So, you may have seen the news reports in the past few days about the goats that have been engineered to produce spider-silk proteins in their milk. Well, about that . . .
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So, if you’ve ever taken a creative writing class or workshop, you’ve undoubtedly been enjoined to “show,” rather than “tell.” It’s one of those writing rules that is commonplace to the point of being cliche. In fact, many instructors feel sufficiently self-conscious about offering that advice that they feel obliged to provide caveats. You know, sometimes telling is the right thing to do, and, of course, it depends on how you tell. Blah, blah, blah.
I’m hoping that this blog has at least one reader who has taken a writing course in Japan, because I’m curious as to what the analogous rule is there. Based on a non-comprehensive sampling of dating simulators, manga comics, and Murakami novels, I imagine generations of Japanese MFA students being told “Tell, don’t show!” You know, “Hi, my name is Haruki. I often come off as brash, but underneath it I am actually quite shy. Also, I had a good, healthy bowel movement this morning.”
Anyway, speaking of “show, don’t tell,” I just came across this brief memoir, published in 2005 by Laurence Klotz in the British Journal of Urology International. He fondly recalls a lecture by G. S. Brindley at the 1983 Urodynamics Society meeting in Las Vegas. Brindley had just made a breakthrough in the treatment of erectile dysfunction through self-injection with papaverine. [Note, I don’t know where the “self-injection” has to be.] After showing a series of photographs of erect penises, Brindley wanted to demonstrate that the effect was not the result of a confounding erotic environment:
The Professor wanted to make his case in the most convincing style possible. He indicated that, in his view, no normal person would find the experience of giving a lecture to a large audience to be erotically stimulating or erection-inducing. He had, he said, therefore injected himself with papaverine in his hotel room before coming to give the lecture, and deliberately wore loose clothes (hence the track-suit) to make it possible to exhibit the results. He stepped around the podium, and pulled his loose pants tight up around his genitalia in an attempt to demonstrate his erection.
At this point, I, and I believe everyone else in the room, was agog. I could scarcely believe what was occurring on stage. But Prof. Brindley was not satisfied. He looked down skeptically at his pants and shook his head with dismay. ‘Unfortunately, this doesn’t display the results clearly enough’. He then summarily dropped his trousers and shorts, revealing a long, thin, clearly erect penis. There was not a sound in the room. Everyone had stopped breathing.
But the mere public showing of his erection from the podium was not sufficient. He paused, and seemed to ponder his next move. The sense of drama in the room was palpable. He then said, with gravity, ‘I’d like to give some of the audience the opportunity to confirm the degree of tumescence’. With his pants at his knees, he waddled down the stairs, approaching (to their horror) the urologists and their partners in the front row. As he approached them, erection waggling before him, four or five of the women in the front rows threw their arms up in the air, seemingly in unison, and screamed loudly.
“I’d like to give some of the audience the opportunity to confirm the degree of tumescence.” Scientific meetings used to be so awesome.
I believe that I found this a couple of days ago via a Twitter or Google+ link, but I’ve lost the origin now. Apologies to the original poster/tweeter. If you know who it is (e.g., if it’s you), please let me know in the comments, and I’ll update with credit.
So, welcome to the first Genetical Book Review of 2012, where we’re going to talk about The Postmortal, by Drew Magary. As the book starts, Science!™ has developed a cure for aging, so that people can live forever. What follows is an exploration of the psychological and sociological consequences of immortality.
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| I love this picture. You can almost hear Death going, “D’oh.” |
I don’t think I’m giving anything away when I tell you that the book winds up being predominantly dystopian. Basically, if you are the sort of person who frets about the future of humanity, who is prone to think things like, “How could I possibly bring a child into this world,” well, don’t read this book. At least, don’t read it in bed after a spicy take-out meal.
If you do enjoy the occasional sci-fi dystopia, this one is of the variety where you make only a small technological (or, in this case, medical) change, and explore the implications in a world that is otherwise very much like our own. One of the interesting things that the author gets to do with this particular premise is to follow history over many decades through the eyes of a single, first-person narrator. So, the protagonist experiences technological and societal changes that would normally take place over the course of generations.
The book is presented as a series of blog posts, some of which are personal, narrative entries, and some transcripts of news reports, others link roundups, and so on. Magary is a contributing editor at Deadspin, and his reporting / media background shows through in the writing. The whole book is engaging, but the writing really shines in the news bits, which are pitch-perfect.
In the book, the cure for aging is achieved through gene therapy, targeted at a single locus, which seems to be closely linked to MC1R, the gene most commonly responsible for redheadedness. What we’re going to use this as a jumping-off point to talk about different evolutionary theories of aging, and the extent to which each might be consistent with the existence of a single gene serving as a master control over the aging process.
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| In The Postmortal, the cure for aging is discovered serendipitously as a byproduct of research aimed at changing hair color. In our actual dystopia, it would have gone differently. Benjamin Button would have been indefinitely detained under NDAA and selectively bred with normal humans. A series of backcrosses would have been used to isolate the gene responsible for his aging reversal. |
But first, a couple of quibbles.
Quibble number 1. There are two biologists who feature prominently in the book: father and son Graham and Steven Otto. Now, I’m not going to argue sexism on the basis of a sample of two, since, even in a world with full gender equality, a random sample of two scientists would both be male about 1/4 of the time (p = 0.25). However, Graham Otto’s devoted wife (and Steven Otto’s loving mother) is (apparent) non-scientist Sarah Otto. It just so happens (presumably unbeknownst to Magary) that there is a real-life Sarah Otto, a prominent biologist who was just awarded a Macarthur “genius” grant. So, that’s . . . unfortunate.
Quibble number 2. The “cure for aging” as presented in the book arrests an individual at whatever age they are when they receive the cure, whether it is three or eighty-three. This actually conflates two different processes: development and senescence. My biological intuition is that, even in the simplest conceivable case, there would be at least two distinct master switches controlling these very different processes. (Actually, possibly a third switch as well, controlling puberty and the onset of secondary sexual characteristics, as distinct from growth to adult size and shape.)
In talking about evolutionary theories of “aging,” I will focus on evolutionary theories of senescence, which is really the most important aspect of “aging” with respect to this book.
[Note: none of this should be interpreted as a criticism of the premise or execution of the book, which I loved. The inherent power of science fiction comes from the idea that you build a world that differs from our own. Rather, as always with The Genetical Book Review, the book’s premise serves as an excuse and a specific context for talking about evolution.]
Basically, there are three major classes of ideas about the evolutionary origins of senescence, which have different implications for how much and how easily natural selection or medical intervention might be able to extend our lifespans. As is often the case, these different theories are not necessarily mutually exclusive or incompatible, but rather have different emphases. Most consistent with the premise of the book are theories that propose a positive adaptive value to senescence and mortality. Somewhat less consistent are theories that focus on senescence as a byproduct of the fact that natural selection becomes weaker for traits that are expressed later in life. Least consistent are theories suggesting that senescence and lifespan are profoundly constrained by biological universals. We’ll take each of these in turn.
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| Just as youth is wasted on the young, discounts are wasted on the elderly. |
1) Senescence as an adaptation.
The idea that there could be a single genetic master switch controlling senescence is most plausible under models where aging and death are specifically adaptive. How would that work, you ask. I mean, after all, the whole idea behind natural selection is that is favors surviving and reproducing, right? Well, in some models, you can actually identify conditions where it makes sense beyond a certain age for adults to go ahead and die. One particular model (cited below) describes an adaptive benefit (at the group / inclusive fitness level) to senescence from limiting the spread of disease.
Perhaps somewhat more generally applicable are models in which senescence is selectively favored as part of a trade off. The idea is that it would be possible to construct a human who lived to be, say, 150, but that it could only be achieved through some sort of compensatory change in another trait. Candidate examples would be size or reproductive output. In fact, all else being equal, smaller humans do tend to live longer than larger ones. Similarly, there are a handful of studies purporting to show that abstaining from reproduction extends lifespan.
In this sort of case, it is easy to see how natural selection might actually favor earlier senescence. To first order, what matters to evolution is how many offspring you produce. If you can grow big and have lots of kids, you’re going to win the evolutionary race, even if it means that you drop dead of a heart attack at thirty-five.
Under one of these models, it is easy to imagine the existence of one or a few genes that function as controllers, or strong modifiers, of senescence. Under the strongest version, you can even imagine a gene affecting only senescence. Under the weaker, trade-off version, it might be possible to dramatically extend lifespan, but not without side effects. Maybe the immortals would all weigh eighty pounds and have dramatically – or indefinitely – delayed onset of reproductive capacity.
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| In a world dominated by evolutionary trade-offs, the immortals will all be Romanian. |
2) Senescence as the absence of selection.
Imagine one trait that affects the probability that you survive to age ten. Now imagine a second trait that affects the probability that you survive from ten to twenty. Whatever selection is acting on the second trait, it has to be weaker than what is acting on the first one. The reason is that the second trait is under selection only in that subset of the population that survives to be ten.
This argument, of course, blends into the trade-off argument introduced earlier. We can imagine traits that trade off health (and survival) at later ages in exchange for enhanced health at earlier ages. In general, such traits will tend to be favored. Basically, it doesn’t matter how robust you are at eighty if you die at twenty.
Even without such tradeoffs, however, we expect to see natural selection growing weaker with age. Given any rate of death (due to choking on litchi nuts, falling off cliffs, being eaten by tigers, whatever), there will be more people alive at age x than at age x + y, for any y > 0. So, the older you are, the less power natural selection has to fight against entropy – both the familiar entropy of the physical world and the evolutionary entropy of the mutation process.
Some of the evidence in support of this idea comes from the fact that there are certain species that tend to live longer than expected. Included among these are birds, porcupines, and humans. What do those have in common? The reason in each case is different, but each has a reduced rate of predation. If you reduce the death rate, you increase the power of selection to slow down the aging process.
One consequence of this is that we expect all of the different systems that make up our bodies to fail at similar rates. For instance, if the human heart just gives out after 100 years, any and all selection goes away for maintaining anything else (brain, kidneys, liver, etc.) for longer than that. This perspective suggests that there will not be a single tweak that could stop aging. Rather, it would require a whole bunch of tweaks, or maybe something more like a Never-Let-Me-Go-style organ harvesting scheme.
3) Senescence as a fundamental constraint.
These ideas come from the existence of certain universal scaling laws, regularities in the relationship between features like body mass, metabolic rate, and lifespan. There are a lot of ideas out there, but what, exactly, is driving these relationships is not yet understood. However, the relationships themselves seems to be fairly robust.
One of the striking findings in this area is the fact that, among species with a heart, an individual’s lifespan corresponds to about 1.5 billion heartbeats. Small species have fast metabolic rates, fast heartbeats, and short lives. Large species live slower and longer.
Once again, these ideas are not mutually exclusive with the “rates of predation” idea. In fact, when we say that species like birds and humans live “longer than expected,” these scaling relationships determine what “expected” is. For instance, a human with a heartrate of 72 beats per minute might live to have about 3 billion heartbeats.
Whatever the origin of these patterns, their apparent universality suggests the existence of very deep constraints on our biology. While natural selection (or medicine) might be able to alter our lifespans, it may be that such intervention is limited to relatively small changes, maybe a factor of two. Perhaps something human sized that could live for many hundreds of years would have to be based on a fundamentally different biological architecture.
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| Following the 2012 Mayan-Zombie/Santorum-Paul apocalypse, humans and other land-based vertebrates will become extinct. Eventually, cephalopod-based land dwellers will eventually emerge to fill our vacated ecological niche. Perhaps they will live longer. Image via Chowgood’s Deviant Art page. |
So, overall, I think the likelihood of a single medical advance that dramatically increases our natural lifespans is pretty remote. But, as you’ll see if you read the book, that might be for the best.
Here are just a few references to get you started if you are interested in the evolutionary constraints on lifespan and senescence.
Glazier, D. (2008). Effects of metabolic level on the body size scaling of metabolic rate in birds and mammals Proceedings of the Royal Society B: Biological Sciences, 275 (1641), 1405-1410 DOI: 10.1098/rspb.2008.0118
Mitteldorf J, & Pepper J (2009). Senescence as an adaptation to limit the spread of disease. Journal of theoretical biology, 260 (2), 186-95 PMID: 19481552
Williams, G. C. (1957). Pleiotropy, Natural Selection, and the Evolution of Senescence Evolution, 11 (4), 398-411
Well, that’s all for today! Check back again soon, as The Genetical Book Review will be posting more frequently in 2012.
Buy it now!!
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So, welcome back to my intermittent live-blog of my adventures in forming a non-profit research institute in order to function as an independent scholar. I’ve written a couple of times before: about my own goals for the enterprise, and about the things that an independent scholar will most be in need of.
One of the things, of course, that an independent scholar needs is colleagues. Depending on the nature of your research, you might be able to do the day-to-day work (math and programming, in my case) entirely on your own, but unless you are a very special sort of misanthropic genius, you need interaction with a set of colleagues. Sometimes you will want to take on collaborative projects that require the expertise of more than one person, but even more, you need knowledgeable people to bounce ideas off of, people who will ask the critical questions that make your work better, or who will drop some jewel of knowledge that lets you see the problem you’ve been working on in an entirely new way.
Now, in principle, much of this can be accomplished on the internet, but I am wondering if there are not certain types of information that more or less require face-to-face contact.
Last week, I was at a “catalysis meeting” at NESCent (the National Evolutionary Synthesis Center) on genomic imprinting. The meeting was superb. It had excellent people who work on the problem from all different perspectives: theorists and experimentalists, molecular and developmental biologists, mouse people, marsupial people, bee people. I learned a ton, and, perhaps more importantly, I learned of the existence of a bunch of things that I didn’t know. I still don’t know them, but now I know that I should know, and I know where to start looking, and whom to ask for help when I get stuck.
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| As an aside, I also had the chance to meet Craig McClain, Assistant Director of Science at NESCent and doyen of the group blog Deep Sea News. He was as nice as their blog is awesome.
Some people say that biologists grow to resemble the organisms that they study. You be the judge. |
You might think that meetings like this are particularly efficient for transmitting information, but that you can accomplish the same thing through more aggressive and far-reaching readings of the literature. After all, the organizers of the meeting were able to find these people. In principle, I could just get all of their papers and read them carefully, referring to textbooks on biochemistry or mammalian physiology whenever there was something I didn’t understand.
But I’m not sure that would actually work.
The thing is, some of the most important pieces of information I got at the meeting were things that are not written in papers, or perhaps anywhere, nor are they likely to be. For example, there were a number of people there who have spent years working with lab mice. They have observed thousands and thousands of crosses (e.g., the outcome of a mother of one mouse strain mating with a father of a different mouse strain). This has given them a deep knowledge of what does and does not happen in these crosses, as well as a sense of how sensitive different traits are to the details of the experimental procedure.
An interesting thing was that there were certain results from the scientific literature that none of these people believe, because they are not consistent with their own observations. Now, no one has gone and written a rebuttal letter, or published a set of negative results contradicting the original papers. They have all just sort of implicitly agreed that results using a certain technique, or sometimes results coming from a certain lab, are unreliable, and they move forward with their research as if those results did not exist.
So, there is this substratum of knowledge that is widespread among experts, but which does not find its way into print. In part, this is due to the thanklessness of writing response letters and publishing negative results. In part, I think, it results from a sense of decorum / political consideration. It is common for scientists to have opinions that whole swaths of research are garbage, and it is common for them to share this knowledge in conversation, particularly over beer. However, most are too cautious to put their genuine opinions down in writing — even in e-mail.
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| As the good folks at Gawker say, “Today’s gossip is tomorrow’s news!” |
Fundamentally, I don’t think that there is anything wrong with this arrangement, as it maintains a pretty high bar for calling someone out for doing bad science, but permits people to move forward with what they collectively perceive to be the best possible information. However, it does point to the importance of getting out there and interacting with people face to face. Otherwise, you may find yourself developing a whole research project that is predicated on some results that no one thinks are true.
I should note that this problem is not unique to the independent scholar. If you are working in a typical university department, there may not be anyone else in your department — or only a small number of people — whose research is close enough to your own that you share the same scuttlebutt. That is, no matter who you are, you need to make sure that you pursue opportunities to talk informally — and in person — with the people who care about the same things that you do.
One last observation from the NESCent meeting. This was the first scientific meeting I have attended under my official affiliation with the Ronin Institute. This meant that people would look at my name tag and ask me about it. I would tell them briefly about the idea and my plans for Ronin, and they were all very enthusiastic. The people who had come over from England, in particular, tended to comment on how very brave I was. After I got back, I came a cross this translation guide:
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| If you work with anyone British, you should print this out and carry it around with you. It serves as a handy guide as to whether you need to be punching them in the nose. |
I’m going to assume that this is just wrong. Let’s posit that a better translation for “That is a very brave proposal” would be “Wow! You are a singular genius and an inspiration to children around the world! Also very sexy! Mee-yow!”
So, Robert Pinsky wrote a cool little piece in Slate the other day titled “In Praise of Memorizing Poetry – Badly.” In it he argues for a particular benefit to be gotten from misremembering a poem: that it brings into focus the choices that were made in the poem, the the consequences of using one word rather than another. He illustrates his argument with Yeats’s “On Being Asked for a War Poem,” which he presents like this:
“On Being Asked for a War Poem”
I think it better that in times like these
A poet’s mouth be silent, for in truth
We have no gift to set a statesman right;
He has had enough of [something] who can please
A young girl in the indolence of her youth,
Or an old man upon a winter’s night.
He talks about misremembering the [something] as “glory” or “indolence” or “striving” before rediscovering Yeats’s original “meddling.”
In the case of “meddling,” the result of the exercise is to highlight the historical context in which Yeats was writing. Yeats was an Irish poet writing about World War I in 1915. At the time, Ireland was still part of the United Kingdom, and was actively involved in the war. However, some Irish nationalists used the war as an opportunity initiate a rebellion against English rule. And, in fact, the Irish War for Independence began pretty much as soon as World War I ended.
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| During Easter week of 1916, Irish rebels seized control of several key buildings in Dublin and declared independence from England. Yeats wrote a poem about it. |
Yeats’s poem was written in response to a request by Henry James, and was originally titled “To a friend who has asked me to sign his manifesto to the neutral nations.” In all of this context, the choice of “meddling” seems to point to a degree of ambivalence towards the war, even presaging Ireland’s own neutrality in World War II.
Now, of course, all of this information is, in principle, available to anyone who has both the original text and access Wikipedia. However, for Pinsky, it is this forgetting, the substitution of “meddling” with “glory,” that serves as the catalyst for this particular close reading. And I doubt that, in the absence of some similar impetus, very many people would have focused on this particular aspect of the poem.
In biology, similar mistakes, in the form of mutations, provide one of our most important windows into the structure and function of biological systems. These mutations are sometimes the product of targeted mutagenesis, but can also result from naturally occurring mutations.
A lot of our coarse-grained knowledge of many systems comes from loss-of-function, or knockout mutations, where a mutation removes a particular gene, or renders it nonfunctional. For example, in 1976, Sharma and Chopra first described a recessive mutation in the fruitfly Drosophila melanogaster. Flies inheriting two copies of the mutation exhibited various developmental defects, the most obvious of which involved wing formation. So, the mutation, and later the gene, became known as “wingless.”
This is typical in genetics, where a gene will be given a name based on the phenotypic consequences of losing that gene. So, a gene required for wings becomes “wingless,” a gene required for heart formation might be called “heartless,” and so on.
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| Kim Jong Il relaxes with some brews. Due to the nature of the discovery process in biology, many genes wind up with names that are more like the opposite of what the gene actually does. This is sort of like how the least democratic countries always wind up with the word “Democratic” in their names, or how Citizens United succeeded in dramatically curtailing most citizens’ abilities to control their own government. |
More subtle mutations, which alter the behavior of a gene or its gene product without completely eliminating it function, are more closely analogous to the misremembering that Pinsky is talking about, however. In a way, a knockout mutation of an important gene is more like just removing one whole line from Yeats’s poem, without regard for grammar, rhyme scheme, coherence, etc. What you would wind up with is a mess that fails in many ways, and is probably not terribly instructive – just like in biology.
Point mutations, which might alter a single amino acid in a protein, provide a more targeted and interpretable set of changes. Such a mutation might cause a small shift in the binding behavior of the protein, or might cause a slight change in the timing of the gene’s expression.
Like in the poetry case, these mutations are more likely to be revealing of the fine tuning part of the creative process, where mutations of small effect arise and are subjected to natural selection. In some populations – things like certain viruses, which have a very large population size and strong selective constraints – it might even be reasonable to think that these alternate, mutant forms have been explored and rejected by past natural selection. In other cases (e.g., large mammals, with relatively small effective population sizes), the most common form we find in nature might not represent some finely tuned optimum, but may simply be a form that works well enough.
Similarly, when we read a Yeats poem, we are inclined to assume that every single word has been chosen with extreme care, that a host of plausible alternatives were considered and rejected by the poet before he settled on just exactly the right word, in this case, “meddled.” I think we are inclined to agree with Pinsky’s final assessment, that “by memorizing his poem imperfectly, I had received a creative writing lesson from a great poet.”
However, a lot of poems in the world, even very good ones, are probably more like large mammals, with many of the word choices working well enough, but not necessarily representing some optimum, even a local one. (There is of course, the question, in biology and in poetry, of to what extent one can talk coherently about optima, but that’s a post for another day.) But this process, deliberate or accidental tinkering, is critical both to the creation of great things, and to understanding how greatness is created.
Sharma RP, & Chopra VL (1976). Effect of the Wingless (wg1) mutation on wing and haltere development in Drosophila melanogaster. Developmental biology, 48 (2), 461-5 PMID: 815114
So, we’re on a somewhat restricted publication schedule here at Lost in Transcription, as we are entering Day 4 of no power following Saturday’s “Snoctogeddon.” Still not clear how many more days until the lights (and heat) come back on, or how long every place with WiFi will be overrun with laptop refugees.
In the meantime, let me point you to a new group blog, which takes it’s name from Theodosius Dobzhansky’s famous quotation, “Nothing in biology makes sense except in the light of evolution.” I wrote about the origin of the quotation here, and featured this anagram-themed Darwin Eats Cake strip:
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The new blog’s name is “Nothing in Biology Makes Sense,” and features the even something-er URL http://nothinginbiology.org/. It features writing from Simone Des Roches, Devin Drown, Sarah Hird, CJ Jenkins, Noah Reid, Chris Smith, Luke Swenson, Jeremy Yoder, and Jonathan Yoder (the fightin’ Yoders!).
The venture is only a few weeks old, but features veteran bloggers, and already has some really interesting posts.
Read it!
So, who doesn’t love it when life imitates art? Apparently, some fishermen near Córdoba, Argentina caught this fish:
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| Image via Geekologie. |
Perhaps coincidentally, the fish was caught near the city’s nuclear reactor.
Sadly, a brief survey of Córdoba’s Wikipedia page reveal’s no mention of a baseball team, glacier, gorge, or iconic lemon tree.
Spanish-language story here.
So, here’s something that’s a little bit awesome. At least it’s awesome if you’re the type of Evolutionary Biologist who likes to poke fun at Evolutionary Psychology. Which is to say, if you’re an Evolutionary Biologist.
If you go to John Tooby’s webpage, and click on the link labeled “Advanced Theory and Method in Evolutionary Psychology,” you get this:
Hat tip to someone whose name I won’t post here, lest it should negatively impact his and/or her job prospects.
So, I’m not sure exactly how I wound up covering this story here. Somehow I have this vague memory of posting a link. Then there was a green fog, and some comments, and tiny dogs riding tricycles, and Katie Holmes struggling to escape from her Katie-Holmes-shaped prison cell, except she had giant fangs, and next thing you know, here we are.
Anyway, a few days ago I mentioned that Gilbert Harman had reposted his mini-paper in which he lays out the case that Marc Hauser had taken many of the ideas in his book Moral Minds from a young researcher named John Mikhail, and that Hauser had not given Mikhail adequate credit for those ideas. Harman argues that Hauser’s qualifies as plagiarism, not of Mikhail’s words, but of his ideas.
A commenter noted that Hauser has responded to the allegations, and Harman provided a link to Hauser’s response, which he has posted on his webpage. You can view the response here. Briefly, Hauser argues 1) that many of the ideas in the book, which Harman claims were copied wholesale from Mikhail, were, in fact, indebted to a number of non-Mikhail sources, many of which predate Mikhail’s work (e.g., Chomsky), 2) that the scope and thrust of Moral Minds is quite different from Mikhail’s, and 3) that Harman seems to be lobbying for a standard of citation that is not at all standard in the field (or any field), and would result in books being completely overwhelmed with citations.
It is worth remembering that Harman himself has stated that his original allegations (which you can read here) were meant to be “a draft of a case for the prosecution and not a final verdict on this topic.” So I think that even Harman would not want any of us jumping to any conclusions without reading and considering Hauser’s response.
What I would love is to hear from someone out there who is familiar with the work in question, but is not connected to Hauser, Mikhail, or Harman. Does any such person exist out there?
So, a few weeks ago, I linked to a short piece written by Princeton Philosophy Professor Gilbert Harman in which Harman made the case that Marc Hauser’s book Moral Minds plagiarized the ideas of a young researcher named John Mikhail.
Then, suddenly, the Harman piece disappeared. Harman commented that he had not meant for the piece to go public. He had posted it to his website in order to get comments from a small circle of colleagues. When it received wider attention, Harman pulled it down so that he could give his ideas some more thought before publicizing his accusations.
Well, an expanded version of the piece is now back up. You can read it here. I haven’t diffed the files, but it looks like the original piece is still there, with some additional discussion at the end.
Connoisseurs of academic scandal, enjoy.
Hat tip to Laila Waggoner.
Edit: Post title had Marc Harman instead of Marc Hauser. Der . . .
