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.)
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 reviewershave 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?
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)
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.
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).
A few weeks ago, I asked a beekeeper at the Portland (Oregon) farmer’s market whether his bees were ok. “Yeah, they are,” he said, “but I get that question a lot.” On Saturday a Seattle beekeeper told me he’d “had some losses” but added soberly, “it could be a lot worse.”
Since colony collapse disorder (CCD) broke out last November, as many as a quarter of our domestic honeybees (Apis mellifera) have disappeared, abandoning hives full of food and larvae. Some beekeepers have lost up to 90% of their hives. Since the adult bees don’t return to the hive to die, it’s impossible to say what killed them; the few victims left behind display a confusing variety of pathological problems, such as a digestive tract clogged with undigested food, elevated numbers of normally harmless pathogens, and discolored tissues. Weirdest of all, opportunistic scavenger species and bees from other hives won’t touch the abandoned stores of honey. What do they know that we don’t?
From a agricultural perspective, it’s a pressing question. Not all crops require bee pollination, but over 100 do, including almonds and many fruits. The bulk of a beekeeper’s own income is derived from renting his or her hives for pollination services, not from honey production - the Oregon beekeeper I interviewed said with a smile that he barely makes any money on honey. California’s almond growers have begun outbidding other industries for the services of beehives, because there are simply not enough to go around - and that was before CCD kicked in, decimating the bee supply in some regions of the US.
• View a narrated slideshow about CCD and the industrial side of beekeeping (NYT)
Depending who you ask, possible causes of CCD include GM crops; malnutrition (poor pollen quality/availability, or poor supplements provided by keepers); unusual numbers of common parasitic mites (varroa); a virus; funguses (a new, more infective strain of Nosema); poor genetic diversity in domestic bee strains; cell phones (or cordless phones - there seems to be some confusion); and pesticides (usually neonicotinoids). Whatever it is, it’s global - Canada and Europe also report losses. France, after serious hive losses several years ago, banned some neonicotinoid pesticides, but continue to lose bees anyway. Australia is largely ok; some US beekeepers have replenished their stocks with Australian bees.
One (somewhat) comforting hypothesis is that CCD is actually old news - a periodic disorder that has happened before, and will clear on its own. Intermittent seasonal losses have been reported since 1868, in both the US and Europe; the occurances were given names like “dwindle disease”, “disappearing disease,” and “Isle of Wight disease.” In some cases, a putative cause, like fungus or unusual weather, was blamed; in other cases the problem simply went away without any likely cause being found (Underwood and van Engelsdorp, 2007). So will CCD just go away? Hopefully, but no one’s counting on it.
Agricultural practicalities aside, there’s something gut-wrenchingly wrong about CCD. A fundamental piece of the ecosystem is being leached away, and we have no idea why. I’m reminded of the epidemic of frog deformities a decade ago. Despite frantic experimentation by ecologists and developmental biologists, it was never solved (the most likely culprits are trematode parasites; but pesticides, habitat loss, and UV radiation probably contributed to the problem). Will a similar complex of interlocking causes be found for CCD? Will we be able to cure it, or will we just have to wait for it to diminish - as we did with the frogs?
The white color of this albino peacock is due to the missing black melanine pigment. The usual rich colors of the peacock are seen because black pigment which absorbs most of the incident light, allowing us to see only the interference colors. In this peacock, the interference is still happening, but the effect is entirely washed out by the abundance of white light. In this albino, you can see that the “eyes” of the tail feathers are clear, not colored.
Via the Evilutionary Biologist, a fun website about the science of color - not just the biology of our eyes, but the physical properties of objects that make them appear colored. Why is water in the sea blue, but water in a glass clear? How is the glow of lightning different than that of a light bulb? What causes the rainbow of color “in” an opal? There’s quite a bit here I didn’t know, or don’t understand as well as I should!
The website is maintained by an organization called IDEA. Some of the pages are under construction, and unfortunately the dates suggest the project may be abandoned, but at least it’s a good start for future reading. IDEA also has a mixed bag of other websites, including color vision and art, pigments, scientific analysis of old masters, and butter. (One of these things is not like the others. . . !)
A) gremlin
B) globulin
C) glomerulus
D) gomphosis
E) gomphus
(answer below the fold. . .)
The answer is C) glomerulus. And this illustration by Jim Stanis is the finest glomerulus I have ever seen - podocytes, pedicels and all!
Bonus point if you know what a glomerulus does - withoutlooking it up on Wikipedia. Quadruple bonus points if you know what all the other answers actually are.
I’ve wanted for some time to post this evocative self-portrait by artist Madeline von Foerster, but I knew if I did, I would have to accompany it with an article about the history of trepanation. An ancient surgical procedure which involves drilling the cranium and removing small sections of bone, trepanation has both mystical and medical associations, and despite its inclusion in Phil Pullman’s popular His Dark Materials trilogy, it remains pretty obscure.
Imagine my surprise and delight when, in the timeliest of manners, the Neurophilosopher swooped in and wrote this excellent Illustrated History of Trepanation that I can simply link to! Thank you, Neurophilosophy Man! You’re my hero! (In your honor, I hereby pledge to read a large chunk of neurophilosophy in the time I would have otherwise spent Googling “trepanation”, “trephination”, and all its other variants).
Anyway - after reading all about trepanation, I highly recommend that you visit von Foerster’s website. Her intricate artwork bursts with medieval influences, symbolism, and erudition, while remaining completely delightful - and her textures, color and detail border on hedonistic. I’m not sure how many levels of meaning there are to some of her pieces, but it’s lovely to try to figure it out.
“Most people think of science as abstract and numerical. In fact, science is a surprisingly visual endeavor: both data and theory are often driven by pictures and images. Felice Frankel’s work conveys the tremendous beauty and excitement of science–letting the layperson share in the wonder of studying the natural world.”
-Eric S. Lander
Continuing yesterday’s theme, but from the art world’s side, gallery owner Edward Winkleman responds on his blog to a NYT profile of Felice Frankel. Winkleman pulls the same things from the piece that got me ruffled when I read it last night.
According to the NYT, Frankel started a stint at MIT as “artist-in-residence,” but ended there as a “research scientist.” No explanation is given for this transition, but it might have something to do with the two reasons Frankel herself disavows “artist” status. She says:
1) her work doesn’t sell, and
2) her work is not about her own ego.
Therefore, she’s not an artist. Double ouch!
Frankel apparently bases this self-assessment on her personal interactions with the professional art world, because the science world is justifiably gaga over her work. And I’m not sure why it wouldn’t be “art.” Frankel’s audio commentary on this slide show discusses the design and planning aspects of her process, and how she uses digital tools to refine her images (Frankel uses a Mac, of course.) But Frankel called her 2002 book Envisioning Science: The Design and Craft of the Science Image. Why design & craft, but not art? Simply because her pieces have a practical purpose?
Frankel says of the image at the top of this post, which appeared on the cover of Physics Today, “I’d like to think you are curious about it because of the way I photographed it. My hope is that you are going to want to ask questions about it.” (NYAS). That sounds like an artist to me. She also notes that she’s sick of it, because it has been reprinted so often. That sounds like a problem an artist would like to have. . .
Bodyscope Anatomical Chart, 1935
approximately 20″ x 16″
Ralph H. Segal, Bodyscope Publications Inc.,
Educational Building, 70 5th Ave., NYC
From 1935, two ornate Bodyscope teaching charts. Three windows in each chart allow a cutaway view of the torso and its accompanying legends (in the arches on either side) to rotate, providing five different views of the internal organs. A numbered key below the figure indicates which of the organ systems is currently displayed. The University of Kansas Clendening Library has a complete set of images in its collection (of the male, the female, and a third organ system chart).
The combination of period fonts, Art deco flourishes, and almost iconographic framing is charming. The spandrels on either side of the arched legends hold portraits of historical luminaries of medicine like Vesalius. Most of the text is anatomical description. However, the legends directly above the figures relate not to science, but to the larger social & moral context in which human anatomy was taught. For the man:
Man’s great Accomplishments and noble Aspirations are achieved through the possession of a Sound Mind and a Healthy Body . . . In these Attributes lie the Bulwark of Man’s Social, Moral, and Domestic Structure: the Foundation which perpetuates Humanity’s Existence.
For the woman:
Woman, her creative body as wisely patterned by God, is the Abode wherein the Seed is endowed with Life and imbued with a Soul. . . Her Maternal nurturing and inspirational influence are reflected in Mankind’s aspirations; the fruits of which become her Reward.
What a contrast between active and passive roles! Man is the disciplined architect, woman the. . . gardener? Man “perpetuates Humanity’s Existence” (I thought that particular activity involved both sexes), while the woman gets Rewarded with symbolic fruits. Nice. It’s interesting, though not surprising, that such moralizing was considered an appropriate way to preface medical education.
For additional detail, have a look at this near-mint specimen offered by Stonegate Antiques.
Incidentally, the Bodyscope chart set is labeled both “copyright 1935″ and “patent pending.” I can’t find evidence of a patent actually issuing. However, one RH Segal is the inventor of record on another patent from 1935, for a perpetual calendar which also employed a system of paper dials. It’s likely the same individual.
- that looks like an ear to me, not a bullseye or a crop circle.
- that looks like a moss to me, not a liverwort. Even zoomed in. But I hear it really is a liverwort.
I’d sarcastically observe that the hypothetical aliens aren’t going to get anyone’s attention by making itty-bitty crop circles on a tree in the middle of a forest. But this story got picked up by the NYT, so I guess I’d be wrong, wouldn’t I?
Sunday’s San Francisco Chronicle has a feature about the Australian light brown apple moth, an agricultural pest that recently appeared in the Bay Area. What makes this article by Matt Stannard (with pictures by Lance Iversen) especially enjoyable is that it’s not just about the invader moths - it’s about the man who discovered their arrival, retired UC Berkeley entomologist Jerry Powell. Powell just happened to find an apple moth at his house in Berkeley; he just happened to recognize the nondescript moth from a research stint he did in Australia; and as a UCB professor emeritus, he knew the right people to call about his hunch.
Last summer, Powell found his first light brown apple moth in his UV “insect lure.” He thought he recognized it, but didn’t get around to dissecting it until last fall - shortly before a second apple moth fell into his trap. He sent the specimen to Australia for a second opinion, then called the California Department of Food and Agriculture, which officially verified the moths’ arrival in March. CDFA is maintaining a network of pheromone-baited traps across 47 counties, and has identified several thousand of the moths so far.
The extent of the invasion, especially in Santa Cruz county, proves that the first invader moth didn’t head straight for Powell:
“By the time Jerry collected this thing in his backyard, clearly it had been established in the Bay Area for a long time,” said Brown of the USDA. “The first one that landed in the Bay Area didn’t fly to Jerry’s house.”
Powell says the presence of the light brown apple moth at his home was not a coincidence. It merely suggested that the insect was everywhere to be found.
“I look every night,” he says. “No one else looks in this area, and so if the thing is established here, I’m going to find it before anybody else does.”
Granted, the moth finding Jerry Powell was not such an unusual coincidence. But Jerry Powell himself - someone who collects insects recreationally, on a regular basis, and is qualified to identify them to the genus/species level - is indeed unusual. Most biologists wouldn’t recognize light brown apple moths if they were sitting on our noses. Most non-biologists wouldn’t notice the moths at all.
This story is a lovely throwback to what was best about Victorian science - collectors everywhere, interested in everything, observing and annotating their backyards just as seriously as they might investigate a tropical island. Now, it seems like every field of science is an island unto itself; most of the scientists I know leave their research at work in an effort to “have a life” (or have left research entirely). So although it may have been inevitable that the apple moth eventually wander into a backyard in Berkeley, it wasn’t inevitable that a lone watcher like Jerry Powell be there to meet it. It warms my heart, somehow, that he was.
Of course, if you’re going to plan a summer jaunt to Europe to commune with medical models, why limit yourself to wax and moulage? Curious Expeditions also “ran into” an ivory obstetric figurine by Zick at the Semmelweis Medical Museum, and have a smashing flickrset of the occasion, from which I abducted the Venus image at the top of this post. I’m convinced Curious Expeditions are the new Rick Steves of the wunderkammer set. . .
My mentor Tom (who taught me most of what I know about teaching) loved to ask this question on biology quizzes. It’s my favorite kind of question: it forces you to apply general scientific principles to a new situation, not a far-fetched one, but a common situation you’d never thought about before. Although I could reason it out, I was embarrassed that I’d never bothered to wonder why honey has such a long shelf life. There are many small puzzles like this in daily life, that go completely unexamined.
Anyway, honey is antibacterial primarily because it’s so highly concentrated - there is significantly less water in honey (which is about 80% sugar and less than 20% water) than in a bacterial cell. To put it crudely, the honey sucks the water out of the bacteria by osmosis, and the bacteria deflate. Honey can also draw water out of humid air - supposedly, placing honey in pastries keeps them from going stale as quickly. The principle of osmosis is essential to biology, and this answer is the most important one.
But honey has other antibacterial properties as well. Its acidity impedes the growth of many microbes, it contains a variety of antioxidants, and it releases low levels of hydrogen peroxide when diluted. You can see why all of these properties would be adaptive: bees don’t want bacteria raiding their pantries any more than we do!
The exact composition and flavor of honey depend on the types of flowers the bees are allowed to harvest; some honeys, like active manuka honey, are reputed to have increased antibacterial properties and are sold as medicinal supplements. (FYI - Meadowfoam honey, while not notably medicinal, tastes mindblowingly like toasted marshmallow. Try it, it’s amazing.)
Honey was used in the ancient world as a medicine and preservative (guess what was used to embalm Dracula’s detatched head?) But for a while honey seems to have been ignored by the medical community, which is strange, because studies are now finding that honey may be just as good as many other antibacterial treatments for topical wounds like diabetic ulcers, which are notoriously persistent.
My mother has impaired circulation (non-diabetic) and her injuries take months to heal over, even with state-of-the-art burn creams and special bandaging. I’ve convinced her to try honey next time: it would be cheaper and easier to find, it would keep bandages from sticking, it would absorb the fluid that leaks from these wounds, and according to several users, it smells much better than the typical topical ointment. (Why do medicines taste and smell so awful, anyway?) The whole idea seems so obvious, I’m surprised I’ve never heard of honey as a folk remedy, the way Aloe vera is touted for sunburn: in my family we cut leaves off the plant and squeezed the gel straight onto the burn. But it turns out there’s not much scientific evidence to support this kind of use of the plant. Maybe we should have used honey?
Here’s a final question: if honey is antibacterial, why can’t you feed it to babies? It turns out honey preserves not just the heads of putative vampires, but also the spores of C. botulinum, which causes the rare but serious disease of botulism. The botulinum spores won’t proliferate in the honey, but they can’t be removed, either (sterilizing them by common methods would compromise the quality of the honey). These spores are harmless to healthy adults, but infants under one year of age can become seriously, even fatally ill. So if you try honey as a topical ointment on yourself or others, be careful not to use it where a baby could ingest it.
You’ve probably heard the recent reports of a winged cat. The cat’s Chinese owner
says the wings, which contain bones, make her pet look like a ‘cat angel’. Her explanation is that the cat sprouted the wings after being sexually harassed.
“A month ago, many female cats in heat came to harass him, and then the wings started to grow,” she said.
However, experts say the phenomenon is more likely down to a gene mutation, and say it shouldn’t prevent the cat living a normal life. (source)
Did the tomcat grow these wings just to fly away from his groupies? How Lamarckian of him!
More on winged cats at the end of this post. . . but first, there are much odder stories blamed on “gene mutations”. I ran across this dreadful mess in a 2005 issue of Pravda:
Geneticists say that mutations seriously change the set of chromosomes, and people with mutations can thus hardly be called humans.
In Yerevan in the former Soviet republic of Armenia, 18-year-old girl Narine Aivasyan shocked doctors with her unusual disease. The girl complained about an abscess on her wrist that had been hurting her for a long period already. When doctors opened the bandage on Narine’s hand they saw two very thin thorns sticking out of the hand. . . Doctors removed from 70 to 100 thorns from the girl’s arm every day. But they still appeared later, which suggested there were two or three parasite cells still staying in the girl’s organism. Doctors from many countries stated there was not a surgical but rather a microbiological problem.
When researchers studied the bigger thorns they arrived at a conclusion that they were no longer of vegetative origin. As a result of mutation, the patient got new unknown cells, some sort of a hybrid of a human and a plant. In other words, the young girl was turning into a cactus.
Yikes! I have no idea what is wrong with Narine, but I seriously doubt she was a Triffid. Honestly, I find the quality of this “journalism” far scarier than the ludicrous idea of cactus-human hybrids.
Unfortunately, it’s on the internet, and there are quite a few people out there who think that anything published on the internet is reliable. Including some of my former students.
So where should one go for reliable information about genetic diseases, without running into questionably sane sensationalism? My favorite authority is the invaluable OMIM (Online Mendelian Inheritance in Man). Users can search OMIM by the name of a gene, the name of its associated disease, or keywords (Tim at Sciencesque uses OMIM’s search function to select random genes for review). But I’ve found that even for senior biology majors, the information in OMIM can be dense and difficult. It’s best to supplement OMIM with some alternative, accessible, trustworthy sources - and ScienceRoll has compiled exactly such a useful list. I highly recommend bookmarking it.
Back to the winged cats. In fact, they do exist. But the usual explanation is matted hair, not mutation. Henry David Thoreau documented the first report of a winged cat in Walden:
she was of a dark brownish-grey colour, with a white spot on her throat, and white feet, and had a large bushy tail like a fox; that in the winter the fur grew thick and flattened out along her sides, forming strips ten or twelve inches long by two and a half wide, and under her chin like a muff, the upper side loose, the under matted like felt, and in the spring these appendages dropped off. They gave me a pair of her ‘wings,’ which I keep still. There is no appearance of a membrane about them. Some thought it was part flying squirrel or some other wild animal, which is not impossible, for, according to naturalists, prolific hybrids have been produced by the union of the marten and the domestic cat. This would have been the right kind of cat for me to keep, if I had kept any; for why should not a poet’s cat be winged as well as his horse?
Thoreau’s “poet’s cat” sounds much like my own cat in appearance and coloring. Her fur forms felt-like dreadlocks that I have to cut out with scissors. Unattended, they could easily become ten inches long and stiff, like wings, before being shed when the anchor hairs fall out. (I doubt Thoreau appreciated what a pain it would be grooming a “poet’s cat”.)
Many cases of winged cats made serious news during the last century. In 1926, Time Magazine reported a case near Wapato, WA (where I spent several childhood summers). Most of the “wings” were probably caused by matted fur, or a genetic collagen deficiency called feline cutaneous asthenia (the cat equivalent of Ehlers-Danlos syndrome). Creative taxidermy artists have also pieced together fakewingedcats.
The Chinese winged cat supposedly had bones in its “wings;” neither matted fur nor FCA (nor taxidermy, since it’s alive) would explain that. I’ve found large sticks and burrs completely encased in my cat’s matted fur, and they feel like small bones, so I’m skeptical. But if the wings really have a bone structure, then the cat may have supernumerary (extra) limbs of some degree. The cause could be a genetic mutation - or a non-genetic birth defect.
In any case, since its owner describes it as an “angel cat,” I hope it won’t share the unfortunate fate of the Russian “Devil Cat,” which was drowned by superstitious locals in 2004.
, 2002
. 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.
