In this section:
Wed, 29 Jul 2020
Today I learned:
Wed, 15 Jul 2020
A couple of people expressed disappointment with yesterday's article, which asked were giant ground sloths immune to poison ivy?, but then failed to deliver on the implied promise. I hope today's article will make up for that.
David Formosa points out what should have been obvious: elephants are megafauna, elephants live where mangoes grow (both in Africa and in India), elephants love eating mangoes   , and, not obvious at all…
It's sad that we no longer have megatherium. But we do have elephants, which is pretty awesome.
The idiot fruit is just another one of those legendarily awful creatures that seem to infest every corner of Australia (see also: box jellyfish, stonefish, gympie gympie, etc.); Wikipedia says:
At present the seeds are mostly dispersed by gravity. The plant is believed to be an evolutionary anachronism. What Pleistocene megafauna formerly dispersed the poisonous seeds of the idiot fruit?
A wombat. A six-foot-tall wombat.
I am speechless with delight.
Tue, 14 Jul 2020
The skin of the mango fruit contains urushiol, the same irritating chemical that is found in poison ivy. But why? From the mango's point of view, the whole point of the mango fruit is to get someone to come along and eat it, so that they will leave the seed somewhere else. Posioning the skin seems counterproductive.
An analogous case is the chili pepper, which contains an irritating chemical, capsaicin. I think the answer here is believed to be that while capsaicin irritates mammals, birds are unaffected. The chili's intended target is birds; you can tell from the small seeds, which are the right size to be pooped out by birds. So chilis have a chemical that encourages mammals to leave the fruit in place for birds.
What's the intended target for the mango fruit? Who's going to poop out a seed the size of a mango pit? You'd need a very large animal, large enough to swallow a whole mango. There aren't many of these now, but that's because they became extinct at the end of the Pleistocene epoch: woolly mammoths and rhinoceroses, huge crocodiles, giant ground sloths, and so on. We may have eaten the animals themselves, but we seem to have quite a lot of fruits around that evolved to have their seeds dispersed by Pleistocene megafauna that are now extinct. So my first thought was, maybe the mango is expecting to be gobbled up by a giant gound sloth, and have its giant seed pooped out elsewhere. And perhaps its urushiol-laden skin makes it unpalatable to smaller animals that might not disperse the seeds as widely, but the giant ground sloth is immune. (Similarly, I'm told that goats are immune to urushiol, and devour poison ivy as they do everything else.)
Well, maybe this theory is partly correct, but even if so, the animal definitely wasn't a giant ground sloth, because those lived only in South America, whereas the mango is native to South Asia. Ground slots and avocados, yes; mangos no.
Still the theory seems reasonable, except that mangoes are tropical fruit and I haven't been able to find any examples of Pleistocene megafauna that lived in the tropics. Still I didn't look very hard.
Wikipedia has an article on evolutionary anachronisms that lists a great many plants, but not the mango.
[ Addendum: I've eaten many mangoes but never noticed any irritation from the peel. I speculate that cultivated mangoes are varieties that have been bred to contain little or no urushiol, or that there is a post-harvest process that removes or inactivates the urushiol, or both. ]
[ Addendum 20200715: I know this article was a little disappointing and that it does not resolve the question in the title. Sorry. But I wrote a followup that you might enjoy anyway. ]
Tue, 05 Nov 2019
A while back a YouTube video was going around titled Octopus Intelligence Experiment Takes an Unexpected Turn. Someone put food in a baby bottle with a screw cap and a rubber nipple. There was a hole drilled in the bottle so that the octopus could reach in to taste the food, but it was not large enough for the food to come out or for the octopus to go in. The idea, I suppose, was that the octopus would figure out how to unscrew the cap.
The “unpexected turn” was that instead of unscrewing the cap, the octopus just ripped the entire nipple out of the bottle.
I have mentioned this before but it bears repeating: this outcome should not have been an unexpected turn:
(Martin Wells, Octopus: Physiology and Behaviour of an Advanced Invertebrate (Springer, 1978), page 241.)
Fri, 14 Sep 2007
Why spiders hang with their heads down
Fortunately, I was at a meeting this week in Durham that was also attended by three of the world's foremost spider experts. I put the question to Jonathan A. Coddington, curator of arachnids for the Smithsonian Institution.
Professor Coddington told me that it was because the spider prefers (for obvious mechanical and dynamic reasons) to attack its prey from above, and so it waits the upper part of the web and constructs the web so that the principal prey-catching portion is below. When prey is caught in the web, the spider charges down and attacks it.
I had mistakenly thought that spiders in orb webs (which are the circular webs you imagine when you try to think of the canonical spiderweb) perched in the center. But it is only the topological center, and geometrically it is above the midline, as the adjacent picture should make clear. Note that more of the radial threads are below the center than are above it.
Sat, 21 Jul 2007
Homosexuality is not hereditary
But natural selection is more interesting than that. This article will ignore the obvious notion of homosexuals who breed anyway. Here is one way in which homosexuality could be entirely hereditary and still be favored by natural selection.
Suppose that human sexuality is extremely complicated, which should not be controversial. Suppose, just for concreteness, that there are 137 different genes that can affect whether an individual turns out heterosexual or homosexual. Say that each of these can either be either in state Q or state S, and that and that any individual will turn out homosexual if any 93 of the 137 genes are in state Q, heterosexual otherwise.
The over-simplistic argument from natural selection says that the Q states will be bred out of the population, and that S will be increasingly predominant over time.
Now let's consider an individual, X, whose family members tend to carry a lot of Q genes.
Suppose X's parents have a lot of Q genes, around 87 or 90. X's parents' siblings, who resemble them, will also have a lot of Q genes, and have a high probability of being homosexual. Having no children of their own, they may contribute to X's welfare, maybe by caring for X or by finding food for X.
In short, for every gay uncle X has, that is one additional set of cousins with whom X does not have to compete for scarce resources.
This could well turn out to be a survival advantage for X over someone from a family of people without a lot of Q genes, someone who is competing for food with a passel of cousins, none of whom ever really get enough to eat, someone whose aunt might even try to kill them in order to benefit her own children.
Perhaps X turns out to be homosexual and never breeds, but X probably has some siblings, in which case X might be an advantageous gay uncle or lesbian aunt to one of his or her own nieces or nephews, who, remember, are carrying a lot of the same genes, including the Q genes.
It might not actually work this way, of course, and in most ways it probably doesn't. The only point here is to show that natural selection does not necessarily rule out the idea of inherited homosexuality; people who think it must, have not exercised enough imagination.
(Now that I have finished writing this article, it occurs to me that the same argument applies to bees and ants; most individuals in a bee or ant colony are sterile. Who would be foolish enough to argue that this trait will soon be bred out of the colony?)
Time and time again, biologists baffled by some apparently futile or maladroit bit of bad design in nature have eventually come to see that they have underestimated the ingenuity, the sheer brilliance, the depth of insight to be disovered in one of Mother Nature's creations. Francis Crick has mischievously baptized this trend in the name of his colleague Leslie Orgel, speaking of what he calls "Orgels Second Rule: Evolution is cleverer than you are."Daniel Dennett, Darwin's Dangerous Idea, p. 74.
Wed, 06 Dec 2006
Serendipitous web searches
Back in the 1950's and 1960's, James V. McConnell at the University of Michigan was doing some really interesting work on learning and memory in planaria flatworms, shown at right. They used to publish their papers in their own private journal of flatworm science, The Journal of Biological Psychology. They didn't have enough material for a full journal, so when you were done reading the Journal, you could flip it over and read the back half, which was a planaria-themed humor magazine called The Worm-Runner's Digest. I swear I'm not making this up.
(I think it's time to revive the planaria-themed humor magazine. Planaria are funny even when they aren't doing anything in particular. Look at those googly eyes!)
(For some reason I've always found planaria fascinating, and I've known about them from an early age. We would occasionally visit my cousin in Oradell, who had a stuffed toy which was probably intended to be a snake, but which I invariably identified as a flatworm. "We're going to visit your Uncle Ronnie," my parents would say, and I would reply. "Can I play with Susan's flatworm?")
Anyway, to get on with the point of this article, McConnell made the astonishing discovery that memory has an identifiable chemical basis. He trained flatworms to run mazes, and noted how long it took to do so. (The mazes were extremely simple T shapes. The planarian goes in the bottom foot of the T. Food goes in one of the top arms, always the same one. Untrained planaria swim up the T and then turn one way or the other at random; trained planaria know to head toward the arm where the food always is. Pretty impressive, for a worm.)
Then McConnell took the trained worms and ground them up and fed them to untrained worms. The untrained worms learned to run the maze a lot faster than the original worms had, apparently demonstrating that there was some sort of information in the trained worms that survived being ground up and ingested. The hypothesis was that the information was somehow encoded in RNA molecules, and could be physically transferred from one individual to another. Isn't that a wonderful dream?
You can still see echoes of this in the science fiction of the era. For example, a recurring theme in Larry Niven's early work is "memory RNA", people getting learning injections, and pills that impart knowledge when you swallow them. See World Out of Time and The Fourth Profession, for example. And I once had a dream that I taught a giant planarian to speak Chinese, then fried it in cornmeal and ate it, after which I was able to speak Chinese. So when I say it's a wonderful dream, I'm speaking both figuratively and literally.
Unfortunately, later scientists were not able to reproduce McConnell's findings, and the "memory RNA" theory has been discredited. How to explain the cannibal flatworms' improved learning times, then? It seems to have been sloppy experimental technique. The original flatworms left some sort of chemical trail in the mazes, that remained after they had been ground up. McConnell's team didn't wash the mazes in between tests, and the cannibal flatworms were able to follow the trails later; it had nothing to do with their diet. Bummer.
So a couple of years ago I was poking around, looking for more information about this, and in particular for a copy of McConnell's famous paper Memory transfer through cannibalism in planarium, which I didn't find. But I did find the totally unrelated Robert French paper. It mentions McConnell, as an example of another cool-sounding and widely-reported theory that took a long time to dislodge, because it's hard to produce clear evidence that cannibal flatworms aren't in fact learning from their lunch meat, and because the theory that they aren't learning is so much less interesting-sounding than the theory that they are. News outlets reported a lot about the memory RNA breakthrough, and much less about the later discrediting of the theory.
French's paper, you will recall, refutes the interesting-sounding hypothesis that infants resemble their fathers more strongly then they do their mothers, and has many of the same difficulties.
There are counterexamples. Everyone seems to have heard that the Fleischmann and Pons tabletop cold fusion experiment was an error. And the Hwang Woo-Suk stem cell fraud is all over the news these days.
Tue, 05 Dec 2006
Do infants resemble their fathers more than their mothers?
A couple years ago, while looking for something entirely unrelated, I ran across the paper of French et al. titled The Resemblance of One-year-old Infants to Their Fathers: Refuting Christenfeld & Hill. French and his colleagues had tried to reproduce Christenfeld and Hill's results, with little success; they suggested that the conclusion was false, and offered a number of arguments as to why the purported resemblance should not exist. Of course, the pop science press was totally uninterested.
At the time, I thought, "Wow, I wish I had a way to get a lot of people to read this paper." Then last month I realized that my widely-read blog is just the place to do this.
Before I go on, here is the paper. I recommend it; it's good reading, and only six pages long. Here's the abstract:
In 1995 Christenfeld and Hill published a paper that purported to show at one year of age, infants resemble their fathers more than their mothers. Evolution, they argued, would have produced this result since it would ensure male parental resources, since the paternity of the infant would no longer be in doubt. We believe this result is false. We present the results of two experiments (and mention a third) which are very far from replicating Christenfeld and Hill's data. In addition, we provide an evolutionary explanation as to why evolution would not have favored the result reported by Christenfeld and Hill.Other related material is available from Robert French's web site.
In the first study done by French, participants were presented with a 1-, 3-, or 5-year-old child's face, and the faces of either the father and two unrelated men, or the mother and two unrelated women. The participants were invited to identify the child's parent. They did indeed succeed in identifying the children's parents somewhat more often than would have been obtained by chance alone. But the participants did not identify fathers more reliably than they identified mothers.
The second study was similar, but used only 1-year-old infants. (The Christenfeld and Hill claim is that one year is the age at which children most resemble their fathers.)
French points out that although the argument from evolutionary considerations is initially attractive, it starts to disintegrate when looked at more closely. The idea is that if a child resembles its father, the father is less likely to doubt his paternity, and so is less likely to withhold resources from the child. So there might be a selection pressure in favor of resembling one's father.
But now turn this around: if a father can be sure of paternity because the children look like him, then he can also be sure when the children aren't his because they don't resemble him. This will create a very strong selection pressure in favor of children resembling their fathers. And the tendency to resemble one's father will create a positive feedback loop: the more likely kids are to look like their fathers, the more likely that children who don't resemble their fathers will be abandoned, neglected, abused, or killed. So if there is a tendency for infants to resemble their fathers more than their mothers, one would expect it to be magnified over time, and to be fairly large by now. But none of the studies (including the original Christenfeld and Hill one) found a strong tendency for children to resemble their fathers.
But, as French notes, it's hard to get people to pay attention to a negative result, to a paper that says that something interesting isn't happening.
[ Addendum 20061206: Here's the original Christenfeld and Hill paper. ]
[ Addendum 20171101: A recent web search refutes my claim that “the pop science press was totally uninterested”. Results include this article from Scientific American and a mention in the book Bumpology: The Myth-Busting Pregnancy Book for Curious Parents-To-Be. ]
[ Addendum 20171101: A more extensive study in 2004 confirmed French's results. ]
Mon, 16 Oct 2006
Why two ears?
The example given in the article that I found most interesting was "Why don't we just have one ear in the middle of our face?". As I said earlier, I think the mark of a good question is that it's quick to ask and long to answer. I've been thinking about this one for several days now, and seems pretty long to answer.
Any reasonable answer to this question is going to be based on evolutionary and adaptive considerations, I think. When you answer from evolutionary considerations, there are only a few kinds of answers you can give:
(Why only one heart? There's no benefit to having two; if you lose 50% of your cardiac capacity, you'll die anyway. Why one mouth? It needs to be big enough to eat with, and anyway, you can't lose it. Why one liver? No reason; that's just the way it's made; two livers would work just as well as one. Why two lungs? I'm not sure; I suppose it's a combination between "no reason, that's the way it's made" (#3 above) and "because that way you can still breathe even if one lung gets clogged up" (#1).)
The positioning of your ears is important. Having two ears far apart on the sides of your head allows you to locate sounds by triangulation. Triangulation requires at least two ears, and requires that they be as far apart as possible. This also explains why the ears are on the sides rather than the front.
Consider what would go wrong if the positions of the eyes and ears were switched. The ears would be pointed in the same direction, which would impede the triangulation-by-sound process. The eyes would be pointed in opposite directions, which would completely ruin the triangulation-by-sight process; you would completely lose your depth perception. So the differing position of the eyes and ears can be seen a response to the differing physical properties of light and sound: light travels in straight lines; sound does not.
The countervailing benefit to losing your depth perception would be that you would be able to see almost 180 degrees around you. Many animals do have their eyes on the side of their heads: antelopes, rabbits, and so forth. Prey, in other words. Predators have eyes on the fronts of their heads so that they can see the prey they are sneaking up on. Prey have eyes on the sides of their heads so that predators can't sneak up on their flanks. Congratulations: you're predator, not prey.
Animals do have exactly one nose in the middle of their face. Why not two? Here, triangulation is not an issue at all. Having one nose on each side of your head would not help you at all to locate the source of an odor. So the nose is stuck in the middle of the head, I suppose for mostly mechanical reasons: animals with noses evolved from animals with a long breathing tube down the middle of their bodies. The nose arises as sensors stuck in the end of the tube. This is another explanation for the one mouth.
Another consideration is symmetry. The body is symmetric, so if you want two ears, you have to put one on each side. Why is this? I used to argue that it was to save information space in the genome: there is only so much room in your chromosomes for instructions about how to build your body, so the information must be compressed. One excellent way to compress it is to make some parts like other parts and then express the differences as diffs. This, I used to say, is why the body is symmetric, why your feet look like your hands, and why men's and women's bodies are approximately the same.
I now think this is wrong. Well, wrong and right, essentially right, but mostly wrong. The fact is, there is plenty of space in the chromosomes for instructions about all sorts of stuff. Chromosomes are really big, and full of redundancy and junk. And if it's so important to save space in the chromosome, why is the inside of your body so very asymmetric?
I now think the reason for symmetries and homologies between body parts is less to do with data compression and storage space in the chromosome, and more to do with the shortness of the distance between points in information space. Suppose you are an animal with two limbs, each of which has a hand on the end. Then a freak mutation occurs so that your descendants now have four limbs. The four limbs will all have similar hands, because mutation cannot invent an entirely new kind of hand out of thin air. Your genome contains only one set of instructions for appendages that go on the ends of limbs, so these are the instructions that are available to your descendants. These instructions can be duplicated and modified, but again, there is no natural process by which a new set of instructions for a new kind of appendage can be invented from whole cloth. So your descendants' hands will look something like their feet for quite a long time.
Similarly, there is a certain probability, say p, of an earless species evolving something that functions as an ear. The number p is small, and ears arise only because of natural selection in favor of having ears. The chance that the species will simultaneously and independently evolve two completely different kinds of ear structures is no more than p2, which is vanishingly small. And once the species has something earlike, the selection pressure in favor of the second sort of ear is absent. So a species gets one kind of ear. If having two ears is beneficial, it is extremely unlikely to arise through independent evolution, and much more likely to arise through a much smaller mutation that directs the same structure, the one for which complete instructions already exist in the genome, to appear on each side of the head.
So this is the reason for bodily symmetry. Think of (A) an earless organism, (B) an organism with two completely different ears, and (C) an organism with two identical ears. Think of these as three points in the space of all possible organisms. The path from point A to C is both much shorter than the path from A to B, and also much more likely to be supported by selection processes.
Now, why is the outside of the body symmetric while the inside is not? I haven't finished thinking this through yet. But I think it's because the outside interacts with the gross physical world to a much greater extent than the inside, and symmetry confers an advantage in large-scale physical interactions. Consider your legs, for example. They are approximately the same length. This is important for walking. If you had a choice between having both legs shortened six inches each, and having one leg shortened by six inches, you would certainly choose the former. (Unless you were a sidehill winder.) Similarly, having two different ears would mess up your hearing, particularly your ability to locate sounds. On the other hand, suppose one of your kidneys were much larger than the other. Big deal. Or suppose you had one giant liver on your right side and none on the left. So what? As long as your body is generally balanced, it is not going to matter, because the liver's interactions with the world are mostly on a chemical level.
So I think that's why you have an ear on each side, instead of one ear in the middle of your head: first, it wouldn't work as well to have one. Second, symmetry is favored by natural selection for information-conserving reasons.
Fri, 08 Sep 2006
I get a new job
(Many people have been surprised to learn that I have a job; they remember that for many years I was intermittently a software consultant and itinerant programming trainer. But since January 2004 I have been regularly employed to do maintenance programming for the University of Pennsylvania's Networking and Telecommunications group.)
Anyway, the job hunt has come to a close. I accepted a new job, put in my resignation letters at the old one, and can stop thinking about it for a while. The new work will be head software engineer at the Penn Genomics Institute. I will try to develop software for genetic biologists to use in their research. I expect that the new job will suit me somewhat better than the old one. I like that it is connected to science, and that I will be working with scientists. The work itself is important; genomics is going to change everything in the world. Also, it pays rather more than the old one, although that was not the principal concern.
So with any luck blog posts will resume here, and eventually some genomics-related articles may start appearing.
Fri, 27 Jan 2006
The octopus and the creation of the cosmos
Although we have the source of all things from chaos, it is a chaos which is simply the wreck and ruin of an earlier world....The drama of creation, according to The Hawaiian account, is divided into a series of stages, and in the very first of these life springs from the shadowy abyss and dark night...At first the lowly zoophytes and corals come into being, and these are followed by worms and shellfish, each type being declared to conquer and destroy its predecessor, a struggle for existence in which the strongest survive....As type follows type, the accumulating slime of their decay raises land above the waters, in which, as spectator of all, swims the octopus, the lone survivor of an earlier world.(Mythology of All Races, vol. ix ("Oceanic"), R.B. Dixon. Thanks to the wonders of the Internet, you can now read the complete text online.)
Everyone, it seems, recognizes the octopus as a weird alien, unique in our universe.
Wed, 25 Jan 2006
A reader, who goes by the name of Omar, wrote to remind me of the "Hox" (short for "homeobox") genes discussed by Richard Dawkins in The Ancestor's Tale. (No "buy this" link; I only do that for books I've actually read and recommend.) These genes are certainly part of the story, just not the part I was wondering about.
The Hox genes seem to be the master controls for notifying developing cells of their body locations. The proteins they manufacture bind with DNA and enable or disable other genes, which in turn manufacture proteins that enable still other genes, and so on. A mutation to the Hox genes, therefore, results in a major change to the animal's body plan. Inserting an additional copy of a Hox gene into an invertebrate can cause its offspring to have duplicated body segements; transposing the order of the genes can mix up the segments. One such mutation, occurring in fruit flies, is called antennapedia, and causes the flies' antennae to be replaced by fully-formed legs!
So it's clear that these genes play an important part in the overall body layout.
But the question I'm most interested in right now is how the small details are implemented. That's why I specifically brought up the example of a ring finger.
Or consider that part of the ring finger turns into a fingernail bed and the rest doesn't. The nail bed is distally located, but the most distal part of the finger nevertheless decides not to be a nail bed. And the ventral part of the finger at the same distance also decides not to be a nail bed.
Meanwhile, the ear is growing into a very complicated but specific shape with a helix and an antihelix and a tragus and an antitragus. How does that happen? How do the growing parts communicate between each other so as to produce that exact shape? (Sometimes, of course, they get confused; look up accessory tragus for example.)
In computer science there are a series of related problems called "firing squad problems". In the basic problem, you have a line of soldiers. You can communicate with the guy at one end, and other than that each soldier can only communicate with the two standing next to him. The idea is to give the soldiers a protocol that allows them to synchronize so that they all fire their guns simultaneously.
It seems to me that the embryonic cells have a much more difficult problem of the same type. Now you need the soldiers to get into an extremely elaborate formation, even though each soldier can only see and talk to the soldiers next to him.
Omar suggested that the Hox genes contain the answer to how the fetal cells "know" whether to be a finger and not a kneecap. But I think that's the wrong way to look at the problem, and one that glosses over the part I find so interesting. No cell "becomes a finger". There is no such thing as a "finger cell". Some cells turn into hair follicles and some turn into bone and some turn into nail bed and some turn into nerves and some turn into oil glands and some turn into fat, and yet you somehow end up with all the cells in the right places turning into the right things so that you have a finger! And the finger has hair on the first knuckle but not the second. How do the cells know which knuckle they are part of? At the end of the finger, the oil glands are in the grooves and not on the ridges. How do the cells know whether they will be at the ridges or the grooves? And the fat pad is on the underside of the distal knuckle and not all spread around. How do the cells know that they are in the middle of the ventral surface of the distal knuckle, but not too close to the surface?
Somehow the fat pad arises in just the right place, and decides to stop growing when it gets big enough. The hair cells arise only on the dorsal side and the oil glands only on the ventral side.
How do they know all these things? How does the cell decide that it's in the right place to differentiate into an oil gland cell? How does the skin decide to grow in that funny pattern of ridges and grooves? And having decided that, how do the skin cells know whether they're positioned at the appropriate place for a ridge or a groove? Is there a master control that tells all the cells everything at once? I bet not; I imagine that the cells conduct chemical arguments with their neighbors about who will do which job.
One example of this kind of communication is phyllotaxis, the way plants decide how to distribute their leaves around the stem. Under certain simple assumptions, there is an optimal way to do this: you want to go around the stem, putting each leaf about 360°/φ farther than the previous one, where φ is ½(1+√5). (More about this in some future post.) And in fact many plants do grow in just this pattern. How does the plant do such an elaborate calculation? It turns out to be simple: Suppose leafing is controlled by the buildup of some chemical, and a leaf comes out when the chemical concentration is high. But when a leaf comes out, it also depletes the concentration of the chemical in its vicinity, so that the next leaf is more likely to come out somewhere else. Then the plant does in fact get leaves with very close to optimal placement. Each leaf, when it comes out, warns the nearby cells not to turn into a leaf themselves---not until the rest of the stem is full, anyway. I imagine that the shape of the ear is constructed through a more complicated control system of the same sort.
an earlier post I remarked that "The liver of arctic animals . . . has a toxically high concentration of vitamin D". Dennis Taylor has pointed out that this is mistaken; I meant to say "vitamin A". Thanks, Dennis.
B and C vitamins are not toxic in large doses; they are water-soluble so that excess quantities are easily excreted. Vitamins A and D are not water-soluble, so excess quantities are harder to get rid of. Apparently, though, the liver is capable of storing very large quantities of vitamin D, so that vitamin D poisoning is extremely rare.
The only cases of vitamin A poisoning I've heard of concerned either people who ate the livers of polar bears, walruses, sled dogs, or other arctic animals, or else health food nuts who consumed enormous quantities of pure vitamin A in a misguided effort to prove how healthy it is. In On Food and Cooking, Harold McGee writes:
In the space of 10 days in February of 1974, an English health food enthusiast named Basil Brown took about 10,000 times the recommended requirement of vitamin A, and drank about 10 gallons of carrot juice, whose pigment is a precursor of vitamin A. At the end of those ten days, he was dead of severe liver damage. His skin was bright yellow.(First edition, p. 536.)
There was a period in my life in which I was eating very large quantities of carrots. (Not for any policy reason; just because I like carrots.) I started to worry that I might hurt myself, so I did a little research. The carrots themselves don't contain vitamin A; they contain beta-carotene, which the body converts internally to vitamin A. The beta-carotene itself is harmless, and excess is easily eliminated. So eat all the carrots you want! You might turn orange, but it probably won't kill you.
Tue, 24 Jan 2006
The really interesting thing I learned was that chrysalises are not featureless lumps. You can see something of the shape of the animal in them. (See, for example, this Wikipedia illustration.) The caterpillar has an exoskeleton, which it molts several times as it grows. When time comes to pupate, the chrysalis is in fact the final exoskeleton, part of the animal itself. This is in contrast to a cocoon, which is different. A cocoon is a case made of silk or leaves that is not part of the animal; the animal builds it and lives inside. When you think of a featureless round lump, you're thinking of a cocoon.
Until recently, I had the idea that the larva's legs get longer, wings sprout, and so forth, but it's not like that at all. Instead, inside the chrysalis, almost the entire animal breaks down into a liquid! The metamorphosis then reorganizes this soup into an adult. I asked the explainer at the Museum if the individual cells retained their identities, or if they were broken down into component chemicals. She didn't know, unfortunately. I hope to find this out in coming weeks.
How does the animal reorganize itself during metamorphosis? How does its body know what new shape to grow into? It's all a big mystery. It's nice that we still have big mysteries. Not all mysteries have survived the scientific revolution. What makes the rain fall and the lightning strike? Solved problems. What happens to the food we eat, and why do we breathe? Well-understood. How does the butterfly reorganize itself from caterpillar soup? It's a big puzzle.
A related puzzle is how a single cell turns into a human baby during gestation. For a while, the thing doubles, then doubles again, and again, becoming roughly spherical, as you'd expect. But then stuff starts to happen: it dimples, and folds over; three layers form, a miracle occurs, and eventually you get a small but perfectly-formed human being. How do the cells in the fingers decide to turn into fingers? How does the cells in the fourth finger know they're one finger from one side of the hand and three fingers from the other side? Maybe the formation of the adult insect inside the chrysalis uses a similar mechanism. Or maybe it's completely different. Both possibilities are mind-boggling.
This is nowhere near being the biggest pending mystery; I think we at least have some idea of where to start looking for the answer. Contrast this with the question of how it is we are conscious, where nobody even has a good idea of what the question is.
Other caterpillar news: chrysalides are so named because they often have a bright golden sheen, or golden features. (Greek "khrusos" is "gold".) The Wikipedia picture of this is excellent too. The "gold" is a yellow pigmented area covered with a shiny coating. The explainer said that some people speculate that it helps break up the outlines of the pupa and camouflage it.
I asked if the chrysalis of the viceroy butterfly, which, as an adult, resembles the poisonous monarch butterfly, also resembled the monarch's chrysalis. The answer: no, they look completely different. Isn't that interesting? You'd think that the pupa would get at least as much benefit from mimicry as the adult. One possible explanation why not: most pupae don't make it to adulthood anyway, so the marginal benefit to the species from mimicry in the pupal stage is small compared with the benefit in the adult stage. Another: the pupa's main defense, which is not available to the adult, is to be difficult to see; beyond that it doesn't matter much what happens if it is seen. Which is correct? I don't know.
For a long time folks thought that the monarch was poisonous and the viceroy was not, and that the viceroy's monarch-like coloring tricked predators into avoiding it unnecessarily. It's now believed that both speciies are poisonous and bad-tasting, and that their similar coloring therefore protects both species. A predator who eats one will avoid both in the future. The former kind of mimicry is called Batesian; the latter, Müllerian.
The monarch butterfly does not manufacture its toxic and bad-tasting chemicals itself. It is poisonous because it ingests poisonous chemicals in its food, which I think is milkweed plants. Plant chemistry is very weird. Think of all the poisonous foods you've ever heard of. Very few of them are animals. (The only poisonous meat I can think of offhand is the liver of arctic animals, which has a toxically high concentration of vitamin D.) If you're stuck on a desert island, you're a lot safer eating strange animals than you are eating strange berries.
Wed, 18 Jan 2006 Daniel Dennett is a philosopher of mind and consciousness. The first work of his that came to my attention was his essay "Why You Can't Build a Computer That Can Feel Pain". This is just the sort of topic that college sophomores love to argue about at midnight in the dorm lounge, the kind of argument that drives me away, screaming "Shut up! Shut up! Shut up!"
But to my lasting surprise, this essay really had something to say. Dennett marshaled an impressive amount of factual evidence for his point of view, and found arguments that I wouldn't have thought of. At the end, I felt as though I really knew something about this topic, whereas before I read the essay, I wouldn't have imagined that there was anything to know about it. Since then, I've tried hard to read everything I can find that Dennett has written.
A teleological explanation is one the explains the existence or occurrence of something by citing a goal or purpose that is served by the thing. Artifacts are the most obvious cases; the goal or purpose of an artifact is the function it was designed to serve by its creator. There is no controversy about the telos of a hammer: it is for hammering in and pulling out nails. The telos of more complicated artifacts, such as camcorders or tow trucks or CT scanners, is if anything more obvious. But even in simple cases, a problem can be seen to loom in the background:(Darwin's Dangerous Idea, pp. 24–25.)
Anyway, there's one place in this otherwise excellent book where Dennett really blew it. First he quotes from a 1988 Boston Globe article by Chet Raymo, "Mysterious Sleep":
University of Chicago sleep researcher Allan Rechtshaffen asks "how could natural selection with its irrevocable logic have 'permitted' the animal kingdom to pay the price of sleep for no good reason? Sleep is so apparently maladaptive that it is hard to understand why some other condition did not evolve to satisfy whatever need it is that sleep satisfies.And then Dennett argues:
But why does sleep need a "clear biological function" at all? It is being awake that needs an explanation, and presumably its explanation is obvious. Animals—unlike plants—need to be awake at least part of the time in order to search for food and procreate, as Raymo notes. But once you've headed down this path of leading an active existence, the cost-benefit analysis of the options that arise is far from obvious. Being awake is relatively costly, compared with lying dormant. So presumably Mother Nature economizes where she can. . . . But surely we animals are at greater risk from predators while we sleep? Not necessarily. Leaving the den is risky, too, and if we're going to minimize that risky phase, we might as well keep the metabolism idling while we bide our time, conserving energy for the main business of replicating.(Darwin's Dangerous Idea, pp. 339–340, or see index under "Sleep, function of".)
This is a terrible argument, because Dennett has apparently missed the really interesting question here. The question isn't why we sleep; it's why we need to sleep. Let's consider another important function, eating. There's no question about why we eat. We eat because we need to eat, and there's no question about why we need to eat either. Sure, eating might be maladaptive: you have to leave the den and expose yourself to danger. It would be very convenient not to have to eat. But just as clearly, not eating won't work, because you need to eat. You have to get energy from somewhere; you simply cannot run your physiology without eating something once in a while. Fine.
But suppose you are in your den, and you are hungry, and need to go out to find food. But there is a predator sniffing around the door, waiting for you. You have a choice: you can stay in and go hungry, using up the reserves that were stored either in your body or in your den. When you run out of food, you can still go without, even though the consequences to your health of this choice may be terrible. In the final extremity, you have the option of starving to death, and that might, under certain circumstances, be a better strategy than going out to be immediately mauled by the predator.
With sleep, you have no such options. If you're treed by a panther, and you need to stay awake to balance on your branch, you have no options. You cannot use up your stored reserves of sleep. You do not have the option to go without sleep in the hope that the panther will get bored and depart. You cannot postpone sleep and suffer the physical consequences. You cannot choose to die from lack of sleep rather than give up and fall out of the tree. Sooner or later you will sleep, whether you choose to or not, and when you sleep you will fall out of the tree and die.
People can and do go on hunger strikes, refuse to eat, and starve to death. Nobody goes on sleep strikes. They can't. Why not? Because they can't. But why can't they? I don't think anyone knows.
The question isn't about the maladaptivity of sleeping itself; it's about the maladaptivity of being unable to prevent or even to delay sleep. Sleep is not merely a strategy to keep us conveniently out of trouble. If that were all it was, we would need to sleep only when it was safe, and we would be able to forgo it when we were in trouble. Sleep, even more than food, must serve some vital physiological role. The role must be so essential that it is impossible to run a mammalian physiology without it, even for as long as three days. Otherwise, there would be adaptive value in being able to postpone sleep for three days, rather than to fall asleep involuntarily and be at the mercy of one's enemies.
Given that, it is indeed a puzzle that we have not been able to identify the vital physiological role of sleep, and Rechtshaffen's puzzlement above makes sense.