But historically? Well, different times, different rumors.

And apparently the one going around in 1865 was that everyone knew this guy who knew a guy who...swallowed a slug and had it come out alive.

I suppose that escargot no longer looks quite so appealing.

Dalton, JC. "Experimental Investigations to determine whether the garden slug can live in the human stomach." April 1865.

(Mmmm, tasty! Source)

I don't know about you, but my first question for these scientists is "WHO WOULD SWALLOW A LIVE SLUG". Seriously. You'd really think people would have the decency to cook it first. Or at least kill it.

And apparently, the guy who wrote this study was also more than a bit incredulous on the subject of live slug survival.

Apparently people were always coming to the good doctor (the author of this study) with stories, and sometimes specimens, of slugs that had taken the road of Lemmiwinks and come out alive. One guy apparently brought him a specimen in a jar, which turned out to be a slug. The guy's friend (it's always a friend) had been having stomach problems, and had given himself an enema to make it better (enemas were disturbingly popular in the 19th century, apparently some people did them daily). Just afterward, he felt something moving around under his clothes and pulled out...a large slug. The guy assumed it had come out of his stomach, but you'd think he would have felt SOMETHING. But the man assumed it was his own fault, because he liked to drink lake water (nevermind that garden slugs do not live in lakes), and so he assumed the slug must have got in that way.

The second instance was actually a 2-year old boy, who's mother found not one, but TWO slugs in his diapers while he was suffering from an upset stomach. The mother was adamant that he must have picked them up two months previously while he was in the country eating veggies, because she never served them fresh veggies otherwise.

The good doctor was not convinced. As he pointed out in his paper, slugs are cold blooded, and don't really do well at 98.6 degrees Fahrenheit. Secondly, slugs are soft. There's no bone there, they are (probably, I don't state from experience) the consistency of a chewy steak, which the stomach is perfectly capable of mashing up. Finally, a slug needs oxygen. There's not really much of that to live on in the gastrointestinal canal (particularly as you head down toward the nether regions of the colon).

I think I would have liked this guy. He heard these stories, he raised his eyebrows, and he said "let's TRY IT".

Sadly, he didn't do it himself. Instead, he collected a bunch of garden slugs, and handed them out to some dogs (carefully putting it down the throat to avoid it getting chewed by accident). History does not record what the dogs thought of this, but considering they got a few bits of steak afterward (to make sure they had swallowed fully), they were probably pretty chill about it.

With the slugs in, the doctor then killed the dogs and took a look inside. If you killed the dog 24 hours later? No slugs. One hour later? No slugs.

Fifteen minutes later? Slugs! The doctor administered four slugs, and found them all, completely dead and "somewhat softened", in the dog's stomach.

Finally, he took four slugs and put them in a jar of stomach juice from a dog, and kept it at body temperature. The long-suffering slugs lasted about 9.5 minutes. By five hours later, there was not much left to be identified as slugs (I really hope he kept that around to show to people. "What's the jar?" "Oh, nothing special, some slugs I've been keeping in dog stomach acid. Like you do".

He even tried water at various temperatures instead of acid, and while the slugs could remain underwater a good 5 hours and still make it out, by the end of 24, the slug was no more.

While the author admits that maybe people could digest slugs differently than dogs...well probably not. He hypothesized that the slugs probably came in on people's veggies (the first man was actually a porter for a hotel who frequently carried such items, and the child's mother apparently used cabbage to make a lot of saurkraut), and just happened to end up in the right place at the right time (as it were).

But I have to say, I'm sad he didn't go the extra mile, and swallow a slug or two for science. I mean, yeah, it'd be gross, but people eat escargot all the time! This is SCIENCE! You have to make SACRIFICES!

So, anyone out there willing to eat a slug or two for science?

Today's weird science comes to you courtesy of Mary Roach's book Gulp: Adventures on the Alimentary Canal. If you haven't read it yet, you should.

But not all dangers produce pheromones, and mice still have to let each other know that something is coming. So, as these authors show, mice may produce pheromones of their own that can communicate alarm to other mice.

If you need to keep the mice away, be prepared to wear...ear d'terror.

Brechbuhl et al. "Mouse alarm pheromone shares structural similarity
with predator scents" PNAS, 2013.

(Or get a cat. That works too. Behold, Scicat).

The authors of this paper had previously described a new ganglion, a group of neurons, which they believed to be involved in pheromone sensing, particularly of alarms. They had called this the Grueneberg ganglion, a small group of cells located at the VERY tip of the mouse nose. The neurons in this area specifically responded to alarm pheromones in previous studies.

But those were alarm pheromones from predator species. What about alarm pheromones from mice themselves? Do mice produce alarm pheromones to warn other mice of danger, and if they do, what are they?

To figure this out, the authors exposed a group of mice to carbon dioxide, which causes a major stress and alarm reaction. They then microextracted the chemicals the animals produced, and identified them. They found a total of 44 chemicals, 32 of which were emitted by control, non-alarmed mice, so those could be discounted. That left 8. 3 of these were unidentified, but the other 5 were gathered together an tested, to see what effects they might have.

First, they exposed the Grueneberg ganglion, where they believed the alarm pheromones to have the biggest effect, to the different chemicals they had isolated. In theory, if the any of the particular chemicals were an alarm pheromone, they would produce chemical potentials in the Grueneberg ganglion, which could be detected my imaging for calcium responses.

While most of the chemicals didn't do anything to the Grueneberg ganglion, one did, SBT (2-sec-butyl-4,5-dihydrothiazole). This one produced a nice big calcium response in the Grueneberg ganglion.

(Figure 2B)

You can see the calcium response on the left. But this is just in mouse slices of ganglion. If you want to prove something is a predator indicator, we need to see some fear.

SBT as a chemical is similar in structure to regular predator chemicals, but does it act the same way? The authors compared SBT with two known predator phermones, TMT and 2-PT, and looked for behavioral responses. They saw a significant increase in the stress hormone corticosterone in response to SBT, and also saw good marks of fear behaviors in the mice exposed to SBT, TMT, and 2-PT, including freezing (a well known fear response in mice), and risk assessment (when mice stretch out to their full length to investigate, leaving the hind paws in relative safety so they can spring back if there's danger).

But what this all working through the Grueneberg ganglion? After all, there's another very well known pheromone detection system: the vomeronasal organ. The authors of this paper believe that the Grueneberg ganglion plays an even bigger role than the VNO when it comes to fear responses.

You can see above the percent of responding cells in each organ (at left), including the Grueneberg ganglion, the Main Olfactory Epithelium (a major scent area), and the VNO. And it looks like SBT, TMT, and 2-PT, all the potential predatory indicators, produced the biggest effect in the Grueneberg ganglion.

So it appears the Grueneberg ganglion responds in a big way to these chemicals. But is it required for the fear response? The authors took a group of mice and looked for fear responses again in response to the pheromones. But this time, half of the mice had had the axons coming from the Grueneberg ganglion CUT. The Grueneberg ganglion was still there, but it couldn't send messages on anymore.

What you can see above are the fear responses in the control mice (grey), and the mice with the cut axons (black). Without the Grueneberg ganglion signals, the mice showed no significant freezing responses to SBT, TMT, or 2-PT, suggesting that the Grueneberg ganglion is required for this fear response. But it's not ENTIRELY required, as the mice with cut axons still showed increased risk assessment (bottom section).

So it appears that the Grueneberg ganglion plays a big role in fear in mice, and that SBT is an important pheromone for mouse to mouse communication. SBT is released in the urine and could be used to indicate to other mice that something wicked this way comes (and the urine is bound to happen, as anyone who has ever handled mice will tell you, one of the first things they will do is pee on you).

The authors note that SBT is structurally similar to TMT and 2-PT, both of which are natural predator odors, and so SBT might be activating similar receptors, giving the mouse to mouse version of the smell of terror. What are those receptors? In theory, it would be the TAAR4 receptor, which is known to mediate responses to predator odor in the VNO. But we don't know yet whether the mouse pheromone works the same way.

But there are still further questions. When they were causing mice to produce alarm pheromones, CO2 was the alarm condition they used (they also tried restraint and cold temperature). It produces a major alarm response, sure, but is it the SAME alarm response to the presence of a predator? It would be interesting to see how the chemical components compared to, say when the animals were exposed to real cat or fox odor. I understand the limitations of using the odors (the responses aren't as reliable, and getting fox odor out of anything is...almost impossible), but they did use some of them for other experiments, and it would definitely be the best way to determine the true similarity (though the chemical similarity and the behavior they got is a good indicator).

This is especially important because SBT is more than just a potential alarm cue. When presented to male and female mice, it promotes aggression in males, while it females it synchronizes estrous. Both of these things (but especially the aggression) can produce the increases in corticosterone they saw in the animals after SBT exposure. So it would be interesting to see both more specifically how SBT is acting, and also how SBT responses compare to true predator odor responses.

Additionally, they still had three unlisted chemicals. I really wonder what those are, though I imagine they are probably being examined separately. It would be interesting if they also played a role.

But it's an interesting thing to think about. Could pheromones like this be used as, say, a good way to get rid of rodents (though, since most of them REALLY smell, even to humans, it's probably not the best idea). And are there other roles for SBT that might be more than just eau d'terror? Future studies will have to find out.

 
Brechbuhl, J., Moine, F., Klaey, M., Nenniger-Tosato, M., Hurni, N., Sporkert, F., Giroud, C., & Broillet, M. (2013). Mouse alarm pheromone shares structural similarity with predator scents Proceedings of the National Academy of Sciences, 110 (12), 4762-4767 DOI: 10.1073/pnas.1214249110

(Source)

And are you willing to wear a tube inserted right up your butt to find out?

(For this, I maded a LOL. Source)

Beazell and Ivy. "The Quantity of Colonic Flatus Excreted by the "Normal" Individual" American Journal of Digestive Diseases, 1941.

Ah. The 40's. Back when you could fit up five dudes with ass-gas bags, make a single graph, cite one other publication in a two page paper, and still get published. I cry a single tear for those days...

Anyway. The authors of this study noticed a certain...lack of literature out there on gas. Specifically on fart VOLUME. We all know we do fart. And I imagine, when you let go a big one, you feel (possibly with relief) there's some major volume leaving the body. But how MUCH?! The only previous study on the topic had one guy, who passed 1 liter of gas per day. That's indeed quite a bit...but the authors of this study doubted those numbers. They needed more!

So they got five, healthy male (of course, who cares how much women fart, you know? All ladies' farts are is puppies and rainbows anyway) med students, and outfitted them with, well...

Nothing says science like a big rubber tube shoved up your butt and TAPED to the abdomen and back (did they just tape the poor guys package up in there as well? I mean, how do you fit the tape around...never mind). I'm having some issues with envisioning the setup, and unfortunately, it is lost to science, for there was no figure. Anyway, a colon tube. Up your butt, with a big rubber dam up against your rectum. The tube was connected to a thick walled rubber balloon which is also, presumably, somewhere about your person. And then whole contraption is taped up your back and over your taint onto your tummy. And the subjects still went about their daily tasks! With "surprisingly little discomfort". I have to wonder how much discomfort they were expecting.

The men they got for this study were as "normal" as possible. The kind of people who never really think about pooping, never really notice farting, and tend to poop at the same time every day like clockwork. The authors hoped that, by using these men with happy little poos, they'd get normal, "happy" (if they can be happy), fart volumes.

So they hooked up the ass-gas bags (that's the technical term) to the dudes immediately after their daily poop. The guys wore the bags around until evening, when they were switched out for new bags. The day bags and the night bags were then added up, and the results over the five subjects averaged to get a total daily anal venting volume.

And the results?

(Click to embiggen)

What you can see is the measures of how much gas the men passed when they pooped (none, a very little, some) and whether they noticed gassiness (two guys noticed it at night rather than in the day, which makes me wonder if they were waking themselves up with their gassy nocturnal emissions). And in the middle columns you can see the total averages of volume of gas passed.

The verdict? On average, 1/2 liter per day (around 527mL). Passing more than that? You might be a bit above average in the gas department.

Half a liter doesn't seem like too much. But of course, for this, they deliberately picked a bunch of guys who NEVER THOUGHT about their bowels. The kind of dudes who, so help them, poop at 2pm each day and are never more than 20 min off of schedule, and who were never aware when they perfumed the air. While I would hope that most humans are lucky enough to be like this, I have to imagine that those who think about their farts, or wonder about their farts, might not be in this population (and I also wonder what on earth those supermen EAT). And what about the latest obsessions with whole grains and high fiber diets? Are we cursing the planet with more odoriferous methane? And are people who more "aware" of their toots actually producing more gas? Or are they just more aware of it? Are people who suffer from gas as something uncomfortable really suffering excess gas? Or is it just going uncomfortable places?

We need more gas! Which means we need more...butt tubes. For science, you know.

*Today's post comes to you via the FABULOUS Mary Roach and her new book "Gulp, Adventures on the Alimentary Canal". I read it and loved it, and had to raid the reference list. Because, farts, of course!

But who DOES squeak the loudest, and what does that do?

(So cute! Source)

Bowers et al. "Foxp2 Mediates Sex Differences in Ultrasonic Vocalization by Rat Pups and Directs Order of Maternal Retrieval" Journal of Neuroscience, 2013.

FoxP2 is is a gene that has been shown before to be correlated with language and vocal communication, particularly in chimps and humans. But it also plays a role in "language" in other species. Birds, for example, show increases in FoxP2 during the time when they learn to sing. So it's possible that FoxP2 could play an important role in "language" and "song" in more than just humans.

So what about in rats?

The authors of this study wanted to look at the role of FoxP2 in rats, particularly in rat PUPS. When a mother rat leaves her pups, even for a very short period of time, the pups will get upset, and start to make little ultrasonic distress calls, that the human ear can't hear. When the mother rat hears these calls, she will usually return to the nest (if she is able), and retrieve her pups, often placing them in a new nest or keeping them nearby.

But there's something a little odd about this. Not all pups squeak equally. In fact, males squeak more often than females. And this has an important effect, the mom retrieves the males FIRST. This means they get put near the center of the nest, where it's warmer.

So what was causing these boys to be so squeaky? It turns out that the male pups at this stage (about four days old), had higher levels of FoxP2 gene expression in their brains than the females did.

But was the FoxP2 causing the squeak? To find this out, the authors used a small interfering RNA (siRNA) that prevents the expression of a single gene. In this case, the prevented the expression of FoxP2.

When the siRNA was inserted into male and female pups, the squeaking equalized. You can see the control males in the clear bars and the control females in the black bars. The females emitted fewer calls. But when the siRNA was on board (the red and blue bars), the number of calls was equal.

And this completely changed how the rat mom treated her pups.

What you can see above is the rank order in which the rat mom retrieved her pups. On the far left are the males. They are low because they have a high rank order, being retrieved first, second, and so on (the numbers get pretty high because rat litters can get pretty big). The females (second from left) have higher rank orders, and are retrieved last. But when the siRNA is onboard, it almost looks like the trend is reversed, but in fact there is no significant difference between how males and females get retrieved.

So the squeaky wheel, or the squeaky rat, gets the grease, and in this case, the squeaky rat has higher FoxP2. Why does this happen? It could be that, in the long run, it's better to retrieve males than females, as more male offspring gives the mom a higher chance of passing on her genes.

But then they tried to extend their findings to humans. In theory, if humans were like rats (in this respect), this would mean that little boys would (a) "squeak" more (perhaps cry more?), and (b) that little boys would have higher levels of FOXP2 in the brain than little girls.

But in this case, it turns out that humans are not like rats. In fact, in a set of postmortem (sadly) samples from 4 year old boys and girls, FOXP2 was LOWER in the boys than in the girls.

I'm actually not surprised by this, and I think there are several reasons why this might be the case. First, girls have been shown to have increased vocabulary development early in life compared to boys, which would predict increases in language related genes compared to boys. So I'm not sure this developmental time point was the best one, an earlier one might have been better. But even then I don't think they would have seen anything. After all, WHY would being a squeaky wheel matter in humans? After all, humans, unlike rats, don't have LITTERS of pups. Just one or two (or rarely three) at a time. A human baby does not (generally) need to compete against other babies for attention and care, and so I'm not sure why something like this would be selected for.

But while they didn't see differences in humans (and after all, rats and humans don't have to be alike in all things), the differences in rats are interesting on their own. In rats, the squeaky wheel (or pup) gets the grease.

And so I set out looking for the study. Until I realized...there was no study. This is an example of what we like to call "science by press release". However flawed one may feel about the peer-review system in academia*, it's definitely important that SOMEONE be able to see the data and find the potential flaws (or, possibly, back you up in how awesome your science is) that are making the study sag (as it were). The science we are about to talk about? Has not been published yet. It is preliminary. The lead author has in fact been bemused by all the media attention (dude, you study boobs, you didn't think we'd just walk BY, did you?), and has stated that he's withholding final judgement until the paper is out.

Rouillon told Reuters that his unpublished work is still in the early stages and he is hesitant about giving one-size-fits-all advice to women, despite the media circus.

But it is not required that science pass peer review before its reported on (heck, there would be no scientific reporting at science conferences if that was the case). So while the science reported may well be...full-figured enough to pass muster, until they DO report it, it's good to keep in mind that it's preliminary.  This means that we only have bits and pieces of the data, and so drawing any conclusions is going to be premature. It's a good idea to keep in mind, honestly, that all science will probably be replaced by better science over time, but stuff that isn't out yet (and on which we have no real details), deserves extra fish-eye.

So. Eyes up here, friends.

(Source)

Boobs. Made of mostly glands and fatty tissue, there's really...not a lot of structure in there.

(You see what I mean. Source)

There are a couple of areas of fibrous tissue (Coopers ligaments), but those, the pectoral muscles, and the tightness of the skin around it, are basically the only things holding the breast pert.

When you're young, obviously, this isn't an issue. But as you get older (or as your breasts get larger), the ligaments will become stretched, and will lose some of their elasticity. This means the breasts become less able to defy gravity, and you therefore get droopage.

Droopage (that's the technical term) is not in itself a problem. Sag happens, and your breasts are not any less functional than they were before. The only issue with this is that of aesthetics. We don't think sag looks good. This could be because we all want to look young and breast perk = young, and this view is certainly exacerbated by our current culture full of push up bras and breast lifts. But no matter why we feel the way we do, boob sag is a sad sag (in our culture, anyway), and women spend a lot of time worrying about it.

Enter the bra. Bras (or ideas preceeding them) date back all the way to ancient Greece, but the purpose is usually support. Not necessarily because of aesthetics, but because having sacks of fat and glands on the front of your chest...can get wearisome. Especially if they are large and heavy. And so over time, bras (preceeded by basic flattening structures and garments like the corset) have developed to do things like support the breasts, relieve back pain (though there isn't a lot of evidence as to whether or not this works), and of course, give you the look of a woman in a lingerie catalog (if so desired). After all, even if bras don't prevent the breasts from sagging, when the bra is on...would you know?

But the question is: is it BETTER to wear a bra? To this end, Jean-Denis Rouillon (and someone who I believe is associated with him, Laetitia Pierrot) has been looking at a lot of boobs. For science. Like you do.

I'm not sure whether the original investigation was all about boob sag or back pain and bra wearing (various media coverage includes both, but again, there's no paper, so I can't be sure), but the preliminary data so far has followed 320 women, ages 18-35, some of whom went braless for a year. During this time, they had their breasts measured with calipers, and Rouillon's preliminary reports report an average INCREASE in perk by 7mm in the braless women.

7mm. That's around 1/4 inch. So not much. Of course, this is average, and we don't know what the variability looks like (again, no paper). With a change in perk that small...I honestly wonder if it's even going to be significant, even if you do have 320 women in the study. But this (and the testimony of the one woman they found to give testimony about how great being braless was) was plenty to make people wonder if boobs are best when bouncing, if bras are generally bad, and other things beginning with B.

And who knows? It could be true. We could end up with perkier puppies if we go braless. But until I see the paper, allowing me to see the extent of the changes (and possible reasons as to why they take place), I'm not burning my bras yet.

And it's possible that it'd be too late for many of us anyway. You'll notice that the study was conducted in young women. The author himself notes that after a couple of kids and in your 40s? Probably not going to do any good.

It's also a question of whether or not bra wearing is actually HARMFUL. Wearing a bra that is ill-fitting or induced WAY too much lift can indeed be harmful, but is a good fitting bra on its own a bad thing? Does it really matter if there's more sag?

It makes me wonder though, what part of not wearing the bra helped? Is there increased pectoral musculature and increased elasticity of the Copper's ligaments, as the researchers have hypothesized? The idea is that the ligaments will be strengthened with natural bouncing. More bouncing, more spring, and so the ligaments stay strong. In contrast, in the presence of a bra, the ligaments have no work to do, and if you don't use it, you lose it, and the ligaments and pectoral muscles could become weak, resulting in funbag sag.

If that's the case, then you might expect women who have stronger pectoral muscles (such as, say, women who weight lift or do other athletics) would have less sag for their age than the average, and the pectoral strength might make up for the ligament weakness. I would be interested to see those women compared, and then comparing atheletic vs non-athletic women in the absence of a bra, or perhaps to compare women who specifically work their pectorals (perhaps with a training program), vs women who don't.

I would also like to note: there are a lot of things about this study that we DON'T KNOW. We know how old the women are, and how many of them there were. We do not know some rather important things, though. We don't know their average cup size! Which can have a pretty big effect on how much your sweater puppies suffer from gravity. I assume they split women evenly in the groups so that all cup sizes were evenly represented...but again, we don't have the data and we don't know. We don't know whether these women were athletic, and therefore how strong the underlying musculature might have been.

We don't know how variable the increase was. I've seen the quote "1/4-inch (7-millimeter)" in terms of RISING. But what is this compared to. Their baseline nipple height? The average nipple sinking of the bra-wearing peers?

We also don't know why the nipples on the braless women ROSE (if indeed they rose, or if they just didn't sink). There might be increase ligament strength, but there also might be other factors. Breasts, for example, change shape pretty drastically in response to life changes, like having children. And over the 15 year period in this study, I'll bet a LOT of these women will be having (or already have had) children. Were the braless and...braful (?) groups any different in this regard? Will something like childbirth and the accompanying changes as this group goes along completely eclipse that 1/4 inch of perk?

So while it's an interesting question, I'm withholding final judgement until I see the paper. And if it makes no difference in terms of harm, it may well be that going braless for perk will remain a personal choice. In the meantime, I look forward to seeing the study, on what will no doubt remain a titular topic. You see what I did there.

*For those outside of academia, the vast majority of scientific journals require peer review prior to publication. This means, when you send the paper to a journal, the journal picks some other scientists (usually around three), that are in or closely related to the field. The peer reviewers then take that manuscript and run it over with a fine-toothed comb, finding everything from major scientific issues (say, the interpretation of the results doesn't match what you actually found, or maybe you did the wrong statistical test, or that you're lacking some major experiment to prove your point), to problems with your use of that/which distinction. They then hand the paper back to the journal editor with their comments, and the suggestion of whether to accept, reject, or make you change big parts of the paper. It's not a perfect system, but it's the best we have for making sure that the science getting out there is, well, scientific. And I can say that my papers have always been improved by peer review (thus far).

- The Great Gastby, F. Scott Fitzgerald

Sci is at SciAm Blogs today, talking about voices. What makes a voice attractive to a man or a woman? What makes it one of those voices that you will never forget, that attract you so much? Head over and check it out!