Those sneaky gingers pop up everywhere


I have a brother with red hair. I also have a son with red hair. Once upon a time, my beard and mustache contained many red hairs among the dominant browns. If you’ve ever wondered how these gingers appear all over the place, Petra Haak-Bloem offers a good explanation (although it needs some editing: how many different ways can they spell pheomelanin?).

The shade of hair color is determined by the amount of melanin, or pigment, in the hair. Your DNA not only encodes what kind of pigment you have, but also how much of it. “For white people the shades are dependent on two sorts of melanin: eumelanine (black pigment) and pheomelanine (red pigment). Hair cells of dark haired people only contain eumelanine. Blondes have less eumelanine. And redheads’ hair contains mostly pheomelanine,” Haak-Bloem says.

“More than a decade ago, researchers discovered that one gene (MC1R) on chromosome 16 plays an important part in giving people red hair. MC1R’s task is making a protein called melanocortin 1. That proteine plays an important part in converting pheolmelanine into eumelanine,” Haak-Bloem tells me. “When someone inherits two mutated versions of the MC1R-gene (one from each parent), less pheomelanine is converted into eumelanine. The feomelanine accumulates in the pigment cells and the person ends up with red hair and fair skin.”

The unexpectedly red beard is the effect of the same mutation in the MC1R gene. When you only have one mutated MC1R, red hair can appear in (unwanted) places. But even Haak-Bloem wasn’t completely sure of the mechanism. Having a deviant red beard has never been linked to any deadly diseases, so it’s pretty low on the research priorities list.

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Reconstructing a brain


Every once in a while, I get some glib story from believers in the Singularity and transhumanism that all we have to do to upload a brain into a computer is make lots of really thin sections and reconstruct every single cell and every single connection, put that data into a machine with a sufficiently robust simulator that executes all the things that a living brain does, and presto! You’ve got a virtual simulation of the person! I’ve explained before how that overly trivializes and reduces the problem to an absurd degree, but guess what? Real scientists, not the ridiculous acolytes of Ray Kurzweil, have been working at this problem realistically. The results are interesting, but also reveal why this work has a long, long way to go.

In a paper from Jeff Lichtman’s group with many authors, they revealed the results of taking many ultrathin sections of a tiny dot of tissue from mouse cortex, scanned them, and then made 3-D reconstructions. There was a time in my life when I was doing this sort of thing: long hours at the ultramicrotome, using glass knives to slice sequential sections from tissue imbedded in an epoxy block, and then collecting them on delicate copper grids, a few at a time, to put on the electron microscope. One of the very cool things about this paper was reading about all the ways they automated this tedious process. It was impressive that they managed to get a complete record of 1500 µm3 of the brain, with a complete map of all the cells and synapses.

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Listicles get published in peer-reviewed journals!


I used a cruel headline, but this is actually a useful list: Fifty psychological and psychiatric terms to avoid: a list of inaccurate, misleading, misused, ambiguous, and logically confused words and phrases. It’s not just the popular media that mangle scientific language, but also more technical works sometimes slip into misleading shorthand. For instance, #1 on their list of bad terms:

(1) A gene for. The news media is awash in reports of identifying “genes for” a myriad of phenotypes, including personality traits, mental illnesses, homosexuality, and political attitudes (Sapolsky, 1997). For example, in 2010, The Telegraph (2010) trumpeted the headline, “‘Liberal gene’ discovered by scientists.” Nevertheless, because genes code for proteins, there are no “genes for” phenotypes per se, including behavioral phenotypes (Falk, 2014). Moreover, genome-wide association studies of major psychiatric disorders, such as schizophrenia and bipolar disorder, suggest that there are probably few or no genes of major effect (Kendler, 2005). In this respect, these disorders are unlike single-gene medical disorders, such as Huntington’s disease or cystic fibrosis. The same conclusion probably holds for all personality traits (De Moor et al., 2012).

Not surprisingly, early claims that the monoamine oxidase-A (MAO-A) gene is a “warrior gene” (McDermott et al., 2009) have not withstood scrutiny. This polymorphism appears to be only modestly associated with risk for aggression, and it has been reported to be associated with conditions that are not tied to a markedly heightened risk of aggression, such as major depression, panic disorder, and autism spectrum disorder (Buckholtz and Meyer-Lindenberg, 2013; Ficks and Waldman, 2014). The evidence for a “God gene,” which supposedly predisposes people to mystical or spiritual experiences, is arguably even less impressive (Shermer, 2015) and no more compelling than that for a “God spot” in the brain (see “God spot”). Incidentally, the term “gene” should not be confused with the term “allele”; genes are stretches of DNA that code for a given morphological or behavioral characteristic, whereas alleles are differing versions of a specific polymorphism in a gene (Pashley, 1994).

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Punks and anarchists unite!


I’m a bit shell-shocked today — man, that was a long drive yesterday — and I stumbled into work today thinking this might be a really good day to bag it early and take a nap. And then I found something in my mailbox that perked me right up.

As a little background, I’ll summarize my talk in St Louis. I pointed out that there was more to evolution than natural selection. Natural selection answers the question of adaptedness — how do organisms get so good at what they do — but there’s another important question, about diversity and variation — why do organisms do so many things in so many different ways? And I made the point with stories about people like Spencer and Galton, who so emphasized optimality and how Nature, red in tooth and claw, ruthlessly culls the weak allowing the survival of only the fittest. Spencerian evolution is a very narrow and limited kind of biology, but unfortunately, it often seems to be the only kind of evolution the general public has in mind.

And then I contrasted it with Kropotkin’s ideas about Mutual Aid (pdf), and the greater importance of cooperation in survival.

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A St Louis weekend

I’m going to be taking off for the Gateway to Reason conference this weekend, and will be speaking on Sunday morning. The title of my talk is “Evolution and Cooperation: A Historical Perspective”, and I kind of suspect that the audience, what few of them show up, will be either a) mildly bored, because too many atheists are uninterested in history and philosophy of science, or b) mildly pissed off, because I’m going to show them that the history of evolutionary theory isn’t as clean and tidy as they imagine, because it got hijacked by conservatives from day one.

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