Saturday, March 15th, 2008

my evolutionary theory of baldness

cavewomen, talking to each other:

A- Look at his head, he must be at least 30!
B- OMG! To have lived that long, he must have really good genes.
A- I saw him first!
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Monday, May 22nd, 2006

how did the peacock's handicap arise?

A- Why do peacocks have huge tails?
B- Because peahens find them attractive.
A- and why do they?
B- because it's a handicap: any peacock that survives with such a ridiculously long tail must be pretty fit otherwise. His genes must be good.
A(1)- well, why do we care about "otherwise"? It's not like the peacock can chuck his tail when he's in danger, so any kids coming out of this mate will suffer all the same negative effects of this handicap. Are these females just hoping that future females will find their kids attractive for no good reason too? Are they betting on the Equal Fool Theory?
B(1)- there are probably mathematical principles (as well as empirical evidence) explaining why a peacock with such a handicap is still fitter than one without one.
A(2)- So the purpose of the tail is to impress females, right? Well, this seems to answer all of our questions, doesn't it? The problem is that this is a case of co-evolution: how did the peahens come to find long tails attractive in the first place? It's not like they could reason "well, if he has such a large handicap, then he must be good to mate with!". Attraction doesn't involve logical reasoning*: it is hard-coded genetically! So it would require an enormous coincidence for the long-tail mutation to come at the same time as the long-tails-are-attractive mutation in a large enough number of individuals simultaneously.
B(2) - Larry Gonick to the rescue!

(in case the link breaks, the answer is: learning biases in neural networks. A NN trained to identify "male" will respond more strongly to huge tails.)

(*) it is interesting to think about whether and how logical reasoning affects. In human, such reasoning processes can definitely affect attraction. Maybe this is due to our strong ability to imagine.
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Sunday, May 21st, 2006

why are Ligers bigger than Lions and Tigers?

from Wikipedia: Liger
It is believed that this is because female lions transmit a growth-inhibiting gene to their descendants to balance the growth-promoting gene transmitted by male lions. (This gene is due to competitive mating strategies in lions.) A male lion needs to be large to successfully defend the pride from other roaming male lions and pass on his genes; also, in prides with multiple male adult lions, a male's cubs need to be bigger than the competing males for the best chance of survival. Thus, his genes favor larger offspring. A lioness, however, will have up to 5 cubs, and a cub is typically one of many being cared for in a pride with many other lions. As such, it has a relatively high survival rate, and need not be huge as it will not need to look after itself very quickly. Smaller cubs are more easily cared for and fed and are less strain on the pride; hence, the inhibiting gene developed.


This is very unsatisfactory! Since it's lacking references, I am including it here as an instance of psychoceramics. It exemplifies a common sort of confusion.

His argument basically says that male lions are predisposed to have large children, and female lions to have small children. The problem is that the article tries to explain this difference by talking about 100% Lion prides, in which these children are the same: each cub will be the child of exactly one male lion and one female lion! At each breeding instance (disregarding opportunity costs), the Darwinian score of the father due to this child is exactly the same as the Darwinian score of the mother due to this child. So if anything, natural selection should make them work in unison!

One could read the article as suggesting that the Darwinian score of male cubs would gain from a marginal increase in size, while female cubs would gain from a marginal decrease in size. This seems plausible, but this would be plain sexual dimorphism, and there's no reason why one parent should contribute more to it than the other.

Anyway, a related idea:
If X chromosomes promote smallness and Y promotes largeness,
then a lion's X + a tiger's X should make a female Liger whose size is between that is tiger and lion females.
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Friday, September 16th, 2005

homophobia meme

I'd like to understand the homophobia meme / anti-homosexuality morality. How did it arise? Is the "western homophobia" from the same origin as Muslim homophobia?

Memes about religion, morality, diets, etc have coevolved with our species, and are far from "random" (whatever that would mean): they follow definite patterns. For instance, dietary memes ensure that people eat together, and thus become friends, helping each others' genetic potential. (this arguments sounds weak, though)

Pinker's "The Mind Works" is a treasure-trove of such arguments, and a delightful read, even though he's wrong in the one or two places that I know something about. But I could dedicate my professional life to his reference page.
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Thursday, September 1st, 2005

Workshop on Language Evolution; Deutscher's "The Unfolding of Language"

Tomorrow and Saturday, The First Scottish-Dutch Workshop on Language Evolution is taking place here.

One of the speakers has written this book "The Unfolding of Language". It looks very interesting.
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Friday, August 19th, 2005

co-evolution of virulence and anti-microbial peptides

I've been analyzing more evolution stuff, inspired by [info]tdj. Maybe I'm going a bit overboard (I probably misinterpreted the original meaning, but such speculations are fascinating anyway)

In response to:
Many living things, from fruit flies to people, naturally produce disease-fighting chemicals, called antimicrobial peptides, to kill harmful bacteria. In a counter move, some disease-causing bacteria have evolved microbial detectors. The bacteria sense the presence of antimicrobial peptides as a warning signal. The alarm sets off a reaction inside the bacteria to avoid destruction.

University of Washington (UW) and McGill researchers have revealed a molecular mechanism whereby bacteria can recognize tiny antimicrobial peptide molecules, then respond by becoming more virulent.


I wrote:

Whoa, such a mechanism could evolve even if it kills the host and stops the bacteria from multiplying. How? Co-evolution: the conditional virulence causes hosts to stop producing antimicrobials (since the ones who produce them die more).

Therefore, the bacteria populations that *do* respond by becoming more virulent have a stable strategy. This is game theory! The 2 players are: HOST'S GENES, and BACTERIA'S GENES, and each player has 2 strategies.

Let's assume virulent reactions to peptide kills the host (-10 for the host).
 \   HOST     peptide   no peptide
BACTERIA

virulent     (-10, -1)    (-1, +1)

non-virulent (0, 0)       (-1, +1)

(HOST_GENES, BACTERIA_GENES)



as long as there is a credible threat of virulence, hosts may "choose" to not produce peptide. I think the evolutionarily stable solution is "mixed strategies".

Individual bacteria do better by not killing the host, but whole bacterial populations that co-evolve with the host do better by having some individuals who become virulent (sacrificing themselves for the greater good of their family), thus "forcing" the host populations' genes to play "no peptide".

I find it plausible that population selection is a strong enough force in bacterial evolution.
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Wednesday, August 10th, 2005

Mosquitoes are more attracted to people already infected with malaria

It looks like malaria somehow makes its host more delicious to mosquitoes, via [info]tdj
Mosquitoes are more attracted to people already infected with malaria. And this appears to be because the malarial parasite orchestrates its own onward transmission from within the human body, a new study suggests.
...
“What’s surprising is that this is not to the advantage of anybody but the parasite,”...“This tremendously important interaction for the person and the mosquito – both can die as a result – is being engineered by the parasite.”


This "engineering" is natural selection: parasites who implement the mechanism multiply more.

But it seems really unlikely that you could orchestrate both sides of the deal via random mutations... so one of them must have been accidentally tuned to start with (before this mechanism evolved): either (1) the different human smell became a side-effect of the parasite while the effect on the mosquito's attraction to that smell has always been the same; or (2) the other way around (effect on human smell always been the same, effect on mosquito behavior evolved). The first seems more likely, especially since the evidence says nothing about the parasite influencing mosquito behavior.

I would bet that, if for some reason mosquitos stop being attracted to that smell, there is nothing the parasite can do about it. (the alternative would be that the parasite could quickly adapt to make infected mosquitos attracted to that smell again, but my claim here is there would have to be a big fluke for them to hit upon such a mechanism (since mutation is random), unless a similar thing were already encoded in the parasites' genes)
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Tuesday, July 19th, 2005

carbon-dating individual human cells

thread at [info]tdj's about carbon-dating individual human cells (it's a very clever idea):

In discussing the required experimental precision / error, I proposed:
Here's a causation network:

A: atmospheric levels of C14 at time of cell's birth
B: initial amount of C14 in cell's DNA (i.e. at birth)
C: time passed since cell's birth
D: amount of C14 in the cell's DNA
E: "measured" amount of C14 in the cell's DNA (this is actually an estimation based on a measurement of radiation emitted by the cell)

A
 \ 
  B   C
   \ /
    D
    |
    E


In order to infer C, we need to know B and D (this inference step is pretty much dead-on if you have enough C14 atoms (by the law of large numbers)). We estimate D as E (noisy, experimental measurement), and B from A (also noisy, say due to non-uniform C14 levels + random variation in the cell birth process (?); one estimation for each point in history, although this "estimation" may be analytic, not statistical).

How many carbons atoms are there in DNA?
...discussion continues...




I really love making models like this.

I'm sure I've linked to CMU's Tetrad Project / Causality Lab before. But it never hurts to give them another plug.
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Thursday, June 2nd, 2005

blegging Richard Nisbett

does anybody know the name of the researcher who studies "cultural cognition", and who has written about that experiment, where you ask someone to describe a picture? Chinese people will describe the background first, whereas westerners will talk about the prominent fish in the picture.

There was also something about US Southerners being quick to anger (than US Northerners) because their Scottish ancestors were shepherds.


EDIT:
Richard Nisbett is the guy.
He wrote "Culture of Honor: the Psychology of Violence in the South."
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Friday, May 27th, 2005

Doug Candland, mental fossils, R Hanson on "The Evolutionary Origins of Religious Thought"

Doug Candland, one of the most interesting people I met at Bucknell, now has a website. He is the one who introduced me to the concept of meme.

He has finally finished the first draft of his new book Psychology of Mental Fossils: Toward an Archeo-psychology

It deals with the question:
Why do some ideas com up time and time again in human cultures? e.g. spiritual healing, phrenology?

This reminds me of Robin Hanson's review of Pascal Boyer's "Religion Explained: The Evolutionary Origins of Religious Thought"

I might call such a topic "the anatomy of human quirkiness".
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