Posts filed under 'Science'
Syphilitic skull with three trephine holes and osteomyelitic lesions
Hunterian museum
One of my favorite London experiences was my visit to the Hunterian museum. If only I had more time there! I liked it so much, I returned on my last day, procrastinating my departure for Heathrow as long as possible.
The Hunterian is tucked away inside the Royal College of Surgeons of England, on Lincoln’s Inn Fields. In its Victorian incarnation, it was a wonderful multi-tiered gallery with railings, balconies, and suspended skeletons:
Illustrated London News, 1845
The Hunterian Gallery before the wars (source)
So I was shocked when I entered the grey, columned Royal College, climbed a graciously curving stairway, and found this extremely modern, two-story crystal-and-glass atrium:
The Crystal Gallery at the Hunterian Museum, Royal College of Surgeons
Definitely not what I was expecting! But it grew on me. I love ornate curiosity cabinets, but there is something very elegant about unadorned bones, and simple glass jars. Biological structures are so rich with intrinsic beauty, there’s no real need to gild the lily (that means you, Damien Hirst).
Though the new Hunterian galleries are peaceful and refined, I felt a slight pang of regret for the railings and wood cabinetry Darwin would have touched, when he studied here in the 1830s and 40s. Unfortunately, many of the specimens Darwin saw were destroyed when the Royal College of Surgeons was bombed in 1941. Like the gallery housing it, John Hunter’s collection is no longer what it once was. But what remains is still pretty darn amazing.
Hunter, a renowned surgeon and fellow of the Royal Society, worked tirelessly to collect medical anomalies like the 7′7″ skeleton of the Irish Giant, Charles Byrne (for which Hunter paid 130 pounds). He also amassed thousands of less exotic teaching specimens: though he did not have access to formaldehyde, he took wet preservation in alcohol to its highest level. After Hunter’s death in 1793, his ~13,000 specimens were purchased by the British state. The collection would be maintained (and enlarged) by the Royal College of Surgeons for the next two hundred years.
Hunter’s collection is organized according to some rather unusual curatorial precepts. As a physician and early experimentalist, Hunter was less interested in taxonomy than in physiology. He grouped specimens not by family or type, but as exemplars of processes - mouthparts and digestion, reproduction, etc. From the Victorian perspective,
The design of Mr. Hunter, in making this collection, was to exhibit the gradations of nature, from the most simple state in which life is found to exist, up to the most perfect and most complex of the animal creation, man himself. By his art, he was able to expose and preserve in a dried state, or in spirits, the corresponding parts of animal bodies; so that the various links in the chain of a perfect being may be readily followed and clearly understood. (Mogg’s New Picture of London and Visitor’s Guide to its Sights, 1844)
But Hunter’s collection does not exemplify linear progression, so much as ramification: the incredible diversity of ways that animal forms have evolved to accomplish given functions. Most of the specimens displayed here are not human; the Hunterian is a shrine not to Man, but to our entire extended family.
I first heard of the Hunterian through the delightful book Stuffed Animals and Pickled Heads: The Culture of Natural History Museums
, by Stephen Asma at Columbia College, Chicago. (I highly recommend this book, if you don’t own it already). Asma’s first impression of the Hunterian was similar to my own:
Without a grasp of Hunter’s underlying principles, the cases seemed slightly irrational. In one case, marked “Digestion,” I found various dissections of mammals, parasitic worms, a cicada, a locust, slugs, a squid, a vulture, a woodpecker, and a puffin. This hodgepodge arrangement follows no taxonomic grouping. . . Individual species, genera, and even families are displayed together to illustrate the unique ways that their structures fit the functions of digestion, circulation, respiration, and so forth. (Stuffed Animals and Pickled Heads, 63)
My copy of Pickled Heads has been with in storage with the rest of my belongings for months, so I’d forgotten Asma’s words. But when I walked up to the first case of Hunter’s jars (mouthparts of squid, beaks, teeth, mouthparts of bees and cicadas), I immediately remembered Asma’s description, and recognized what he meant. The intestines of fish were right next to the stomachs of mammals, including a rat which substantially outweighed the tiny human fetus next to it. There is no mistaking the idiosyncratic style of this little museum, so different from the aggressively educational dioramas of the London Natural History Museum or the Smithsonian Natural History Museum. Modern biology museums are full-color, multimedia entertainment factories - it’s a way to engage the audience, true, but it sometimes teeters toward the tawdry and didactic. Asma expresses the difference far better than I could:
Perhaps the most notable aspect of the Hunterian Museum–besides the bleached and bloated “monsters”–is that it’s not intended for a lay audience. The Hunterian doesn’t really care whether the average person is “getting it.” This is unexpectedly unnerving, since most other museum encounters come complete with torrents of helpful information. Almost every museum specimen that you have ever encountered, be it a fossil, a jar, or a mount, is accompanied by a plaque, a chart, or a recording that announces to you–even before a question has been formulated in your head-”what you are seeing is so and so. . . .”
What was Hunter trying to communicate when he grouped his specimens? This question alone gives one a more interactive relationship with the museum than any computer gadgetry could. (Stuffed Animals and Pickled Heads, 78-79)
It’s a little unfair to say the Hunterian doesn’t care if visitors “get it.” I saw a class of kids around twelve years old when I was there, moving in and out of a room set aside for teaching purposes, and they seemed to be “getting it” pretty well. The point is, they were being allowed to draw their own conclusions, and with a little guidance, to simply wander and wonder. Refreshing indeed.
What do I do when confronted with a mute collection of natural wonders? Why, break out the sketchbook. But I didn’t have one! It’s been so long since I felt peaceful enough to sketch in a museum - I’m normally buffeted by thousands of obnoxious children, and worse, tourists who act like children. I wasn’t prepared. I had to buy a little 5″x8″ Moleskine at a nearby bookshop, and sketch with a mechanical pencil while sitting on the floor. Since the museum does not allow photography, not even for earnest, sincere bloggers, these little doodles are all I have to represent Hunter’s myriad curiosities. I can’t believe I didn’t even get to the bound foot, or the lion with rickets, or the male and female ivory anatomical models. Argh.
Sepia officinalis (preparation showing the mouthparts of a cuttlefish)
Hunterian Museum
If you are active in the biomedical professions (and yes, they will ask for proof of this, like an ID card) you may also visit the Wellcome Anatomy and Pathology Museum upstairs.
At first glance, the Wellcome collection seems like the neglected younger sibling of the Hunterian prodigal son (or, if you prefer, the Harry-under-the-stairs to the spoiled Hunterian Dudley Dursley). It’s one outdated, drab room, filled with hundreds of specimen jars. No sexy lighting or pedagogical dioramas here - to figure out what you’re viewing you have to thumb through well-used, slightly sticky binders of notes. These binders are tucked in shelves or tables, wherever the last user left them; I couldn’t find one of the binders at all, so I’m still in the dark about some of the skeletal abnormalities I saw.
But the biggest difference is that the Wellcome specimens are all Homo sapiens, representing a variety of obscure, rare, or dramatic medical conditions - conditions, like keratin horns, that I never expected to personally see in the flesh! And they’re generally in better condition than the Hunterian specimens (most date from the 20th century). I could have spent five to ten minutes examining a single specimen, and there are hundreds of prosections in the Museum. I was completely overwhelmed, and didn’t sketch a single thing (sorry).
I wondered why the Hunterian and Wellcome collections were spatially isolated in this way, and the Wellcome closed to the public. It couldn’t be about shock value - some of the Hunterian exhibits were pretty gruesome. So I asked the head of conservation, who told me that it has to do with the legal status of the collection.
The UK has a long history of scandalous “body-snatching” (see this Curious Expeditions post for more on that nefarious activity). Since the 1832 Anatomy Act, enacted to discourage the illicit sale of body parts, specimens like those in the Wellcome collection have been more and more tightly restricted. Since 2006, the Human Tissues Authority has regulated the donation, disposal, and use of medical specimens and cadavers, and requires special licesning for the public display of remains from persons who died since 1906 (according to their FAQ, they also require licenses of plastination exhibits, such as Body Worlds). But since John Hunter lived, collected, and died years before the Anatomy Act, his collection can be displayed without the restrictions that impact the pathology collection.
Skull of 25-year-old man showing enlargement due to hydrocephalus
Liston collection at Hunterian Museum
I highly recommend both the Hunterian and Wellcome collections to any biologist, artist, kunstkammer fan, or interested layperson visiting London. The Hunterian is perfectly suitable for older children, and surprisingly peaceful for a (free!) museum so close to both the British Library and Inns of Court. There were tourists everywhere, but only a handful stopping by to see John Hunter’s life’s work. You might make a day of it and also visit the Wellcome Collection, around the corner near UCL, or Sir John Soanes Museum, which is literally across the street - but then, I still need to post about those, don’t I?
So much to see, so much to blog, so little time. What a wonderful world.
September 9th, 2007
Science Magazine just published research suggesting that a foreign virus, which apparently arrived via Australia, could be causing the mysterious colony collapse disorder (CCD). About 96% of CCD colonies were positive for this virus, which is confusingly named Israel acute paralysis virus (IAPV). Still unanswered: why Australia’s bees, if they’ve all got this, are doing just fine. Also, although there is a strong correlation between CCD and IAPV in the US, there is no clear chain of causation - CCD bees may be more susceptible to IAPV than unaffected bees.
Researchers have found an imported virus that may be associated with the sudden disappearance of honey bees in the United States, known as colony collapse disorder (CCD). This baffling syndrome, which earlier this year made headlines around the world, may have afflicted as many as 23% of beekeepers in the United States and caused losses of up to 90% of hives in some apiaries. The identification of a suspect is an important step, says Nicholas Calderone of Cornell University. “Before, we didn’t even have circumstantial evidence.”
The suspect is a pathogen called Israel acute paralysis virus (IAPV). A team of researchers reports online in Science this week (www.sciencemag.org/cgi/content/abstract/1146498) that they found the virus in most of the affected colonies they tested, but in almost no healthy ones. If the virus proves to be the cause of CCD, it could have international economic implications, for the researchers point to Australia as a possible source. Since 2005, U.S. beekeepers, especially those struggling to keep up with the insatiable demand for almond pollination in California, have imported several million dollars’ worth of bees from Australia. The researchers report that they have found IAPV in imported Australian bees.
Full text, if you have a Science subscription: Puzzling Decline of U.S. Bees Linked to Virus From Australia
If you don’t, a pretty good news article about it
September 6th, 2007
My excursion in honor of the first ever International Rock-Flipping Day (IRFD), September 2, was disappointing. I was full of hope, given the cicada-filled trees outside my apartment and the bizarre insectoid life I’ve already encountered in the few weeks I’ve been in Washington, DC. But in increasing frustration, I flipped no less than three rocks in the well-watered garden outside my apartment complex, then two more rocks in the dryish park - in desperation, I even flipped a derelict toaster oven!
The only animal I found under any of these objects was one incredibly common pillbug. And I couldn’t even get a decent photo of it before it ran away.
I suppose it could have been worse. After all, the unpretentious, unpoisonous, friendly pillbug is the semi-official mascot of IRFD, depicted on the snazzy badge created by Jason at cephalopodcast:
I’ve always loved pillbugs - the glossier and rounder, the better. (I have much less affection for their cousins the sowbugs, because they cannot roll themselves into perfect little balls). Pillbugs were also the occasion for the first great biological discovery of my life. During my childhood rock-flipping phase, I encountered a pillbug brooding its offspring (ghostly white, pin-head-sized versions of their parent). I was mystified; I thought insects simply laid eggs and left them without the slightest regard. So I looked up pillbugs (actually I probably looked up “roly-polies,” because that’s what we called them) and learned they aren’t insects (hexapods) at all. They’re crustaceans. Isopods like sowbugs and pillbugs are closer relations to lobsters and shrimp - even to barnacles - than to anything you’d usually find in your garden, including the very similar millipedes (myriapods). The astonishment of that taxonomic discovery has never left me, and probably went a long way to making me a biologist.
But the wonder doesn’t stop there. As we all know by now, the ocean harbors giant versions of nearly everything - including pillbugs! I wouldn’t care to run into the giant isopod, Bathynomus giganteus:
Deep Sea Giant Isopod - Coda’s flickr stream
or this:
Giant Isopod - NOAA explorer
Why are giant isopods so darn big? I have no clue, but Deep-Sea News took a good try at the question. (You might also ask why terrestrial arthropods are not larger; a recent paper in PNAS identified the oxygen-delivering tracheal system as the limiting factor for certain species of beetle).
Today I was a little disappointed that there were no hexapods or myriapods or arachnids to be seen - not even under the toaster oven. But walking dejectedly back to the apartment with my empty camera, I saw a doe and her still-dappled fawn - definitely too large to have squeezed out from under a rock, but enough to satisfy my frustrated biophilia. Perhaps next year’s IRFD will give more conventional results (mark your calendar now).
In the meantime, check out everyone else’s experiences here: most had much better luck than I did!
September 3rd, 2007
Made in Transit: oyster mushrooms
Agata Jaworska
On Saturday I went to the farmer’s market to snag some nectarines and peaches. Unfortunately, by Tuesday they’d gone bad already, which left me wondering what farmers do with all the peaches and nectarines that become ripe on Monday: they can’t possibly last to Saturday’s market. Are they composted? Juiced? I have no idea.
The short shelf life of fresh produce is incompatible with our centralized, artificial metropolitan structure and shopping habits. That’s why supermarkets have tried everything, including genetic engineering (remember the flavr savr tomato?) to make fruit ripen more slowly, so it can survive transport and remain appetizing long enough to sell. Now here’s a nifty new idea, called “Made in Transit”: grow the food while it’s being shipped!
No, it won’t work for a peach, but mushrooms could keep right on growing in your grocery bag until you get around to using them. Sounds like a good idea to me.
Via culiblog.
August 11th, 2007
I winced in sympathy at this account, “A biologist in Nigeria”, by Dave Ng (The World’s Fair) of his experience teaching a genetics course. The conditions were simply awful. But I’m afraid any non-biologist readers won’t understand how awful - why, you may reasonably wonder, do we insist on shiny, spotless, well-lit, glass-and-brushed-metal labs full of inscrutable gadgetry and hypnotically blinking lights? Are we striving for some kind of James Bond ubervillain aesthetic?
The answer is obviously yes. But it’s not that scientists are excessively fastidious and high-maintenance - not entirely - it’s that the techniques are so demanding. A few stray skin cells or a moment’s power surge can ruin an expensive day-long cloning experiment. Everything has to be sterile; everything has to work in a timely manner. Now imagine training students to do such experiments inside a Dumpster with broken tools, and you get some idea what Dave was facing.
Once, as an undergrad, cradled in the luxuries of a top-notch US research university,* I found my experiments contaminated time and again - despite every tool being autoclaved and every reagent brand-new. I troubleshot my protocol in the conventional way, and concluded that - I barely believe this myself - large (multi-kb) chunks of DNA were flying zeppelin-like across a large lab space into my Eppendorf tubes, contaminating my work. When I did everything inside the laminar airflow hood, the problem went away. That’s when I learned that even if you have all the right equipment, science can still go mysteriously awry.
At that time, I took everything for granted - the laminar hood, the limitless stocks of new reagents on the shelves, the bags of pristine Eppendorf tubes - and the considerable funds I spent repeating my little student experiment until I solved the problem (using that shiny sterile glass-and-brushed-metal laminar hood). Sterility, reliable power, and access to common reagents are well within reach of every US lab, even grant-poor ones. Without such infrastructure, it barely matters how imaginative or innovative a nation’s scientists are. In some countries, it is practically impossible to do molecular biology.
Nonetheless, Dave miraculously managed to make his teaching lab work - and is returning to do it all again. Afterward, there will be several dozen young Nigerian scientists who truly understand what biotechnology is, and hopefully, how to bring more of it to their nation. If only they could clone Dave, and send him out to all the other countries without clean labs or basic reagents.
*I didn’t actually attend that school, I was just there for the summer - to ogle the ubervillain labs, of course!
July 29th, 2007
Back when I was six or seven, my personal computer was a cassette-tape driven TRS-80, and my favorite game was Pyramid. Pyramid was an endearingly primitive choose-your-own adventure game, in which you gave the program commands it rarely understood, hoping to randomly stumble on something useful, like THROW BIRD. I made it pretty far into the game, only to discover at the heart of the infamous maze of twisty passages, a coin-operated vending machine!
I felt totally ripped off: everyone knows there were no vending machines in ancient Egypt! The game lost some of its luster from this cheap anachronism, and eventually I gave up, moving on to the more fast-paced Centipede clone, Slay the Nereis (OK, I just paused in the middle of writing this post to waste thirty minutes playing Atari’s online version of Centipede. I still get a thrill from the sound of those falling fleas, but how I miss the arcade version’s rollerball).
Anyway, it turns out that Egyptian vending machine wasn’t such a stretch after all. Ancient machines that were derided as toys or flights of fancy are now taken seriously by archaeologists and engineers. The Antikythera mechanism is the best example of this (there was an excellent article about it in the May 15 New Yorker). And Cabinet of Wonders just posted a wonderful essay and collection of links on ancient automata. It’s incredibly interesting reading.
Apparently there was a coin-operated vending machine (for holy water!) two thousand years ago - designed by the Greek engineer Hero of Alexandria (or Heron). That was long after the Pyramids were built, but who knows? Maybe Hero wasn’t the first to figure it out. The Antikythera Mechanism survived, albeit in terrible condition, but how many gadgets, including proto-computers and primitive robots, have been lost? It’s a dizzying question - but also an important reminder that biologically, we are neither more intelligent nor more creative now than our ancestors were a few thousand years ago. We’re just starting at a much higher technological baseline.
July 19th, 2007
from xkcd.com
A few months ago, I dreamed that I attended a cocktail party, where I mistook Simon Baron-Cohen (the neurobiologist) for his cousin Sacha Baron Cohen (better known as Borat). I don’t know why either of them was in my dream (I haven’t even seen Borat), but if the opportunity ever comes up, I would like to pick the neurobiologist’s brain over cocktails. I don’t know quite what to think about his suggestion that autism might be caused by assortative mating among technogeeks - not to mention the bit about men and women having differently abled brains.
Autism is getting more and more attention, both in the media and in research. But we still don’t understand the developmental causes of autism. We don’t know how to define what has gone awry in autistic children, much less fix it. This confusion has fueled a rash of hypotheses (and lawsuits) over possible causes - most of which are unsupported by scientific evidence. But parents want some explanation: as many as 1 in 100 of their children will be diagnosed with autism spectrum disorders. Whether there is a new autism “epidemic,” or we’re just catching cases that twenty years ago would have gone undiagnosed, is still unclear.
For the past several years, Baron-Cohen and his collaborators have been fleshing out a genetic model for autism. Twin studies support the idea that autism is genetic - the best predictor for autism is a twin with autism. But why do children of non-autistic parents become autistic? And why is the rate of autism increasing? Unlike more straightforward genetic conditions such as Tay-Sachs or hemophilia, where a “bad” allele of a gene causes a well-defined disease, autism probably involves multiple genes with additive effects - alleles that are benign, even beneficial, in normal individuals, could contribute to autism in the right (or wrong) combinations.
As summarized in this 2003 Guardian article, Baron-Cohen maps autism along the same continuum as gender differences in cognition. So let’s start with that. According to his model, women tend to be “empathizing,” while men are more “systematizing”:
Systemizing involves identifying the laws that govern how a system works. Once you know the laws, you can control the system or predict its behavior. Empathizing, on the other hand, involves recognizing what another person may be feeling or thinking, and responding to those feelings with an appropriate emotion of one’s own. (”The Systematizing Brain,” NYT, 2005)
This is, of course, a simplification - individual men and women could fall anywhere on the E-S continuum; most of us are a middling balance of E and S. But the idea is that, in bulk, most men tend to be S while most women are E.
Such claims about gender differences in mental processing are understandably controversial, especially when they reinforce cultural stereotypes. Baron-Cohen’s papers are peppered with phrases like “typical male interests (e.g., in mechanics)”. He knows he’s treading dangerous ground, and isn’t shy about it:
Two big scientific debates have attracted a lot of attention over the past year. One concerns the causes of autism, while the other addresses differences in scientific aptitude between the sexes. At the risk of adding fuel to both fires, I submit that these two lines of inquiry have a great deal in common. (”The Systematizing Brain”, NYT, 2005)
I’m not going to get into that gender-bias mudhole. But just to balance things out, here’s a typical response from his critics.
Anyway, within the E (female) - S (male) spectrum, Baron-Cohen characterizes autism as a hyper-systematizing brain (an extremely male brain). When S dominates E, the ability to form interpersonal relationships and communicate with others could be hindered. If you’d like to get a feeling for how “systematizing” you are, Baron-Cohen’s autism quotient (AQ) test (Wired) is a blunt-force gauge of autistic traits for adults. The relevant research paper is linked at the bottom of this post; the average AQ test score is supposed to be 16-17. The automatic scoring at Wired wasn’t working when I checked, but the test is also mirrored here at OK Cupid, so try there first.
Although the AQ test emphatically CANNOT diagnose autism, autistic individuals tend to have scores over 32. And as you’d expect from the previous paragraphs, AQ is also correlated with gender: men usually score higher than women do.
EQSQ also has a little systematizing/empathizing quiz: I have no idea if this one’s based on science at all, but it tries to assess if you are more S or E.
If you’d like more detail on why brains are either empathizing or systematizing, you should read this article from Entelechy, “The Biology of Imagination.” In it, Baron-Cohen hypothesizes that developmental deficits in certain brain circuits might impair the acquisition of empathy, shifting the balance toward systematizing. The general idea is that humans (and cats, dogs, etc.) can easily generate primary mental representations of the world around them. But it’s harder to handle “second-order” representations, like the imagined perspectives and feelings of other people:
Let’s define mind-reading as the ability to put yourself in someone else’s shoes, to imagine the other person’s thoughts and feelings. . .
To mind-read, or to imagine the world from someone else’s different perspective, one has to switch from one’s own primary representations (what one takes to be true of the world) to someone else’s representation (what they take to be true of the world, even if this could be untrue). Arguably, empathy, dialogue, and relationships are all impossible without such an ability to switch between our primary and our second-order representations. (Entelechy)
Baron-Cohen suggests that genetic influences on the growing brain could specifically affect the development of this capability:
In the vast majority of the population, this module functions well. It can be seen in the normal infant at 14 months old who can introduce pretence into their play; seen in the normal 4 year old child who can employ mind-reading in their relationships and thus appreciate different points of view; or seen in the adult novelist who can imagine all sorts of scenarios that exist nowhere except in her own imagination, and in the imagination of her reader.
But sometimes this module can fail to develop in the normal way. A child might be delayed in developing this special piece of hardware: meta-representation. The consequence would be that they find it hard to mind-read others. This appears to be the case in children with Asperger Syndrome. They have degrees of difficulty with mind-reading. Or they may never develop meta-representation, such that they are effectively ‘mind-blind’. This appears to be the case in children with severe or extreme (classic) autism. Given that classic autism and Asperger Syndrome are both sub-groups on what is today recognized as the ‘autistic spectrum’, and that this spectrum appears to be caused by genetic factors affecting brain development, the inference from this is that the capacity for meta-representation itself may depend on genes that can build the relevant brain structures, that allow us to imagine other people’s worlds. (Entelechy)
If each person has some alleles pushing the developing brain towards E, and other alleles pushing toward S, then an imbalance of those normally harmless alleles could cause a brain to become excessively S. How would such a genetic imbalance arise? As in this article from last November’s Seed, Baron-Cohen suggests that assortative mating - strongly systematizing men preferentially choosing systematizing women, or vice versa - could, through basic genetic principles, produce even more systematizing offspring. It’s as simple as a tall couple getting together and having even taller children. And Baron-Cohen has data to support it:
First, both parents of children with autism are likely to be super-fast on attention tasks, in which the aim is to spot a detail as quickly as possible. Second, both parents have an increased likelihood of having had a father who worked in the field of engineering. Third, both parents are more likely to have elevated scores on subtle measures of autistic traits. And fourth, both parents show a trend toward a more male pattern of brain activity when measured using MRI.
The chances of both parents displaying these similarities are vanishingly small. Something must be causing two such individuals to be attracted to one another. I propose that “something” is strong systematizing—the drive to analyze the details of a system in order to understand how it works. (Seed)
Parents of autistic children score higher on the AQ test than other parents - indicating that, while not themselves autistic, they have systematizing tendencies. The higher the AQ score, the stronger those tendencies are. Scientists and engineers (both male and female) tend to score higher on the AQ test than non-scientists. (Remember, systematizing is only a detriment if taken to extremes; most of us would like to be better at pattern recognition and analysis.)
If systematizers are marrying each other in increasing numbers, and bearing increasingly systematizing children, could it explain a suspicious increase in autism in, of all places, Silicon Valley? Hmmmm.
On the AQ test, I scored a measly 20. I guess from a genetic standpoint, it would be safe for me to reproduce with an engineer, or another scientist. But on the other hand, biologists have the lowest average AQ out of several scientific disciplines tested - my score is actually high for a biologist. Even worse, according to EQSQ.com, I’m a Y-chromosome level systematizer! I’m supposedly less empathetic than the average man - which will no doubt disconcert everybody who has seen me practically burst into tears over a “sad” inanimate object, like the IKEA lamp. (it’s all alone! in the rain!)
Maybe I do have a few autistic personality quirks. But I also have a few stereotypically “male” mental tendencies, like a talent for reading maps and mentally rotating objects. I’m obviously not male. Nor am I autistic. (And I think EQSQ’s test claims I’m a systematizer because I’m rabidly curious - not because I’m systematic about my curiosity). Where exactly should we draw the line between personality quirks and symptoms? What does something like the AQ test really indicate? There seems to be some hypothetical tipping point, at which a geeky personality morphs into autistic pathology, and I have difficulty with that. Which is probably why I’m a biologist, not a psychologist.
Diagnosing Asperger syndrome (AS) is especially problematic. AS is a high-functioning autism spectrum disorder, in which IQ is not compromised. But experts can’t agree on whether AS is a mild form of autism, or a related disorder. One of my professors fit the AS stereotype perfectly: brilliant, observant, obsessed with details, completely oblivious to interpersonal problems, and utterly lacking in empathy. I’d say he was illogical about people - an adjective that would never apply to his meticulous research. Did he have autism/Asperger syndrome? Or was he just a preoccupied geek with atrocious managerial skills?
What about an obsessively organized polymath like Thomas Jefferson - did he also have AS, as Norm Ledgin claims in Diagnosing Jefferson? Or was he just an eccentric genius? Baron-Cohen and his collaborator Ioan James have suggested that science’s most revered figures, Isaac Newton and Albert Einstein, were autistic. But not everyone buys it:
Glen Elliott, a psychiatrist from the University of California at San Francisco, is not convinced. He says attempting to diagnose on the basis of biographical information is extremely unreliable, and points out that any behaviour can have various causes. He thinks being highly intelligent would itself have shaped Newton and Einstein’s personalities.
“One can imagine geniuses who are socially inept and yet not remotely autistic,” he says. “Impatience with the intellectual slowness of others, narcissism and passion for one’s mission in life might combine to make such an individuals isolative and difficult.” Elliott adds that Einstein had a good sense of humour, a trait that is virtually unknown in people with severe Asperger syndrome. (New Scientist)
Narcissistic, isolative, difficult, wicked sense of humor, impatient with the intellectual slowness of others. . .sounds perfect!
Speaking of fictional characters, even prickly Mr. Darcy from Pride and Prejudice has been labeled autistic, in which case autistic tendencies are catnip to tens of thousands of Darcy-loving females across America. I’m somehow skeptical.
However flawed the book’s historical premise, the Amazon reviews of Diagnosing Jefferson include some glowing, grateful comments from the parents of children with autism. These parents want to believe that their children can and will be successful (after all, if a father of our nation was autistic. . . ). Baron-Cohen seems to share their concern; he constantly emphasizes the unique perspective and gifts of autistic/AS children. It’s true that a few articulate, successful autistics, like animal behaviorist Temple Grandin, do gain unique insights from their condition. If I ever teach neurobiology again, Oliver Sacks’ essay-portrait of Dr. Grandin, titled “An Anthropologist on Mars” (Grandin’s own phrase) will be required reading. It’s a wonderful lesson in forming those second-order representations, trying to imagine an autistic individual’s perspective on the world.
Yet the diagnosis of autism is almost always a stunning tragedy for affected families. And if Baron-Cohen’s assortative mating hypothesis is correct, and autism is caused by concentrating otherwise neutral, even advantageous, “systematizing” alleles - how can we possibly prevent autism? We can’t prohibit extreme systematizers from marrying because they might have autistic children. There’s no meaningful way to measure that risk in advance, as there is for single-gene disorders. How do we combat a “disease” that’s the unpredictable product of completely normal human genetic variability? I don’t have an answer for that, and I don’t think anyone does.
Additional resources: Simon Baron-Cohen, “The hyper-systematizing, assortative mating theory of autism” (pdf)
Simon Baron-Cohen, et. al., “The Autism-Spectrum Quotient (AQ)” (pdf)
July 16th, 2007
Earlier, it seemed like everyone in the biology blogosphere (including me) voiced their opinion on whether biology is perceived to be easier than physics, and whether that explains why we see so much inaccurate popular biology perpetrated by non-biologists. It turns out SCQ explored the physics envy issue way back in 2005, in an article they have just reposted. They reveal the shameful truth: all biologists really want to be physicists! We’re just not good enough at math:
Russell[6] documented the now well-accepted finding that biologists rarely use integers per se, particularly when making chemical solutions. When they believe themselves to be unobserved, biologists prefer to use their own unique counting system consisting of the following quantities:
1. Some.
2. A bunch.
3. A whole bunch.
4. All of it.
5. See if somebody else has any.
6. We’ll have to buy some more.
7. Let’s write a new grant.
These quantification terms are roughly delineated by increasing powers of 10. The biologists’ counting system was compared to the primitive counting system used until quite recently in Samoa.
In my case this is sort of true. I’m not good at math. I wish I was better at it. One of my undergraduate professors told me I would be humiliated in graduate school for being so bad at math (I was humiliated, but for other reasons). And he was just the last in a long line of instructors to denigrate my talents in that area, starting with Mr. Florence in 6th grade - who made fun of me for not being familiar with exponents. Plus, I was not supposed to be good at math - or so I was told - because I was a girl. (Apparently both penis envy and physics envy were unavoidable).
All of this led to an overwhelming dislike for math, which remained intact until I discovered that, despite my gender, physical chemistry is actually kind of cool, and partial derivatives are downright neat-o. Unfortunately that was my senior year of college - a bit late to switch fields.
So who knows? If my 6th grade math teacher hadn’t been an insensitive jerk, or if I hadn’t been fed the girls-are-bad-at-math line so often, I might have become a physicist instead. If so, in the grand tradition of Schrodinger, I would no doubt have eventually started spouting off about biology. When it comes to curious minds, I think the grass is always greener. Not that I know botany or optics. Or psychology.
But I wish I did.
July 10th, 2007
The Wellcome collection of medical images has been made available for non-profit use under a Creative Commons license. This is a really fabulous resource. Just for fun I searched “trepanation” and got nine images like these:
Thanks to Stranger Fruit for the heads-up (oops, no pun was intended).
Also of interest: 43 submissions to the Worth 100 medical anomaly competition (via Boing Boing).
July 9th, 2007
The LA Times recently reviewed Body of Work: Meditations on Mortality from the Human Anatomy Lab
, a memoir by medical resident Christine Montross. I’ve been trying to decide if I want to read it, and I’m still uncertain. Although a relative novice when it comes to medicine (my degree is in molecular biology), I taught anatomy using human cadavers, and have dissected them. I never found cadavers the least bit disturbing. But I may be unusual in my detachment - my students reacted with disgust, distress, nervousness - and constant anxiety that their reactions weren’t normal.
But what is normal? How should we relate to a donated cadaver in the anatomy lab - as a person, or a thing? Some reactions seem to be universal - gallows humor, for example. Humans have been laughing at death since long before Shakespeare. (What other weapon do we have? Death always wins, and the cadaver’s the un-living proof of it.) We have some general rules of conduct - for example, treating the cadaver with respect, keeping the pieces of the various cadavers separate, covering face and genitals when they are not being examined. But such rules seem to be mostly for the students’ comfort, since it’s hard for a cadaver to retain modesty or dignity, at least in a traditional sense, when skin is missing and viscera are exposed.
Students respond to cadavers in personal ways, based on their own family histories, so one student’s experience of dissection is unlike any other’s. Everyone sees the cadaver differently: is this a person, or a patient, or a body, or a teaching specimen, or an illustration. . .? When students take limbs from a skeleton and hold them up to their own arms, turning them to determine the correct orientation, they enact a little unconscious ritual: memento mori. One student was fine with the cadavers until her grandmother passed away; after that, she found the cadaver so disturbing she couldn’t be in the same room with it. The boundaries of life and death, previously comfortably clear, had blurred intolerably. Before class began, students came to me, concerned that they might find the body of a deceased relative in the lab: when and were and who, they wanted to know. (Why came much later.)
Montross’ book takes on some of these issues. As reviewed by Harvard professor, poet and doctor Rafael Campo,
“Body of Work” is at its best when Montross, who is also a poet, allows us to observe the astonishing beauty her dissection reveals, and to relish the language she uses to describe it. “The language of these bones slides along their edges,” she writes. “Os coxae, the hip bones. Their three parts, with names like flowers: ilium, ischium, pubis…. The pelvic brim, as if water spills over it…. Brim, arch, spine. The ligament names like a call to prayer: sacrospinous, sacrotuberous. Sacrosanct.”
This wonder cabinet of anatomical language is familiar to any biologist. It is indeed beautiful. So is the body it describes. But Campo rebukes Montross for allowing such language to establish a clinical distance between herself and the life history of her assigned cadaver, “Eve:”
I believe it is the depersonalization first modeled for aspiring doctors in their encounters with cadavers that accounts for much of the lack of professionalism and career burnout in physicians, and the callous treatment patients too often receive nowadays.
Really: studying the body as beautiful, complex object is a precursor to treating living patients callously? I have never known anyone to leave an anatomy lab feeling less respect and wonder for human beings than before they began. Yet Campo wants the anatomical curriculum to explicitly address the spiritual, not just the physical:
In this age of frequently misapplied technology, here is a chance to make productive use of video cameras and monitors: Might not a video of Eve, telling of her life and created at the time she decided to donate her body, help mitigate some of the mistreatment Montross documents, as well as the subsequent distancing she (however uneasily) comes to approve?
A pleasant idea - and what I’d expect from the author of The Desire To Heal: A Doctor’s Education in Empathy, Identity, and Poetry. Empathy should be part of the training of doctors and nurses alike. But is anatomy lab the right venue in which to share the life history of a cadaver? Personal details would increase the discomfort of beginners - in my experience, overly powerful empathy for the deceased disrupts their ability to cut and handle the body (a point Campo seems to dismiss). Would cadavers without life stories receive less respect or care than those who had documented their lives?
Isn’t the point that regardless of our living identities, whether we are good or bad, our bodies are kin, after death and in life? When the cadaver was alive, it was home to a unique mind. Now that its cells are dead, is its role in the laboratory to elegize that mind - or to represent universal anatomical mechanisms? As a biologist, the answer seems fairly clear. Perhaps a doctor feels differently; I don’t know. But I was disappointed as Montross appears to conclude her book by backtracking from scientific objectivity to elegaic ritual (with Campo’s approval):
Great teacher,” she intones, “I give you flowers. I carry your body to the funeral pyre. When you burn, may every space in you that I have named flare and burst into light.” Thus she aligns herself with the humane tradition of honoring the dead, and the act of love inherent in tending to them. The detached concern she professes to want to emulate seems refreshingly absent here. Perhaps, in recognizing our universal and very human contradictions, there is hope for the beleaguered medical profession, after all.
Honestly, this leaves me cold. I can’t speak for anyone else, but if my body ever ends up in a cadaver lab, I don’t want people intoning poetry to it. I want them to dissect it. And yes, I said “it,” not “me.” I’ll be dead. My body is a wonderful clockwork, but it ain’t me.
The imagined ritual may be beautiful and humane, but it is a pleasant fiction, meant for the observer, not the observed. It has nothing to do with the cadaver’s living identity - we have no idea who “Eve” was, nor if she even desired commemoration. Most importantly, the manifest beauty of the human body doesn’t require validation by tradition or flowers (or words). We don’t have to turn a cadaver into a spiritual symbol to make it a wonder: it already is wonderful, even in death. And if someone fails to understand that, I doubt they should be practicing medicine at all.
July 8th, 2007
An Experiment on a Bird in the Air Pump (1768)
Joseph Wright of Derby
An Experiment on a Bird in the Air Pump - detail
(view zoomed image at the National Gallery of London)
Wouldn’t it be excellent if science was still conducted in darkened, intimate chambers lit by candles, as in these wonderful paintings - part of a series of posts on chiaroscuro at { feuilleton }?
Sure, you could get the same dramatic effect by holding lab meeting huddled over a UV transilluminator - but oh, the inconvenient mutagenesis.
July 6th, 2007
portrait of James Ferguson, astronomer
Oh, look! Legions of Dead White Males with (natural laws, anatomical parts, minerals, equations, geological features, organisms, diseases, scientific societies) named after them! And some little prankster drew spectacles on Ferguson.
Scientific Identity: Portraits from the Dibner Library of the History of Science and Technology
via
July 6th, 2007
From the Guardian: scientists and non-scientists attempt to answer basic science questions. Example:
Q: Roughly how old is the earth?
A: Oh blimey. Well, I know that human beings have been going for about a million and a half years, so … I’m just grasping here. Something like 60 billion years or something like that, but that’s a grasp. I’m not a physical scientist and it shows. I’m probably not scientifically literate.
That answer was from a professor of neuropharmacology. (I’m not good with numbers either, so I’ll shut up now.)
Via
July 4th, 2007
Normalcy
One Size Does Not Fit All
, 2002
Beverly Naidus
A while ago, I promised to share my impressions of Gina Kolata’s Rethinking Thin
. I finished the book last month, but I wanted to let my response percolate before posting. The biology of metabolism is one of my hot-button issues, and I had high hopes for this book. With a hefty subtitle like “The New Science of Weight Loss - and the Myths and Realities of Dieting,” I expected a forceful argument, perhaps even a jeremiad, against those dietary myths. The book is, somewhat disappointingly, not a jeremiad. But it is interesting, and, I hope, part of a gradual shift in attitudes toward metabolism.
The fruit of Kolata’s research is partly a history book, recapping America’s obsession with weight loss from the 1800s on. As a history of dieting, it’s eye-opening: the same kinds of diets have been recycled for over a hundred years. You thought Atkins was new? Not so much! It’s also partly a review of the latest obesity research - but that research points too many directions, and is far too complex, for a review of such brevity to satiate scientifically informed readers. Thirdly, it’s a sensitive portrait, though a somewhat superficial one, of dieters who embody a statistical inevitability: failure to keep lost weight off. Their initial euphoric success and subsequent depression are what tables and figures in scientific papers never capture.
In introductory classes, I often assign non-fiction books that model how science should be practiced, while also demonstrating how real-world preconceptions, politics, and personalities inevitably derail perfect objectivity. Rethinking Thin is a book in that vein: Kolata takes on preconceptions about fatness, some deeply ingrained in our culture, and discusses how research has been directed and constrained by those preconceptions. Occasionally, the prose goes off the deep end:
Without phen-fen, Carmen was at a loss to control his weight. “I stopped, and the weight came back,” he recalls. What to do? He had no interest in trying another water-cooler diet, so, like the swallows of Capistrano who, legend has it, return each year to an old ruined church where they had been saved in the past from an innkeeper who destroyed their nest, Carmen returned to Jenny Craig.
But aside from a few inexplicable clunkers like that one, the book is pleasantly readable. It’s full of engaging details, like Chicago teen Yvonne Blue’s 1926 diary (”Three months in which to lose thirty pounds - but I’ll do it - or die in the attempt”), or the “Dr. Atkins of his day,” Horace Fletcher, who advocated weight loss through “divine mastication” (chewing), which was popularly called Fletcherizing.
What Rethinking Thin is not: a diet book. It is not a how-to book, nor a consumer report recommending one diet over another. And it is not - as some reviewers have suggested - a license to give up and be fat. There’s an important distinction between acknowledging the substantial genetic influence on obesity, and abdicating personal responsibility because of it.
For readers who have struggled with weight issues, much of this book will seem disturbingly familiar. Several individuals in the book confide their intense feelings of relief when they realize that other people have the same difficulties with food that they do. (My response to the book was also very personal, as will become obvious from this review). But though catharsis is pleasant, the people who should read this book are the people who don’t struggle with weight loss - especially health professionals who advise patients on dieting. I doubt many will read it, since a problem that one does not share (and an entire nonfiction book about that problem) is generally much less interesting than one’s own problems. I understand that if you’re naturally thin, it can be hard to relate to someone who is fat - you wonder why they don’t simply eat less. You may even have contempt for their lack of self-control. But the fact is, losing weight is not the same challenge for everyone, and the biology backs that up.
If you don’t struggle with your weight, consider this: do you congratulate yourself on avoiding unhealthy foods that you don’t like? Probably not, because you don’t have to resist cravings or desires to do so. It’s much harder to avoid your favorite foods - the ones that make your stomach growl and mouth water! So wouldn’t it be harder to resist food in general, if you experienced a constant, 24/7 struggle against gnawing hunger - the same sensation you’d have if your favorite food was sitting temptingly in front of you?
The truth is, some people really are hungry ALL the time. I know this because I’m one of them. I don’t know what “eating until you’re full” feels like. When I say “I’m full,” it means “I’m not going to continue eating now, because it would be imprudent/indelicate/unnecessary.” But am I still hungry? Heck yes! My stomach growls pretty much all day, at night while I’m trying to sleep (fun), while I’m jogging. . . talk about embarassing.
Why does this happen? I have no idea, but I think it’s genetic. Kolata’s book presents consistent evidence that “the children who are going to get fat are those whose biological parents are fat”; 80% of adopted children with two obese birth parents became obese; only 14% of the children with nonobese parents did. Metabolism is genetic. Body shape is genetic. But does a genetic “hunger overdrive” give me license to eat food nonstop and gain ridiculous amounts of weight? Absolutely not! I may be at a disadvantage, but I’m still responsible for what I eat. I get the distinct impression that people who decry or deny the “genetics of weight” (and blame Rethinking Thin for promoting it as a cause of obesity) fear that genetics will mean a complete abdication of personal responsibility. I don’t agree at all: clarifying the role of genetics helps to give an individual control, by defining the parameters of their problem. However unreasonable or destructive, constant hunger is a real, physiological impulse that some people have to resist. Telling these people “it’s all in your head” isn’t helpful. What’s wrong with “I realize you feel this way, and it’s not your fault, but if your goal is to be thinner, you need to develop strategies to control this hunger” ? Wouldn’t the latter advice be more constructive than denying the problem exists?
Guilty
One Size Does Not Fit All, 2002
Beverly Naidus
You can probably sense that I’ve had a few unpleasant run-ins with nutritionists myself. In fact, I’ve been reprimanded for “lying” about my food intake, because according to those one-size-fits-all medical charts, it’s simply impossible that I weigh what I do, exercise as much as I do, and eat as little as I do. If I estimate my basal metabolic rate (BMR), I should be eating almost a thousand more calories each day than I do! I’ve kept meticulous food/exercise diaries that would make a dietician’s head spin, because the numbers don’t add up.
How do I explain this? Simple. These BMR estimations don’t work for everyone, because not everyone’s metabolism runs at the same rate. (If I assessed my BMR directly by measuring oxygen consumption, it would be much more accurate, but I’ve never had the pleasure of an expensive VO2 test). Rethinking Thin recounts seminal studies that demonstrated this decades ago - subjects’ bodies readily buffered experimental changes in caloric intake, revving up or slowing down to maintain weight near their set point. Naturally thin subjects had to eat a truly shocking amount of food to put on weight; they couldn’t keep it on! Why, then, is it hard to accept that people’s metabolisms are heterogenous to start with? I’d have gotten my weight under control much faster if the nutritionist I saw ten years ago had said “huh. You must have a slow metabolism. It’s not fair, but you’ll have to eat less than the recommended amount. Let’s work on doing that, in a healthy way.” (I’m sure there are nutritionists somewhere who say things like that, but I’ve never had the pleasure to meet them).
So how much do I eat, when I’m trying to lose a few pounds? I never give a number anymore, because of the knee-jerk response I get. I’ve been called anorexic, despite being well on the chunky side of the bell curve. (”Do I look anorexic?” usually silences those critics). I’ve also been accused of crashing my own metabolism (and causing my weight problem) by eating so little my body goes into “starvation mode.” Aside from the unlikelihood of being in “starvation mode” while having plenty of energy, plenty of fat, and running several miles a day, I only started eating substantially less in my late twenties - after I got the confidence to define my own diet based on what felt right, not what I was told to do. Since then I’ve lost weight, not gained it.
The only proven way to lose weight is to 1) reduce calories and 2) increase expenditure through exercise. Yet society seems reluctant to endorse option 1, as if there is an unforgivably slippery slope between endorsing a low caloric intake, and promoting Nicole Ritchie-style emaciation. Why our society persists in defining beauty by supermodels who are extreme outliers on the curve of human morphology, and what that does to young girls’ self-esteem, is another post entirely. Kolata points out that despite the revisionist conception of Marilyn Monroe as a curvacious “size 12,” the sex goddess was really only 115 to 120 pounds - hardly today’s 12; but Rethinking Thin spends only one chapter on the changing history of body images. This is disappointing but understandable - it is a different issue, and an important one, that deserves its own conversation. Especially in a holier-than-thou age where talking heads on Fox News accuse 17-year-old Jordin Sparks, winner of American Idol, of setting a bad example simply by existing:
When I look at Jordin, what I see is diabetes, I see heart disease, I see cholesterol. . . .she’s a vision of unhealth. (Meme Roth)
Jordin is 5′ 10″ and according to People, a size 12.
Although I would never endorse eating disorders, or the bizarre delusions of people who think 17-year olds should be pilloried on national media outlets, I would argue that some of us can responsibly reduce food intake pretty far, and in fact need to do so, if we want to be a socially acceptable size or have an athletic build. By denying this, health professionals enforce all-or-nothing choices that are fodder for eating disorders. If you can’t get to a healthy weight by dieting in the “approved” way - and not all of us can - you might give up completely and be unhappily fat, or stop trusting medical advice at all, take extreme measures, and hurt yourself in the process. Your self-esteem shouldn’t be about numbers on a scale (bathroom scale OR food scale); it should be about cardiovascular, mental, and immune health!
This brings me to a group of people who get suprisingly scant coverage in Rethinking Thin: devotees of caloric restriction. Kolata touches on the origins of counting calories, first popularized by early twentieth-century diets books like How to Live by Fisher and Fisk, or Lulu Peters’ Diet and Health, with Key to the Calories (1918), which recommended a diet of 1200 calories per day:
You will be surprised how much 1200 calories will be if the food is judiciously selected. You may be hungry at first, but you will soon become accustomed to the change. I find that dry lemon or orange peel, or those little aromatic breath sweeteners, just a tiny bit, seem to stop the hunger pangs; or you may have a cup of fat-free bouillon or half an apple, or other low calorie food. (L.H. Peters)
According to Kolata, “Diets became stricter and stricter, with doctors, around 1928, recommending eating just 600 to 750 calories a day to cure severe obesity.” Who eats that much? Some practitioners of caloric restriction eat almost that little - and do very well.
Caloric restriction (CR) is a diet plan in which the caloric intake is reduced by at least 20% from the recommended amount. CR definitely works, and not only to lose weight. In lab animals, it also significantly extends lifespan - a benefit which may or may not apply to humans. (Health and longevity are the stated goals of CR - not weight loss per se).
But disappointingly, “caloric restriction” isn’t even in Kolata’s index. Her book is about popular diets and the science behind them; despite the efforts of CR proponent and diet guru Roy Walford, CR is hardly popular. It can be grueling, and Americans love their food - drugs like Alli, which have limited benefits but let you eat, will always be more attractive. CR is also controversial. The Mayo clinic is hesitant to recommend CR. And a Slate article last month compared CR to anorexia. (Of course, this is the same publication that ran this story in February, in which 1500 calories a day were termed “starvation.”)
So what do we do? For the genetically unlucky, is obesity inevitable - something we can only combat with starvation? Animal models haven’t answered that question. Carl Zimmer, writing about mouse genetics for Discover, describes Gary Churchill’s efforts to find the elusive fat gene:
Rather than focus on a single gene, Churchill and his colleagues decided to explore the entire weight-control network. They selected a big, lean strain of mice and mated them with small, fat ones. The offspring of this union grew to many different sizes and weights. Churchill and his team then measured how large the animals grew and how much of their body weight was fat versus muscle. They also measured how the fat was spread out on each mouse. Like us, mice tend to accumulate fat in certain places, like their haunches and their bellies. Finally, the scientists scanned the genome of each mouse for hundreds of markers to see which ones were linked tightly to each trait.
The map they came up with looks like a flowchart from hell. Churchill’s group identified a dozen sites in the mouse genome where genes are influencing the body weight of mice. But the genes have different effects. Some make mice large-bodied, and being big makes mice more likely to get fat. But they also found genes that had separate effects on both body size and fat levels. In some cases, the same gene could make a mouse both big and lean. Other genes influenced only how fat the mice were, with no effect on their body size. Still other genes determined the size of different fat pads. One region of mouse DNA appears to make mice fat overall while actually making the fat pads on their haunches smaller.
This sounds very much like human beings, doesn’t it? The genetic “flowchart from hell” could be why one diet doesn’t fit all; why the Atkins diet may work for your aunt but makes you get fatter; why your friend who never exercises is still thinner than you are. It’s why some people put fat on their thighs and some deposit it on their midriffs.
Can we fight the flowchart from hell? Kolata seems doubtful, and this is where I am most disappointed with her book. In the end, the dieters she’s tracked don’t keep their lost weight off, and the book concludes in a tone of sadness and powerlessness. Kolata even speculates that the obesity epidemic could be inevitable - some unforeseen consequence of a modern lifestyle which we can do little about. She never says we’re definitely doomed to be fat - just that, for many of us, we’ll have a constant struggle to avoid it, and almost all of us will fail (a grim reality borne out by statistics).
I agree that no diet will be a quick cure for the obesity epidemic. I hope Kolata’s book persuades a few more people of that, or at least conveys the hardships naturally heavy people face as they fight their own bodies. But I wish her book had reframed the obesity problem more optimistically, as an individual problem, with individual solutions. To paraphrase Tolstoy, every naturally thin person is alike, but every heavy person is heavy in their own unique way, for their own reasons - genetic and otherwise. If we accept that, we might see more creative ways to approach obesity.
June 25th, 2007
My PhD is four years old, and has long lost what transient lustre it held for me. Yet I’m somehow still involved in never-ending rounds of revision on a paper based on graduate work to which I will never return. As captured in this SCQ piece, Mother Goose and the Scientific Review Process, the whims of reviewers truly are beyond the ken of mortal man (or woman).
June 23rd, 2007
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