Blueprint: How DNA Makes Us Who We Are

I’m going to review Robert Plomin’s  new book,  Blueprint: How DNA Makes Us Who We Are.  It’ll show up in Quillette . By the way, I should someday write a piece for them about how I am not a moderate left-winger who was eventually left behind by the Left getting ever crazier.  I would also not talk about how the New York Times used to be a great paper.  Was that when they called for McClellan to be made dictator, or when they informed Goddard of the “need to have something better than a vacuum against which to react against.” ?

Probably there will be a podcast. The GoFundMe link is here. You can also send money via Paypal (Use the donate button), or bitcoins to 1Jv4cu1wETM5Xs9unjKbDbCrRF2mrjWXr5.

In-kind donations, such as hefty lumps of ambergris and uncirculated 1909 S Vdb Wheat pennies,  are always appreciated.

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Last Survivor

It seems that although the Amerindians had dogs (after a while), those puppies did very poorly after Columbus.  Modern dog breeds have slim-to-no ancestry of this kind ( from comparisons with ancient dog DNA) . You have to suspect infectious disease. However, one descendant is still going strong:  it turns out that canine venereal sarcoma, the cell line infection or contagious cancer, originated in a North American dog: it’s closely related to those old Injun dogs and shows a bit of coyote introgression!

I had made a similar suggestion  a few years back: I said that there still might be living Neanderthals ( contagious ones, I was thinking ) and challenged some readers to guess how. After two years, none had, so I relented and gave them a hint: “What for you bury me in the cold, cold ground?”

 

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Alzheimers, or did I already say that?

More studies are suggesting  that Alzheimer’s disease may be caused by a persistent  viral infection of the brain.  Autopsy studies show that Alzheimer’s victims have higher viral load. A couple of other recent studies in Taiwan suggest that antiviral drugs may  significantly reduce the incidence of Alzheimer’s.

And of course we have the long record of complete failure of therapies based on the amyloid hypothesis.

Many of these recent articles mention that most people in the Alzheimer’s research community are violently opposed to any pathogen hypothesis, or probably anything other than the amyloid hypothesis.  I see phrases like “venomous hostility” used.

Truly I don’t get why.  I see no political angle of any kind, no emotional hook  – the only thing I can imagine is that personal and community investment in a given approach makes it very hard, almost impossible to admit a mistake.  Is that enough, all by itself?

 

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Why Adopted Children Still Struggle Over Time

I noticed an article in the Atlantic, about much higher rates of disability, behavior and learning problems, suspensions.  Lower achievement on reading, math, and science assessment tests.  They can’t figure it out.

There must be something attractive about living in a constant fog of mystery.  Who knew that dogs bite men?

 

 

 

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Occam’s Butterknife

” Picture this nursery school scene: 10 1-year-olds are squeezed next to one another on a bench, their backs against a wall. They sit motionless. None cry, push or shove.

A woman attendant takes a small windup toy chicken out of a box, turns the key and lets it strut across the floor past the infants’ feet. Again, none of the children move or try to grab the toy, as their American counterparts surely would. They simply follow it with their eyes.

Finally, one boy cannot resist. He toddles over and pounces on the chicken. The attendant gently picks him up and deposits him back on the bench.

The episode took place one recent morning in the neat gray brick nursery school and kindergarten run by the Peking Printing and Dyeing factory for 270 children of its workers. But it is similar to scenes acted out in tens of thousands of preschool classes all across China. Visitors Are Impressed

American visitors to China are continually impressed, indeed often amazed, by the almost universal good behavior of Chinese children. They are quiet, obedient, quick to follow their teachers’ instructions, and they seldom exhibit the boisterous aggressiveness or selfishness of American children.”

In the New York Times, by Fox Butterfield himself, who must be the avatar of some totally clueless god.

I mean, really: quiet one-year-olds???

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Turkheimer speaks!

Time to respond to Eric Turkheimer’s  post.

In my review of Carl Zimmer’s book, I said that the existing fixation index values between continental races are compatible with very significant physical and behavioral differences between those races, because wolves and coyotes have exactly the same value of Fst as Yorubas and Mormons. Lewontin said that two groups with that Fst couldn’t be very different, yet coyotes and wolves are very different – so Lewontin was wrong.  Turkheimer seems to agree with me on this, although he probably doesn’t think Lewontin is full of shit. He should.

Turkheimer says that human behavioral differences are highly polygenic: true enough. And he says that makes them very significantly different from single gene effects – ” big mechanistic single gene effects and complex polygenicity” .  He talks about how complex and non-deterministic that process is.

That’s bullshit: complexity doesn’t imply non-determinism.  The closest thing to non-determinism you’re going to find outside of quantum mechanics (and to a sharp many-worlder that too is completely deterministic) is a physical system where tiny changes in initial conditions cause big changes later.   Butterfly effect; the Kirkwood gaps in the asteroid belt: chaos theory. You know the story.

Is brain development in humans like that? Do little changes in initial conditions generally, or often, eventuate in big differences later?  No: of course not.  Big changes usually leave you dead or seriously fucked up: selection hates that.  Development is robust because selection has made it so: generally small changes make no difference.  There has, over a long time, been selection for reliable development of phenotypes that work, have high fitness.  Obviously not always: shit happens, mutations happen.

One important example of that reliability of development : identical twins, even those raised apart, are very similar.  Turkheimer says that 10% of the time, identical twins have significantly different IQs: well most of the time matters more than 10% of the time, and most of the time identical twins are very similar.  Identical twins raised apart are more similar than dizygotic twins raised together.  Some of them are insanely similar.

I’m going to mention some facts from agricultural genetics – not because I think that people are sheep ( although they are), but in order  to make some points.

Lots of important traits in domesticated animals are highly polygenic. Milk yield in dairy cows is highly polygenic: no single allele explains a lot of the variance in milk production.  Does this mean that milk production is not predictable, or that it varies in odd ways  compared to traits that are monogenic or oligogenic?   No, that doesn’t happen: the consequences of polygenicity that Turkheimer expects don’t actually occur. If they did, much of agriculture would come to a screeching halt.  Speed in horses is highly polygenic: does that mean that development of running ability is a nondeterministic process?  Is it logically impossible to know that certain breeds or horses ( say  Thoroughbreds) are faster than other breeds (say  Shetland ponies)?  It may be logically impossible for Turkheimer, but it’s easy for everyone else.  Along the same line, Kevin Mitchell, for equally mysterious reasons, has said that it’s really hard to select on highly polygenic trauts – even though we have a mathematical theory of selection that says otherwise, even though we do it every day in agricultural genetics.

Both are making use of nonexistent general principles to further a particular conclusion.

Let me tell you a real difference in a highly polygenic trait compared to a monogenic or oligogenic trait: the highly polygenic trait is generally more predictable, not less.  Although quite a few alleles affect skin color, there are a few with large effects,  SLC24a5 for example.  Siblings will look a lot different if one has SLC24a5 and the other does not. This happens often in India.  Underlying principle: central limit theorem.  You’re throwing more dice.

Turkheimer also says that we don’t really know anything about polygenic differences unless we  understand the mechanisms.  And usually we don’t know the mechanisms: even when we know that a given allele boosts a horse’s speed, or a Guernsey’s milk production, or makes dachshunds have short legs, we usually don’t know exactly how  it works.  Often we haven’t the faintest. Which is why we couldn’t select for fast horses or cows  that produce lots of milk- except that we could and did, hundreds of years ago, thousands of years ago. You don’t need to know how a plus allele or minus allele for trait X works to be able to [reasonably] accurately predict the consequences. Investigating mechanisms is going to be difficult in highly polygenic traits: those alleles favoring high trait value could work through a number of different mechanisms.  We don’t  know the mechanisms involved in the behavior of Turkheimer’s dogs – but in that case it doesn’t bother him.  In humans, not knowing mechanisms bothers him: He wants humans to be special.  And hey, they are, but not in the way he would like.

Actually I don’t quite believe this of either Mitchell or Turkheimer. I think they’re trying to arguing away stuff they don’t like.

That said, although knowing the details of mechanisms is not usually essential, I can think of cases where it’s worthwhile. There is a haplotype, now common in dairy cattle, that significant boosts milk production in heterozygotes while being lethal in embryo in homozygotes.  Milk production went  up while calf production went down.

What about the idea that  some unknown small thing might cause someone with an identical genotype to be quite different?  Not impossible – but we know it doesn’t happen very often, since identical twins, even though raised apart, are on average very similar.  We know that genetically more similar people have more similar IQs. A robust development process, favored by selection, does this.

A note: we know that different races have significant average differences in behavior at birth.   

Turkheimer says that I think he doesn’t have the intellectual courage required t0 face unpleasant facts. I don’t know the man: I don’t know whether he has intellectual courage. A priori, it’s unlikely, because few people and fewer professors do.   But I do think he’s unsound on general questions in quantitative genetics, which is what I think of Kevin Mitchell – even though Mitchell just has a perfectly sound post on transgenerational inheritance. Once is not enough.

 

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Lossless Compression

In my review, I complained a bit about Zimmer being prolix. Here is an example.  In Chapter 4, “Atta Girl” , if you strip out the human-interest anecdotes, he’s saying

“Mendelian diseases exist and can be serious. They’re usually recessive.  Sometimes we can do something for the kids, but generally not. PKU is bad. ”   24 words:   Zimmer takes about 11,000.

 

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