MRAs don’t understand evolution or development

Since form is a consequence of differential growth of tissues, and since different tissues grow at different rates, one of the ways evolution can shape morphology is through changes in growth rate, so changes in timing can produce very different forms. There are genes that affect specific tissues discretely; for instance, the gene ASPM regulates mitotic activity in regions of the brain, so mutations in it can produce smaller brains, or microcephaly. There are also global regulators of growth, and just changing the rate of maturation of the organism can produce changes in the proportion of different tissues, because of allometric variation in different regions.

So, for instance, if developmental maturation of the somatic tissues is slowed, while sexual maturation is maintained at the standard rate, individuals retain juvenile characters at reproductive age, a process called neoteny (similarly, you can get a similar effect by maintaining a standard rate of somatic growth, but accelerating the rate of sexual maturation, a process called progenesis.) Note that what’s key here is that different tissues are regulated differently; if you just slow the rate of development of both somatic and reproductive organs, you get individuals with the standard morphology, it just takes longer for them to get there. Everyone who knows anything about development and evolution understands that neoteny/progenesis requires independent regulation of different tissues.

One of the factors thought to play a role in human evolution is neoteny. Compared to other primates, adult humans retain a juvenile morphology: heads large in proportion to our bodies, larger eyes, smaller jaws, etc. This is not particularly controversial, although I’d really like to see more specific identification of the genes involved. Our shape could, after all, alternatively be explained by character by character changes in gene expression. The neoteny hypothesis implies that a large cranium and small jaw are correlated, that is, by changing one regulator of growth you get both effects. It would also be possible that they’re uncorrelated, that (as a simplified example) one gene that generates larger brains evolved, and that a second gene for reduced jaws evolved completely independently.

Neoteny can also be a mosaic process. Big head and small jaws are a retention of a juvenile character, but other features, like our bigger noses and ears as adults compared to babies (creepy visualization: imagine a baby with a nose as big in proportion to its head as an adult’s; all cuteness disappears). Even if the neoteny hypothesis is generally valid, it can’t explain all the features of an adult human, and does not imply that humans are all big babies in every respect. Donald Trump excepted.

That’s the background. Now for the pseudoscientific appropriation of a concept from development and evolution.

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Agriculture was a mistake…except to the 7 billion people who wouldn’t exist without it

Jared Diamond’s 1987 article, The Worst Mistake in the History of the Human Race, got me wondering. How do you define “mistake”? He doesn’t. What would a successful species look like? He doesn’t say. While it’s thought-provoking, it’s very hard to pin down his meaning without some explanation for those concepts.

The biggest mistake, he claims, was agriculture. He argues against a progressivist view of history, which argues that agriculture couldn’t possibly be a mistake, because it must have improved human lives or we wouldn’t have adopted it, and on those grounds, I think he’s right in principle — we adopt stupid ideas all the time. But then he tries to take an extreme opposite tack, that agriculture was bad for human beings, and there I think he’s going wrong. Agriculture produced a different environment for our species, and it had a mix of consequences.

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I am not fooled: the zombie apocalypse is nigh

Yesterday was awful. All the aches and pains of being confined to a tiny space for more than a day jumped up and bit me in the butt, and I’m also struggling with a bad case of jet lag and the crankies. So I spent yesterday in an achey, woozy fog, and today looks only slightly better.

Then to top it all off, the internet connection at my house died. I could not communicate with the rest of the world from my comfy chair, and I was too messed up to stagger someplace with a live connection. I dropped off the internet for most of yesterday, which, considering my mood, might have been a good thing.

Also, this morning I read this story about resurrecting Renaissance technologies. Internet down, and people are building wooden printing presses and trying to bring back bookmaking? Definitely signs that we’re in the End Times.

The way I feel right now, though, I’m just going to bow to the zombies, presenting them my head, and tell them to eat and get it all over with.

What is a “computer”? What is “information processing”?

Just before I left the States, I read this, shall we say, interesting article about how your brain is not a computer. The subhead, which does more or less summarize the content, is:

Your brain does not process information, retrieve knowledge or store memories. In short: your brain is not a computer

Curiously, in order to comprehend the article, I had to retrieve knowledge and stored memories about neuroscience (I have a degree in that) and computers (I worked in the field for several years), and I had to process the information in the article and in my background, and I found that article confusing. It did not compute.

Jeffrey Shallit, who knows much more about the information processing side of the story, also found it somewhat enraging.

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Glyphosate turns out to be kind of a boring molecule


Derek Lowe has a sensible article about glyphosphate, the herbicide otherwise known as Roundup. Glyphosate is scary: it’s a chemical, don’t you know, and it kills weeds, so who knows what it’s doing to your children and your cats; even scarier, some crops are being genetically modified to be resistant to glyphosate, and then proteins that protect against Roundup might end up in your cornflakes.

And now some people are raving that glyphosate causes autism, because of course every chemical compound that they don’t understand causes behavioral problems that we don’t like. We must have a scapegoat. It doesn’t matter that it has never been found to have an effect on humans.

An extensive scientific literature indicates that glyphosate is specifically not genotoxic, is not a carcinogen or a teratogen, nor has any specific adverse health effect ever been demonstrated to have been caused by exposure to or low-level consumption of glyphosate. It has little effect on non-target organisms other than plants; a contributing factor to this is that glyphosate inhibits an enzyme found in plants. This enzyme is not found in humans, other mammals, birds, fish, or insects.

The use of glyphosate on herbicide tolerant crops has proven problematic to anti-GMO activists since adoption of the technology promotes the switch to a chemical with a lower environmental impact quotient and lower toxicity.

Lowe explains the statistical nature of risk, and the cautious style of chemical classifications, that allows almost any chemical to be judged as risky to some degree, and feeds sensationalist misreadings. All the data really seems to be saying that it does nothing to animals, but let’s cover our bets and keep an eye on it.

I even have an anecdote about Roundup. We tried to see if it has any early teratogenic effects. The results are sadly unpublishable (for very bad reasons) so it’s safe to summarize them here.

We have a simple assay for developmental errors. Zebrafish pop out a bunch of eggs every morning when the lights come on, and we clean them up and separate them out into beakers, with about 100ml of water for 50 embryos. For our controls, we use fish tank water, the same stuff the adults are swimming around in. It’s got fish pee in it, bacteria, fungal spores, even tiny invertebrates (check your home aquarium water — would you drink it?). We use that because it does have some challenges for growing embryos, and provides a good background for comparisons — we lose 5-10% of the embryos, usually to fungal growth, in these situations.

I had a student who wanted to test local water sources for potential teratogens. So they collected jugs of water from nearby ponds and streams, which are rich with agricultural runoff. We then grew embryos in simple, unfiltered water from Lake Crystal, or the Pomme de Terre river, or nearby ponds, just to see if we had any preliminary effect worth pursuing. This is why we use crude tank water for the controls — those sources would also be complex and biologically rich.

Here’s the boring result: nothing happened. Fish grew happily in water from a shallow pond full of duck poop with an ethanol plant on one side and a dairy farm on the other, with no detectable disorders or effects on the rate of development. In fact, the pond water embryos were healthier in one sense — they had reduced mortality from fungal infections than embryos in tank water. Tentative explanation for that: tank water might specifically be a breeding ground for fungi that thrive on fish, or the fungi might be more sensitive to agricultural chemicals than the fish are. Anyway, it was a negative result.

Then we thought to push it, and see if we could get any deleterious effect from those agricultural chemicals, so I bought a gallon of Roundup at the hardware store, and we did a dilution series. Nope, nothing. We had embryos growing in a concentration of several percent glyphosate, and they didn’t seem to mind at all. We used concentrations that were approximately ten times what Monsanto recommends that you spray directly on your lawn, and the zebrafish didn’t care.

Now of course this was a limited and preliminary experiment. All we were examining was survival and basic morphology, and we were only looking at early developmental events, like gastrulation and neurulation and the earliest twitching behaviors, and we can say with some confidence that those were unaffected. We did not look at older animals, so if it were an endocrine disruptor (it isn’t) for instance, we wouldn’t know it. We also don’t have a test for fish autism.

I can also say that I wouldn’t drink glyphosate, but not because I’m afraid it would give me cancer. It’s because the straight stuff is kind of oily and smells nasty. So those stunts where people give Monsanto executives a glass of Roundup and dare them to drink it are really misleading — they’re not going to drink it because concentrated-just-about-anything is unpleasant.

I think the bottom line is that making a claim about the deleterious effects of a substance requires actual data, and not cherry-picking suggestive and vaguely defined effects.

It also says that the file drawer effect is a problem. I suspect there have been lots of preliminary experiments that see nothing, and are abandoned as unpublishable, like ours. That effect is also complicated. You can’t tell me just to take the data we got and publish that, because it really was just a quick pilot experiment to see if there was something worth pursuing. It’s not just that a negative result is unpublishable, but that we didn’t see enough of an effect to make it worth our while to invest enough time and effort to make the results thorough and robust enough to even consider getting it into publishable shape. And thus science staggers on.

Mendel vs. Weldon, a pointless rematch


Classes are over, and that means I have more time to think…about my classes. So I’m on the lookout for ideas to improve my teaching, and gosh, look, Nature has an article on better ways to teach genetics. So I read it eagerly, and was left scratching my head. It’s a short news article, so it’s a bit thin on the details of how to teach genetics the way it recommends, but I’m also confused about how this approach would be useful.

The author, Gregory Radick, advocates teaching Weldonian genetics, rather than Mendelian genetics.

In a recent two-year project, we taught university students a curriculum that was altered to reflect what genetics textbooks might be like now if biology circa 1906 had taken the Weldonian rather than the Mendelian route. These students encountered genetics as funda­mentally tied to development and environment. Genes were not presented to them as what inheritance is ‘really about’, with everything else relegated to ignorable supporting roles. For example, they were taught that although genes can affect the heart directly, they also affect blood pressure, the body’s activity levels and other influential factors, themselves often influenced by non-genetic factors (such as smoking). Where in this tangle, we ask them, is a gene for heart disease? In effect, this revised curriculum seeks to take what is peripheral in the existing teaching of genetics and make it central, and to make what is central peripheral.

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