How to spot a crackpot

I've found a nice follow-up to Dan Graur's latest post. The anthropologist Pascal Boyer has been investigating the wonders of crackpot physics. In this blog post he gives us a flavor for how he is getting on. Interestingly, what he finds is very similar to what goes on in crackpot biology.

Read full post at Evo.Sphere

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New venue

After a long break where I dealt mostly with my primary duties (research, writing papers, teaching, presenting at conferences, ...) and got my tenure application in order, I'm back to blogging. I've teamed up with some colleagues at the University of Houston to write on evolution in a blog (Evo.Sphere) sponsored by the Houston Chronicle. Check out my first post there: The Fittest Theory.

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The mystery in the comments

Derek Atkins (apparently my only reader these days) has forced me out of blog inaction by a series of comments to an old piece on Sanford's curiously titled book. You may recall that I started reading it out of politeness after Salvador Cordova gave it to me. I quickly lost interest once I realized just how bad it was and decided to spare you a complete series of negative reviews. After all, I have serious work to do writing papers and grant applications, going to seminars, pushing worms (they've missed me!), analyzing data, mentoring and teaching. Somehow I doubt that my tenure package will look stronger if I waste valuable time refuting bad (really, really bad; failing student bad) population genetic arguments -- a subject which, by the way, I'm teaching right now to a dozen (suffering) undergraduate and graduate students.

Now Atkins has bombarded me with so many comments that I may never get around to answering all of them, but I see a few that are worth responding to, because they are representative of the kinds of arguments that Sanford and other creationists make routinely. After a discussion on how many different kinds of creationists can dance on the head of a pin, Derek gets to what is really bothering him: "What I take exception to is your list of Sanford’s assertions that twists what he really does say. This speaks to your integrity." So I'm in trouble now... Here goes:

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Let’s start with the first assertion to which you’ve taken exception. Analogies are what they are—an attempt to aid the reader (since there may be a wide range of exposure to the materials) in understanding the salient points. It is a device that is effective and is used in all disciplines. [...] The use of differing language/information analogies to the genome does not start nor end with YE or ID proponents (they are not one-in-the-same) but is seen in the analogies of those who are strident evolutionists as well, such as Carl Sagan (1974) when he compares the genome with having more information than contained in the Library of Congress. [...] What I find interesting is not having read any evolutionist being singled out for using these analogies, but anyone who is YE or ID is denigrated for doing so. Unless you have taken non-YE/IDers to task regarding this point, it seems irrelevant to single out Sanford. I credit Sanford for being quite clear about the limitations of the analogy, as quoted above.

Yes, Dawkins used the cake recipe in 1982 in The Extended Phenotype, Dennett used Borges' Library of Babel concept in an interesting analogy for genotypic space in Darwin's Dangerous Idea, and Steve Jones wrote a whole book on The Language of the Genes. Good science writers make their careers on good analogies. Of course to suggest that they never get into trouble over their analogizing is ridiculous: entire volumes of criticism by scientists and philosophers have been devoted to the "gene/meme" and "spandrels" analogies alone. The problem is that, despite his mild disclaimers, the analogy Sandford introduces is a terrible one to discuss the evolution of genomic complexity. So I pointed it out. The reason I did this without hesitation and with what you might perceive as some impatience is that creationists of all stripes use analogies as substitutes for the rigorous scientific work of formulating hypotheses, testing them in the laboratory, or with computer simulations, or with observations from nature, and developing theories based on these activities.

Moving on:

In the second argument you offer as one example the nematode Caenorhabditis elegans, citing de Bono M, Barmann CI,.(1998). In the abstract we read, “A loss-of-function mutation in the npr-1 gene, which encodes a predicted G protein-coupled receptor similar to neuropeptide Y receptors, causes a solitary strain to take on social behavior.” [...] Loss-of-function and various other degradations to the genome is more the rule than the exception to genetic mutations. This is the point Sanford makes clear, though you sidestep this and ask, “Does it matter?” It is an important area of discussion that is not well served with a flippant response. Any gene that mutates causing loss-of-function has certainly lost, not gained usefulness, and by definition the genome has lost information."

This is wrong at so many levels that it is even hard to know where to begin. First of all, it is by no means certain that the genome has lost any information in this case (or any other involving mutations). The main reason is that Sanford and other people who use this argument don't actually define the term in a meaninful way (precisely one of my main criticisms of Sanford). According to any technical meaning of information that I am aware of, a single aminoacid substitution does very little, if anything to it.

The second error you (both) make is that you misunderstand what is meant by the expression "loss-of-function". This has nothing whatsoever to do with information. It also does not mean degradation. de Bono & Bargmann are referring only to the activity of the npr-1 gene product, which is a transmembrane receptor that binds to small peptides outside the cell and creates a signal inside the cell. Loss of function in these cases means that the peptides bind with lower affinity to the receptor or elicit a weaker signal inside the cell. The "social allele" is a loss of function allele when you treat the "solitary allele" of the N2 strain as the reference allele (the reference strain in C. elegans biology). If the Hawaiian strain CB4856 happened to be the standard strain, instead of the English N2 strain, the mutation would be referred to as a gain-of-function mutation. Note that gain-of-function mutations in all kinds of genes are routinely isolated by geneticists (something Sanford neglects to mention). What de Bono & Bargmann are saying is that the NPR-1 receptor from a social worm has a lower activity than the receptor from a solitary worm. But if you look at the level of the behavior, it is not obvious which one has the greater "function": they are both functional, they just have different functions. The irony is that the best information available suggests that the social allele (with lower activity) is actually ancestral to the solitary one in the Caenorhabditis genus, so the mutation most likely occurred in the direction of increased function in the evolutionary history of C. elegans.

So let's recapitulate. On the first point, you did not actually address my substantive, specific criticisms of his analogy. To say that others have also used analogies is beside the point. The question is: where exactly did I twist what Sanford was saying? On the second, until you define information, Sanford's point remains nonsensical. Your misunderstanding of the meaning of loss-of-function does not inspire confidence in your command of the issues at hand. Do yourself a favor and read a population genetics textbook before embarrassing yourself any further: Gillespie's Population Genetics or Hartl & Clark'a Principles of Population Genetics are both pretty good.

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Snakes and ladders

PZ Myers has just written an excellent essay on the evolution of complexity. He makes several interesting points with which I agree. For example, human scientists have long assumed that we (humans) are the most complex organisms in the biosphere. They used to think we had about 100,000 genes. (Kauffman was a bit out of date by 1995, but that number was kicking around. For example, I remember seeing it in the first edition of Jonathan Slack's From egg to embryo from 1983). In 2001, initial estimates from the draft sequence of the human genome put the number of protein-coding genes at 30,000-40,000. It has been shrinking ever since. By 2004, the estimates were down to 20,000-25,000. Of course, this is only the latest in a long series of slights to human delusions of grandeur: from being at the center of the Universe to being in one of many, many, many planets; from being the pinnacle of creation to being genealogically related to every organism on the planet (actually, I find this rather cool, and not demeaning at all, but that's just me...), from being a complexity champion among the metazoa, to being perilously close in genomic complexity to the nematode C. elegans, which has about 19,000 genes and 959 somatic cells.

Like PZ Myers (and Larry Moran), I find most of the current hypotheses that try to do away with the so called genomic paradoxes, unconvincing, bordering on wishful thinking. An understanding of the nearly neutral theory of molecular evolution should makes us intensely skeptical of any claims to deep significance in the non-coding portions of genomes of species with low effective population sizes like us (what counts is the historical population size during our evolution over the last few million years, not the explosion over the last few centuries, in case you're wondering). Just because our genome is crawling with small RNAs (I'll assume it, even though the estimates are not terribly reliable at the moment), and some of them can regulate gene expression, doesn't mean that these RNAs are doing anything terribly important or in any way related to our supposed complexity. Of course, this is no reason to stop looking -- don't take my word for it. I'm just giving you an evolutionary biologist's hunch as to the outcome of this flurry of activity.

Where I have to disagree with PZ (and with others before him, such as SJ Gould in Full House) is in dismissing the problem of increases in complexity.

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On this I'm with Wallace Arthur in his latest book Creatures of Accident (his defense of agnosticism is less persuasive). Just because increases in complexity are not the dominant theme in the evolution of life (more snakes and ladders, than just ladders), does not mean that we should ignore this important feature of the pattern. The fact remains that from simple molecules we got simple prokaryotic cells, then more complex eukaryotic cells, then simple multicellular organisms, ..., then exquisitely complex multicellular creatures like cephalopods, crocodiles and chimpanzees. There are even well-documented cases of generalized increases in complexity across whole groups of animals, such as in the complexity of septal sutures in ammonoids (cephalopods again). Finding out what evolutionary forces could possible drive such increases in complexity is a central problem in biology, and one that has not been adequately addressed yet. Sure, gene duplications are part of the story. But what are the selective pressures on complexity? What are the distributions of mutational effects on complexity?

I have actually been working on the evolution of complexity and have just written a theoretical paper on it. I've been promising to say something about it. Now, that I've started talking about it, I might just get around to doing so.

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Publish or perish?

PZ Myers has just taken the time to reminisce over Paul Nelson's three year long silence on his curious concept of "ontogenetic depth". It so happens that I was first introduced to this IDea through the Pharyngula post about our 2005 paper (mentioned in my last post). Unlike Nelson, we have not been idle since we came up with our measure of lineage complexity. In fact our first follow up paper has just been accepted for publication at the Proceedings of the Royal Society B. I promise to write about the paper in more detail here before it comes out. Now I must finish going over it one more time, and prepare a talk on it for Monday (you can check out the summary).

This walk down memory lane brings to mind a challenge of my own to another intelligent design creationist. The last time I wrote about "ontogenetic depth" here, I warned Salvador Cordova not to be so sure that Andreas Wagner's results on the evolution of robustness of circadian oscillators (see here and here) would not generalize to other systems. Guess what? Andreas Wagner has just proved Salvador wrong for a completely different kind of gene network model (one pioneered by Wagner about a decade ago, and essentially the same model we used in our recent paper on the evolution of robustness).

So, on the one hand you have real scientists at work, publishing their results in peer-reviewed journals, moving their fields forward. On the other hand, you have the pseudoscientific creationists at the Discovery Institute, not doing any original scientific work of their own, not publishing in peer-reviewed journals, criticizing and misrepresenting the work of others, attacking great scientists ad hominem.

Update: For a vivid metaphor of the contrast I made in the last paragraph, check out PZ's brilliant exegesis of 300.

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Preaching to the unconverted

I first came across PZ Myers' posts when I was teaching Evolution of Development in the Fall of 2004. I forget which posts caught my eye initially, but I started checking back occasionally. This was before I started paying regular attention to blogs -- I didn't even know what they were... Then I read his piece about our 2005 Nature paper and was hugely impressed. So I started reading him more regularly, and I've done so ever since. Some two years later, he's still my favorite blogger, the one I read most from. Happy Birthday, PZ!

Update: for more tributes see here, here and here.

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What's in a word?

The Science Cafe on Tuesday was a lot of fun. I got stumped a couple of times -- strangely enough I'm not an expert on penguin homosexuality -- but I'm told I didn't do too badly (although my graduate students may not be good informants). I managed to control myself and not mention negative epistasis... The other speakers were great. I might just have to go over to Salento more often (I was already a fan of their coffee).

Janis Antonovics and friends (Hello, MissPrism! Long time no see. Nice blog, by the way...) have just published a fascinating essay on the use of words related to “evolution” in the context of research into the evolution of antibiotic resistance. Their main finding is disquieting:

The results of our survey showed a huge disparity in word use between the evolutionary biology and biomedical research literature (Figure 1). In research reports in journals with primarily evolutionary or genetic content, the word “evolution” was used 65.8% of the time to describe evolutionary processes [...]. However, in research reports in the biomedical literature, the word “evolution” was used only 2.7% of the time [...]. Indeed, whereas all the articles in the evolutionary genetics journals used the word “evolution,” ten out of 15 of the articles in the biomedical literature failed to do so completely. Instead, 60.0% of the time antimicrobial resistance was described as “emerging,” “spreading,” or “increasing” [...]; in contrast, these words were used only 7.5% of the time in the evolutionary literature [...]. Other nontechnical words describing the evolutionary process included “develop,” “acquire,” “appear,” “trend,” “become common,” “improve,” and “arise.”

They do point out that there was no evidence that the scientists involved were trying to cover up evidence for evolution or anything. Just poor choice of words. And, unfortunately, this does nothing to improve the public understanding of evolutionary biology (see this figure).

Some of their other findings are more encouraging. For example, decided to look at whether the use of the word “evolution” changed in NSF and NIH grant proposals and in papers published in general science journals such as Nature and Science. They report:

The results showed that the use of the word “evolution” was actually increasing in all fields of biology, with the greatest relative increases in the areas of general science and medicine (Figure 3). This reflects the growing importance of evolutionary concepts in the biomedical field, and highlights even more the strange rarity with which the word “evolution” is used in the biomedical literature dealing with antimicrobial resistance.

But they follow this up with a deeply troubling passage for me:

It has been repeatedly rumored (and reiterated by one of the reviewers of this article) that both the National Institutes of Health and the National Science Foundation have in the past actively discouraged the use of the word “evolution” in titles or abstracts of proposals so as to avoid controversy.

I too have heard the similar rumors -- mustn't upset all those scientifically illiterate representatives in Washington! But it gets better:

Indeed, we were told by one researcher that in the title of one proposal, the authors were urged to change the phrase “the evolution of sex” to the more arcanely eloquent wording “the advantage of bi-parental genomic recombination.”

Talk about politically correct evolutionary biology! I wish I'd known of this story before the Science Cafe...

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Sex talk

Sex: Why Bother? Evolution Mysteries










One of the greatest mysteries of biology is why humans need a sexual act to reproduce while some organisms such as bacteria do not, and while others, like plant lice, can reproduce with or without a sexual act. Scientific evidence indicates that sexual reproduction is in fact a much less efficient way of producing new individuals and, consequently, of passing on genes to the next generation. Why then are some species, like humans, only able to reproduce with a sexual act? This is one of the greatest intrigues of evolutionary biology. And science aside, what does sex mean to us after all? Do we mate with the only goal of passing genes onto the next generation? Or is there more to it under the sheets? Come and discuss these questions with outstanding scientist, medical ethicist, and religious studies scholar at the next Science Café.

WHEN: Tuesday February 27, 2007 from 7:30 pm to 9:00 pm

WHERE: Salento Coffee House, 2407 Rice Boulevard in Rice Village

WHO:

• Dr. Ricardo Azevedo, Assistant Professor in the Department of Biology and Biochemistry at the University of Houston
  
  
• Dr. Simon Whitney, M.D. and Medical Ethicist, Medical Director of Baylor Family Medicine at the Baylor College of Medicine
  
  
• Prof. Jeffrey J. Kripal, J. Newton Rayzor Professor and Chair of the Department of Religious Studies at Rice University. Author of “Esalen: America and the Religion of No Religion”, a book dealing with modern fusions of science, eroticism, and mystical experience
  
  
• Moderator: Patricia Gras, Senior Producer at HoustonPBS and Host of TV show Living Smart – airing Sundays at 3:30pm and Thursdays at 1:30pm. Living Smart episodes also available on google video

COST: Free to the public. No registration needed.

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Open your mind

Bora Zivkovic, of A Blog Around the Clock, has put together an anthology of the best science blog writing (ever). It has a great name: The Open Laboratory. To my surprise, my two-part post "Blind Watchmaker or Swiss Designer?" (see here and here) was picked for it. I'm delighted to be among such distinguished company.

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How selfish is this meme?

Go ahead, link to this post and do your bit for the new science of memetics.

[Via Pharyngula]

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