When genes fight

For those of you just tuning in: on a genetic level, all parental investments in their offspring are equally valuable.  From the offspring’s perspective investing in them is two to four times as good as investing in their sibling (depending on if they’re half or full siblings).  The fight to get the amount of resources they think they deserve is parent-offspring conflict

One manifestation of parent offspring conflict is weaning conflict, where offspring would like to keep getting nutrients with no effort and their mom would really like them to go out and get a job.

But it can start before then.  Conflict over exactly how much nutrition a fetus should get may contribute to preeclampsia (high blood pressure during pregnancy) and insulin resistance (PDF).  This is not just about mothers not wanting to give up nutrients- more nutrition leads to larger babies, which is almost always good for the baby but kind of hard on the person forcing it out through their vagina.  There is even speculation that the human custom of making a thick uterine lining (nutritionally expensive) only to flush it away each month evolved as self defense against a placenta that would otherwise invade your uterus like ivy invades bricks.

This is your uterus on babies.
This is your uterus on babies.

Creepy, yes.  Abhorrent, at the level of individuals.  But totally logical and predictable from the level of a gene.

Kin Selection

The idea of kin selection was implicit in my post on haplodiploidy but let’s make it explicit.  The unit of selection is the gene, not the individual.  The individual is a co-operative venture by many genes to reproduce themselves [I attempted to explain why this was and it became 4 paragraphs on the origin of DNA, so let’s just take it as a given].  There’s no reason for genes to prefer directly reproducing themselves: if you can get more copies of yourself by helping someone else’s co-operative venture than your own, that’s a better investment.  Doing so is known as kin selection.

The most obvious example of this is parental investment in offspring.  Offspring aren’t you, but they have your genes.  For a diploid sexually reproducing organism, a given allele of yours has a 50% chance of being in your offspring via common descent (sharing an allele via coincidence doesn’t count for reasons we will get to).  But a full sibling is just as related to you as your child, so raising them is just as good.  The technical term for this is helpers at the nest*.  It’s especially likely when raising offspring is exceptionally costly and resources (e.g. territory) are very limited, so the choice is between raising siblings or nothing, rather than raise siblings or raise your own offspring.

As you might guess from the name, helping at the nest is most common in birds, but you do see it elsewhere. Golden Lion Tamarins live in groups of 2-8, but will usually have one, with a maximum of two, breeding females.  Females are unable to provide sufficiently for their offspring on their own.  They’re helped out by other group members, which are likely to be their own children, siblings, or sibling’s children.

Honestly I have no idea if that's a helper or the parent but it's adorable.
Honestly I have no idea if that’s a helper or a parent but it’s adorable.

Nest-helping may be at intermediate step between the “good luck, fuckers” school of parenting (technical term: r-strategist) and eusociality.  For example Carpenter Bees (carpenter is a genus, there are 500+ species within it) are usually solitary, but some build nests near each other in trypophobia-inducing pattern,. show specialization and cooperation between nesting adults (e.g. one guards all nests while others forage) , and daughters sometimes share a single nest with their mothers.

Don't trust pictures in nature articles.  I couldn't find a picture of cooperation so I used one of fighting.
Don’t trust pictures in nature articles. I couldn’t find a picture of cooperation so I used one of fighting.

One way to help your own siblings is to raise them, like helpers at the nest do.  Another is to free up parental energy by taking less for yourself.  From a genetic perspective, you should stop asking for things from your parents if the energy would benefit a full sibling twice as much, or a half sibling four times as much.  But from the parents perspective children are all equally valuable, so they will want to switch giving as soon as resources benefit one child more than another.  This is parent offspring conflict, as explained by noted evolutionary biologist Dylan Moran at 30:00 in this lecture:

More on parent offspring conflict tomorrow.

*Note: kin selection is not necessarily the only reward for helping to raise siblings; individuals may also learn parenting skills or give themselves a leg up claiming their parents’ stuff when they die.


Let’s start way at the beginning.  All eukaryotic cells (which includes any multicellular organism) carry their DNA wrapped up in a chromosome


In any given species the chromosomes are numbered, and chromsome N contains predictable information.  For example, the human chromosome 16 contains the DNA to alpha-globin, a component of hemoglobin, the thing that lets your red blood cells carry oxygen.  Some people have a variant in their alpha-globin genes that leads to sickle cell anemia.  It’s still chromosome 16.  The general location and form of the DNA that produces a protein is the gene, different variations are called alleles.  So technically it’s wrong to say “the gene for sickle cell”, you need to say “allele for sickle cell”, but everyone knows what you mean.

Many organisms contain more than one version of their chromosomes: the second (or more) chromosome has the same genes but different alleles (unless something goes weird, which does happen but we don’t have time to get into).  You are probably most familiar with the human chromosomes: 2 versions of 22 normal chromosomes, an X chromosome, and either an X or a Y chromosome, with Y chromosomes conferring maleness.    Having two versions of each chromosome is referred to as being diploid, and it’s not the only choice.  Certain sugar cane hybrids have as many as 12 copies of the same chromosome.  Some species show variation in ploidy between individuals.  This is more common in plants, which can self-fertilize, but is also seen in insects.  In humans individual chromosomes are occasionally doubled when they shouldn’t be: this causes death if it’s a big chromosome and things like Down’s Syndrome if it’s not.

Note that the Y chromosome does not contain all the information you need to be male: it releases the signals to be male, and numerous genes on multiple chromosomes respond accordingly.*   That’s not the only way to determine sex.  Birds, some fish, some reptiles, and a few others species use the ZW system, which is the same as XY except females are the one with the Y chromosome.  Many reptiles sex depends on the temperatures their egg experienced (and not every species responds to temperatures the same way).   We don’t know how sex is determined in the platypus, which, yeah, that’s about what I expect from the platypus.

Then it gets weird.  Fruit flies, and have the equivalent of X and Y chromosomes- but they have anywhere from one to four versons of sex chromosomes, and 2-4 versions of each non-sex chromosome (autosome). All autosomes have the same number of versions, but there may be a different number of sex chromosomes.  The sex of a fruit fly depends on the ratio between the # of autosome copies and sex chrosomsome copies.

But what I really want to talk about (600 words in) is haplodiploidy.  A haploid cell has only one version of each chromosome, a diploid two.  In haplodiploidy, females are diploid, and both male and female produce haploid gametes (egg and sperm).  Unfertilized eggs grown into males, and fertilized eggs grown into females- so females have twice as many chromosomes as their brothers.  Males have one grandfather and no father at all.

This has a couple of implications.  One, most deleterious recessive genes get weeded out right quick, because no male will produce them.  On the other hand, such a gene could persist if it boosted female reproduction sufficiently.  Second, females can reproduce without males, although they will produce only sons.  Which they can then mate with (and inbreeding isn’t nearly as dangerous as it is in diploid animals, because of the aforementioned filter on negative recessive genes), and produce daughters, so a single female can repopulate the planet.

Then there’s relatedness.  A human is 25% related to a half sibling (for any given gene there’s a 50% chance it came from the shared parent, and a 50% chance the parent passed it on to the sibling).  But a haplodiploid father passes on the same genes to every child, so each sibling is 50% related to each other through him.  If the siblings also share the same mother, they are 75% related to each other.  That is more related than they could be to their own offspring (50%).**

It was initially thought that this was why/how eusociality developed: it was literally more advantageous to raise sisters than daughters.  That’s not strictly true:  There are haplodiploids without eusociality, and strict diploids with eusociality.  Some  eusocial haplodiploid queens breed with multiple males, so their daughters are raising sisters only 25% related to them.  But eusociality is heavily overrepresented in haplodiploid animals, so it clearly affects the math.

*Fun fact: the signal for male development in utero is not exactly the same as the signal for male development at puberty, and it’s possible to be unable to produce the fetal signal but successfully produce the puberty signal, producing babies that are born with female external genitalia but grow a penis and testicles at puberty (nearly all of these children identify as men as adults).  This was common enough in certain villages in the Dominican Republic that they have a name for it, which translates to “penis at 12.”  It’s considered a joyous thing because sons are more valued than daughters.

**But aren’t their sons 100% related to them?  Yes.  But relatedness is not necessarily reciprocal.  A gene in a female has only a 50% chance of being in a given son, so she is only 50% related to him.

Autism as Developmental Injury

Left untreated, people with phenylketonuria (PKU) can develop intellectual disabilities, seizures, and “other medical problems”.  But PKU does not cause any of those.  Phenylketonuria + a normal diet causes a build of of phenylalinine in the body, which causes those problems.  If PKU is caught at birth and the sufferer is kept on a phenylanlinine-light diet, they will never develop these problems.

Henry Markram suggests that something analogous is going on with autism.  He and his collaborators think that the actual problem is that autistic babies have extraordinary sensory sensitivity, and this sensitivity causes defenses that cause them to miss certain critical information during developmental periods.  What is challenging but achievable (the zone necessary for learning) for other people is overwhelming for them, so they don’t learn.  The developmental window closes and they’ve lost their chance to truly master that skill.  But if they were given stimulus in their zone of achievable challenge, they would learn those skills and maintain them for life.  They might continue to need accommodations, the way phenylketonurics need to stay on a phenylalinine-light diet their whole life, but with those accommodations they could function “normally”.  This is known as the intense world hypothesis.

The example they give is the critical period for learning language.  You *can* learn a new language after the critical period, but it will never be as easy, most people will never attain genuine fluency, and if you never learn any language it may be truly impossible to pick one up later.  If normal human speech is overwhelming to an autistic infant they will miss that period and their language will be impaired for life.  But if they’re given regular access to speech they are comfortable with (probably quieter and slower) they could learn it just fine, the same way hearing impaired children do fine with sign language.

I was also really impressed with the writing of this lay-press article.  I’ve been avoiding doing take downs, especially of popsci articles, because there are millions of wrong things every day and criticizing them is easy.  For a while I could justify them as case studies in critical reading, but now it just feels bad.  This had led to a lot of aborted blog entries, as I read something amazing and then realize it’s too flawed to pass on uncritically.   I don’t agree with everything the article says (insisting there’s only one cause of autism strikes me less as brave and more as idiotic), but it lays out its case in an informative and responsible manner.

What We Talk About When We Talk About Effectiveness

The biological/scientific definitions of heredity and heritable differ slightly from the popular usage.  Lay people tend use it  to mean “how much is this caused by genes?”  In science, heredity is how closely people resemble their parents, divided by the total variation in the population.  Biological sex has almost zero heritability because knowing someone’s parents sex does not allow you to predict their own sex.*  Number of arms is barely heritable, because there’s almost no variation in number of arms among humans, and what variation exists is overwhelmingly caused by environment, not genetics.

A corollary to this is that a measure of heredity is only valid for the exact environment you measured it in.  If you plant a variety of seeds in identical pots and give them identical water and supplements, most variation will be due to genetics, and a small amount to chance (which will be counted as environment), so traits like height and time to flower will be highly heritable.  If you plant those same seeds in widely varying pots and vary the water and nutrients they get, a lot of the variation will be due to environment, and the heredity values of the same traits will be much lower.  Skin color in Norway is more heritable in the winter than in the summer, because teenagers deliberately tan more than their parents.

I have struggled before to make effectiveness estimates when the intervention’s usefulness depends on multiple factors.  Blood for car accident victims is only helpful in the context of emergency rooms and medical schools and sterile gauze.  Suicide hotlines require phones and electricity and suicidal people at a bare minimum, and active rescues require police and mental hospitals and often pharmaceutical research.  I think I’m just going to have to put effectiveness in the same category as heredity: the quantification is only valid for the environment in which it is measured.

I’ve worried before about Effective Altruism’s tendency to take the existing system as a given.  That was a reasonable simplification when the movement was first starting, and there was plenty of low hanging fruit that didn’t require more sophisticated analysis.  But I’m really happy to see organizations like the Open Philanthropy Project branch into studying how to change systems and how to measure the effectiveness of attempts to do so.

*Intersexuality confounds this a little but my impression is it’s mostly not a genetic issue, in part because intersex people generally have difficulty reproducing.

r/fatlogic endorses creationism

Normally when I’m investigating something I like to read well regarded books on both sides, in the hopes that the ignorance will cancel out.  Finding a suitable counterpoint to Health At Every Size is hard, because its opposition is “everyone in the world”, and there has been no selective pressure to elevate the actual science away from the shame and aesthetic preferences.

For example, I spent a little bit of time on r/fatlogic which, as decisions go, was not my best ever.   r/fatlogic frames itself as a criticism of horrible “fat logic”- things like “700 pounds is no less healthy than 200 pounds.  Possibly healthier.”  This is not a great start.  I have a deep personal understanding of how frustrating it is when people are wrong, but I have found I am happier and a better person when I say “yup, wrong”, and then move on with my day.  For the truly awful I might e-mail a friend making fun of it (thanks, Rachel!).  Forming a whole club around criticizing people, especially people that are already having a pretty tough time in life, is bad for everyone.

r/fatlogic is even worse than that, because it has an extraordinary case of the cowpox of doubt.  Wrong people keep insisting body fat is independent of calories consumed and exercise?  Well then body fat must be solely dependent on calories consumed and exercise, and anyone who suggests it is affected by anything else is a fatty fat fathead making excuses for their fat.  They are literally denying  the possibility of individual variability in the translation of external environment into physical state.  For bonus points, they invoke “but thermodynamics”, which is the same argument creationists use against evolution itself.

Here I tried several ways to explain exactly how wrong they were and how that was terrible, but then I decided to take my own advice and stop before I endorsed the hollow Earth theory.  My current contender for an opposition book is Good Calories, Bad Calories, but I’m open to suggestions.