EA GWAS published over a year ago, I came up with an IQ PGS for HG00096 Born in the UK. It would be appreciated if someone could double check the numbers though the quantitative result would stand whatever numerical adjustments were needed.

    This individual is calculated to have a genoIQ of 91 (PGS of 0.304). Below I have noted the strand by strand PGS scores for chromosomes 11-16 for purposes of illustration. One of the first things that should be noticed for this person is how much of a counteracting effect the negative strands are having on the PGS. Even in the chromosomes listed below, there is more negative PGS than this person has in their entire PGS! Chromosome 14 is especially bad luck! They lose 0.28 PGs on this one chromosome! The specific numbers might be revised on double checking, though the observation that there is a very large tug of war going on between the pluses and minuses is entirely collaborated by the research evidence. (The final column by the way is the running sum of the maximal chromosomal strand.)

    This individual is not assumed to have been highly selected for any particular trait. Yet, even this individual highlights the idea that IQ would not need to regress to any average with proper mate selection. Consider for example this person’s 2 strands of chromosome 16. They are both quite respectable. The child of this person is ensured of inheriting a favorable chromosome 16. Finding a mate also with homozygous high IQ on chromosome 16 would mean regression to the mean {for this chromosome at least} would not occur in the next generation. Notice that chromosomes 12 and 13 also both have positive values and could also be locked in if a potential mate could be found for these chromosomes.

    This style of thinking makes much more sense than simply considering IQ. Mating by IQ was an enormously unsuccessful IQ enhancement strategy. It is not difficult to see why from the numbers below. A child of this person would lose either the high PGS on chromosome 16 of either 0.09 or 0.138 and could also lose 0.137 PGS on chromosome 13. It is easy to imagine that an offset might not be provided by the genetic contribution of a mate (if they were to be selected for IQ). With completely disorganized genomes it is no great wonder that regression to the mean has been inevitable till now. Yet, as seen below especially with chromosome 16, strategic reproduction and embryo will allow for locking in PGS values so that regression to the mean could not happen. Simply consider what would happen if all the chromosomes for this person and for their mate resembled chromosome 16 below! Regression to the mean is not possible.

    0.016 -0.036 11 0.554
    0.026 0.015 12 0.58
    0.004 0.137 13 0.717
    -0.161 -0.121 14 0.596
    -0.047 -0.031 15 0.565
    0.09 0.138 16 0.703

    I was interested in what the IQ of this person’s haploid genome would be.
    By choosing the largest number of all their chromosomes I arrived at 0.881.
    This person with an IQ of 91 then has a haploid IQ of 119.
    A full genome IQ (decided to simply double this one person haploid genome to form a full genome)
    was 162.

    PGS of 0.881 –> IQ 119.1 (This is only a haploid genome!)
    PGS of 1.762 –> IQ 161.7 (This is the full genome)

    This might be thought to be entirely theoretical. One would need to able to choose the best chromosome in the whole genome. How many embryos would be needed to do this? Surprisingly, this technology has already been developed in mice. If an averagish IQ person already has the potential to have 162 IQ children, then perhaps we need to carefully consider how far off IQ uplift truly is. PMID: 26485770

    I would greatly appreciate comments about this. Anyone with coding skills would be encouraged to crunch through the numbers again. Ask if you need help. It takes a little effort to extract the information from UCSC. If any published research exists on this topic I would be very interested in obtaining some citations.

    • Replies: @YetAnotherAnon
  178. @res

    I haven’t got that data, though they may exist. The usual approach is to use the best estimate of parental intelligence (or give Raven’s to willing parents) and predict from that, using a heritability estimate of 0.6 for the adult expectation. Also, if there is sibling data, usually on scholastic attainment, that helps calibrate the prediction.

  179. @Emil O. W. Kirkegaard

    I think you are confused about what I am saying, perhaps due to lack of clarity on my part.

    Whether a Wilson effect is observed for any given trait (whether a ‘uterine factor’ is present) is entirely an empirical question. I only used the two examples that you gave on your blog, namely weight and length. I make no claims regarding other traits; the formulas hold, or fail to hold, regardless, and the birth MC effect (zero or otherwise) is a merely parameter to be entered. (My comment is long, so I am putting a more tag).

    [MORE]

    The standard deviation grows with the mean in the growth standard. I assume, though it is not necessary in principle, but only likely, that the standard deviation in that growth standard, is due to direct genetic contribution.

    The question is whether the increasing genetic variance with age is sufficient to explain the (found) Wilson effects in weight and length, absent reduction in gross environmental variance with age (regression to genetic setpoint). Hence the necessity of the equations. For effects in which no Wilson effect is observed, the point is moot.

    Where genetic sensitivity to environment (e.g. uptake of lead) can come into play, in particular for Wilson’s data, it can only occur after birth, as the mother’s genes would determine uptake during gestation, rather than the children’s, and thus MZ and DZ would be subject to the same effect.

    I argue that the increase in (presumably direct effect) genetic variance in weight is more than adequate to explain Wilson’s weight data, but not enough to explain the length data.

    That is, if one calculates the size (mean squared and variance) of the Wilson effect at birth from the MZ formula using variance at birth (I simplify a bit, as there is a variable parameter, and one should look at the outcome for various values, although it is not visible in the simplistic model of the above equations), one can calculate the correlation at later ages, on the assumption that the initial effect (in absolute terms) is not diluted, and thus obtain a Wilson-like effect.

    The above model Wilson effect will be stronger than the data in the weight case, and weaker than the data in the length case. One possibility is regression to genetic setpoint in the length case. Another is that the lead poisoning of Wilson’s data’s era provided more genetic variance (uptake variability), and it may be useful to see if the same strength length data Wilson effect can be achieved with twins born after the phase-out of leaded petrol.

    • Replies: @Emil O. W. Kirkegaard
  180. @Emil O. W. Kirkegaard

    A quick addendum—the bulk of the growth will be shortly (weeks) before delivery, and thus the mother’s exposure will be minimal, which would explain a negligible common environmental effect, so direct genetic contribution should dominate, due to maternal leave protecting the mother from exposure to lead.

  181. @res

    Interesting post. Any thoughts on how it relates to my observations in this comment on the previous post here?

    Link doesn’t take me to a particular post.

    Is it possible there are uterine effects acting in opposite directions? That could end up canceling in the observations. As you say though, should really be arguing this from the data.

    Of course. However, the usual claim from uterine environments is that they make twins, especially MZs more similar, because this would cause an upward bias in h² from MZ-DZ studies. If you think e.g. MC causes less similarity, this leads to downward bias for h² in MZ-DZ studies, as seen for very early height/weight in my Wilson blogpost. Generally, DZ twins are not much more similar with age than regular SS siblings, so whatever the simultaneous uterine factors are (sharing uterine at same time vs. time shifted), they aren’t very important for population level variation.

    My analysis of their MC findings just mostly indicate that the variation seen is due to sampling error. It would be possible to do a simulation to try to quantify whether it is _only_ due to sampling error, but that requires simulating twin data etc., which is difficult (time consuming).

    • Replies: @res
  182. @Johan Meyer

    There’s lots of studies that look at unstandardized genetic variance as function as age, and these generally show that genetic variance increases with age, while the others stay roughly the same. Hence, h² goes up with age.

    Random examples:

    - http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.704.9516&rep=rep1&type=pdf
    - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4618266/
    - https://www.researchgate.net/profile/Rene_Mttus/publication/323112699_Kids_becoming_less_alike_A_behavioral_genetic_analysis_of_developmental_increases_in_personality_variance_from_childhood_to_adolescence/links/5aa9ab590f7e9b88266f642a/Kids-becoming-less-alike-A-behavioral-genetic-analysis-of-developmental-increases-in-personality-variance-from-childhood-to-adolescence.pdf

    Note: personality is weird due to measurement issues.

    I don’t know why you are so obsessed with lead and lead GxE. I see no particular reason to have such a strong prior on that environmental toxin.

    • Replies: @Johan Meyer
  183. @Emil O. W. Kirkegaard

    There’s lots of studies that look at unstandardized genetic variance as function as age, and these generally show that genetic variance increases with age, while the others stay roughly the same. Hence, h² goes up with age.

    Exactly. And thus the difference between MZ and DZ correlations, thus the Wilson effect. One does not need a reduction in environmental variance with age (regression to genetic setpoint). That is exactly the point I have been trying to communicate.

    I don’t know why you are so obsessed with lead and lead GxE. I see no particular reason to have such a strong prior on that environmental toxin.

    1. Ethnic groups who have weak or no background with a bronze age tend to have blood lead distributions that tend much higher than the distributions of ethnic groups that did have substantial bronze ages, in the same time and place.

    2. Reduction of sperm quality due to lead poisoning would tend to drive evolution to reduce uptake, and tend to give men a leg up on women to reduce uptake. The question is whether genes can aid discrimination between ionic lead (Pb^{2+}) and ionic calcium (Ca^{2+}). If they can, then genetic effects in uptake should be expected.

    3. Either the lead effect (dose response) on IQ is real, or it is an artefact. The general weakness or lack of apparent common environmental effect in twin studies (twins born and raised during the leaded petrol era) forces the matter to be either artefact or genetically variable uptake, so that the variance appears to be genetic rather than common environment.

    4. The efforts to reduce lead poisoning should have lead to convergence in ethnic distribution of blood lead, as residences of individuals with the highest blood lead at the time of measurement, get priority. Further, lead poisoning was seen as a black problem. Yet the efforts have not resolved the discrepancy, but have only reduced the overall scale of the problem.

    Further, it is a low hanging fruit. Indoor shooting ranges are associated with raised blood lead. Any major urban US police force could rapidly gather test data using a small number of officers of the major ethnic/racial groups in the US as a proof of principle.

  184. res says:
    @Emil O. W. Kirkegaard

    Link doesn’t take me to a particular post.

    What are you seeing? For me the link goes to http://www.unz.com/jthompson/scientific-racism/#comment-2614416 which is a comment of mine on Dr. Thompson’s last post.

    If you think e.g. MC causes less similarity, this leads to downward bias for h² in MZ-DZ studies,

    I am not sure how different directions of MC similarity effect would balance out. And how much that might vary by trait. I wonder how much effects like that might affect the time trajectory of h^2.

  185. @Factorize

    First — since IQ is not merely genetic based, if that is the case at, Mr. and Mrs Einstein did not produce more Einstein’s.

    Second, your model is pure speculation, there is no way as of yet to deconstruct the nature of the relationship of the chromosomes you are referring to as soley or even uniquely linked to IQ.

    Third, you speak of innovations as though innovations require a certain or guaranteed to IQ of the result of IQ as opposed to hard work or intensive work on a particular problem or issue. That simply is just not the case.

    Fourth, “Now it is readily acknowledged without qualification.” in no universe of this subject has that debate been settled nor will it ever be because it simply is not possible to untangle environment from the equation. It’s clear even in the presented data – that environment – including bio-environmental are factors in chromosome development.

    What concerns me about the core of these conversations is the tend to link DNA to justification for how one is rated to be treated. My ill treatment of others is by default to dna. The introduction of “christian ethos” into the conversation that one can inherent by way of dna just defies the actual record in which long standing christian practitioners have offspring, who are not only not practicing the said ethics, but reject christian ethos entirely.

    • Replies: @HallParvey
  186. @EliteCommInc.

    The introduction of “christian ethos” into the conversation that one can inherent by way of dna just defies the actual record in which long standing christian practitioners have offspring, who are not only not practicing the said ethics, but reject christian ethos entirely.

    Many children of christians do not actively participate in organized worship activities which, in too many cases, tend to be more “do good” than anything else.

    However, they still carry, within themselves, the same genetic codes that cause their parents to seek eternal life. A conscious awareness that, just maybe, they are part of something much greater than themselves. That rejection you mentioned generally lasts only until they have reached some level of maturity.

    The young often reject the religion of their parents because too often the religion salesmen, of all stripes, equate sin with everything natural. Except overeating.

    God worship does not require a cathedral. It doesn’t even require a tent.
    It doesn’t require anything except the individual and his or her appreciation of the world they inherited.

    This should in no way prohibit those who prefer the grandeur of the cathedral. But that’s just the difference between the preference for Coke or Pepsi.

  187. @utu

    Yes, yes, I know you told me to get lost, but this is too funny not to mention.

    The genetic covariance of MZ twins should not be affected by selective mating, as being twins should be independent of genetic outcome, and should thus simply be equal to the population variance.

    However, the DZ genetic covariance may be larger than half the population variance, due to selective mating, per the argument in your link; the question is what fraction of the selective mating correlation is genetic (direct genetic causation model); call that fraction $c$.

    Then, assuming that the correlation and fraction (of selective mating, for a given trait) is identical for all chromosomes, the DZ genetic covariance is roughly (ignoring meiosis cross-over of genes between chromosome homologues)

    $$\sigma_\mathrm{genetic}^2\,\frac{1+r_\mathrm{selective\,mating}\,c}{2}$$

    Thus the Falconer equations may add a factor (normal mathematical sense, not a random variable) of $1-r_\mathrm{selective\,mating}\,c$ to the estimate of fraction of variance that is genetical, if the argument about selective mating in your link is correct. This factor is less than unity, i.e. the Falconer equations would tend to underestimate the genetic fraction of variance, under selective mating.

    Any environmental effect that has substantial variance must, in light of the above, and the lack of detected non-genetically varying common effect between twins, have a genetically varying effect, e.g. uptake. If it can be demonstrated that a given environmental variable does not have such genetic effect, it is likely not related to the outcome under consideration.

  188. Factorize says:

    November 26, 2018

    The day that genetics ceased to matter.

    https://www.nature.com/articles/d41586-018-07545-0

  189. @Factorize

    Thank you, you have obviously gone into this much more than I have and from a starting point of much greater knowledge – so much so that it’ll take me a day or three to understand/decode (is PGS polygenic score?) what you’ve written.

    Can’t guarantee it, but I’ll try to get the data and crunch the numbers – but only if/when I understand what I’m trying to do. Like Captain Oates, I may be some time.

    Just a couple of questions

    i) you show polygenic scores for each pair of chromosomes –

    a) do these scores relate to IQ or are they a more general measure of what exactly? I presume it’s EA – Educational Attainment?

    b) they show (presumably) increased (+ve) or decreased (-ve) probabilities of improvement in (a) – but compared to what? A sample of native British population? Presumably the average of the “1.1 million EA GWAS”?

    c) how (without the maths) are the scores for each chromosome derived? Human chromosome 16 for example is over 90 million base pairs and 795 genes (according to NCBI). Do they statistically correlate the make up (in base pairs) of each of those genes against the individual’s EA and thus get a score for a chromosome, or what? I presume everyone has 795 genes in chromosome 16, or am I wrong and some people miss out, and it’s a count of the various genes that’s used?

    ii) PMID – is that a PubMed identifier?

    Sorry to know so little but I’m trying to work it out as I go along!

    • Replies: @Factorize
  190. Anon[257] • Disclaimer says:
    @Sanguinius

    Conception and pregnancy rates were high in the past. But survival of fetuses, newborns infants and children under 5 was only about 60% for most of human history. If children reached 5, that still didn’t mean they would live to adulthood. In some eras and in some populations survival rate from birth to adulthood was only about 40% of live births.

    Until the last 100 eyears miscarriages and still births were common. The survival rates of fetuses was as low as the survival from birth to adulthood rates. In the old days parents were lucky if 8 pregnancies resulted in 4 adults. There were as many second and even third marriages to to death in childbirth as there are second marriages due to divorce today.

    The Amish have been breeding for conformity, submission and docility for centuries. They began in a very close knit conformist Swiss peasant village where cooperation and conformity meant survival long before Christianity came along.

    The Amish don’t tolerate non conformity. People who don’t conform even to styles in facial hair and number of pleats on a skirt are pushed out and never spoken to again.

    Do the Amish really have such big families anymore? Since their children are shunned and banished if they go out as adults and make a living in “English “ ways, I highly doubt it. Farms and family businesses can’t be divided up generation after generation after generation.

    How many children to have depends on finances and housing. Unless you’re Chinese and accustomed to 30 people in an 1800 sq ft house.

    Much of the drop in European birth rates, especially in the cities is caused by the tiny little 2 bedroom apartments most European city dwellers live in. Plus the low take home incomes after the massive taxes to build those tiny little apartments are taken out of the paychecks.

    There is nothing to prevent people who think other people should have 5 to 10 children from having babies themselves. Especially men who can make babies from about 13 to 85 unlike women who can conceive only about 27 years 13 to 40.

  191. Factorize says:
    @YetAnotherAnon

    YetAnotherAnon, thank you for replying! Usually when I suggest that it would be fun to do some programming/math/work, I find that people just remembered that they had a cake in the oven, or that they need to take the washing off the line, or almost any imaginable excuse not to help. You will be the first volunteer!

    This type of an activity is like a baton race. I can hand off what I have learned and then you can leg it out until we find some more volunteers or I am ready for another circuit.

    I) a) The PGS were for the original data published for the 1.1 million EA GWAS. You are correct that EA not = IQ, though it is a starting point and there is moderate correlation between the two. Once we had everything set then IQ effect sizes could easily be switched into our program.

    b) The + and – are the sums of the PGS for each chromosome for each individual. The table of SNPs and effect sizes from the 1.1 million EA GWAS presumely reports effect sizes in SD. The method that apparently will be used in calculating PGS to select embryos etc. is simply a sum weighted by allele number of the effect sizes for all chromosomes. This PGS could then be used to estimate IQ or EA or other traits. Chromosome IQ partitions out that part of the PGS associated with each chromosome.

    c) The math behind this is much easier than one might first assume. Each of the chromosome would only have roughly 50 SNPs to sum up. Perhaps we could even do this by hand! These 50 SNPs would represent the PGS for the entire chromosome. I am sure that utu will question the validity of such an assumption, though we do need to start somewhere. The main objective for me would be to start to gain some appreciation of how mate selection, embryo selection, recombination, chromosome selection, perhaps CRISPR applications would relate to real life genome data. There are a few thousand phased full genomes on UCSC, so once we got things rolling we could develop a fair amount of insight into these questions.

    At the moment there seems to be a large void in investigating these questions. I think it is very important to fill in some of these gaps. How much of an IQ boost would occur if potential singles were to optimize mate choice based upon genotype? We need to find out!

    Yes, here’s the pubmed article.

    https://www.ncbi.nlm.nih.gov/pubmed/?term=26485770

    First up is to download the phased genomes from UCSC.

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