Known Unknowns

Why no one can say exactly how much is safe to drink while pregnant


I was waiting in the dining car of an Amtrak train recently when I looked up and saw that old familiar sign:


One finds this warning everywhere: printed on bottles and menus or posted on placards at restaurants and even train cars barreling through Midwestern farmland in the middle of the night. The warnings are, of course, intended to reduce the number of cases of fetal alcohol syndrome in the United States. To that end, the Centers for Disease Control and Prevention (CDC) and the American Congress of Obstetricians and Gynecologists (ACOG) recommend that women avoid drinking any alcohol throughout their pregnancies.

Here’s how the CDC puts it:

“There is no known safe amount of alcohol to drink while pregnant.”

And here’s ACOG’s statement in 2008:

“. . . ACOG reiterates its long-standing position that no amount of alcohol consumption can be considered safe during pregnancy.”

Did you notice what they did there? These statements don’t actually say that no amount of alcohol is safe during pregnancy. They say that no safe amount is known and that no amount can be considered safe, respectively. Ultimately, these are statements of uncertainty. We don’t know how much is safe to drink, so it’s best if you don’t drink any at all.

Lest you think this is a merely a reflection of America’s puritanical roots, check out the recommendations of the U.K.’s National Health Service. While they make allowances for the fact that some women choose to drink, they still advise pregnant women to avoid alcohol altogether. As they say:

“If women want to avoid all possible alcohol-related risks, they should not drink alcohol during pregnancy because the evidence on this is limited.”

Yet it seems odd that the evidence is so limited. The damaging effects of binge drinking on fetal development were known in the 18th century and the first modern description of fetal alcohol syndrome was published in a French medical journal nearly 50 years ago. Six years later, in 1973, a group of researchers at the University of Washington documented the syndrome in The Lancet. Even then, people knew the cause of fetal alcohol syndrome: alcohol. And in the forty years since, fetal alcohol syndrome has become a well-known and well-studied illness. NIH alone devotes more than $30 million dollars annually to research in the field. So how come no one has answered the most pressing question (at least for pregnant women): How much is safe to drink?

One reason is that fetal alcohol syndrome isn’t like HIV. You can’t diagnose it with a blood test. Doctors rely on a characteristic pattern of facial abnormalities, growth delays and neural or mental problems – often in addition to evidence of prenatal alcohol exposure – to diagnose a child. Yet children exposed to and affected by alcohol during fetal development don’t always show all of these symptoms. Doctors and agencies now define fetal alcohol syndrome as the extreme end of a spectrum of disorders caused by prenatal alcohol exposure. The full spectrum, called fetal alcohol spectrum disorders (FASD), includes milder forms of the illness that involve subtler cognitive or behavioral problems and lack the classic facial features of the full-blown syndrome.

As you might imagine, milder cases of FASD are hard to identify. Pediatricians can miss the signs altogether. And there’s a fundamental difficulty in diagnosing the mildest cases of FASD. To put it crudely, if your child is slow, who’s to say whether the culprit is a little wine during pregnancy, genetics, too much television, too few vegetables, or god-knows-what-else? Unfortunately, identifying and understanding the mildest cases is crucial. These are the cases that worry pregnant women who drink lightly. They lie at the heart of the uncertainty voiced by the CDC, ACOG, and others. Most pregnant women would like to enjoy the occasional merlot or Sam Adams, but not if they thought it would rob their children of IQ points or otherwise limit their abilities – even just a little – down the line.

While it’s hard to pin down the subtlest cases in the clinic, scientists can still detect them by looking for differences between groups of children with different exposures. The most obvious way of testing this would be to randomly assign pregnant women to drink alcohol at different doses, but of course that experiment would be unethical and should never be done. Instead, researchers capitalize on the variability in how much women choose to drink during pregnancy (or at least how much they report that they drank, which may not always be the same thing.) In addition to interviewing moms about their drinking habits, the scientists test their children at different ages and look for correlations between prenatal alcohol exposure and test performance.

While essential, these studies can be messy and hard to interpret. When researchers do find correlations between moderate prenatal alcohol exposure and poor test performance, they can’t definitively claim that the former caused the latter (although it’s suggestive). A mysterious third variable (say, maternal cocaine use) might be responsible for them both. On the flip side, interpreting studies that don’t find correlations is even trickier.  It’s hard to show that one thing doesn’t affect another, particularly when you are interested in very small effects. To establish this with any confidence, scientists must show that it holds with large numbers of people and that they are using the right outcome measure (e.g., IQ score). FASD impairments can span language, movement, math skills, goal-directed behaviors, and social interactions. Any number of measures from wildly different tests might be relevant. If a given study doesn’t find a correlation between prenatal alcohol exposure and outcome measure, it might be because the study didn’t test enough children or didn’t choose the right test to pick up the subtle differences between groups.

When studies in humans get tricky, scientists often turn to animal models. FASD research has been no exception. These animal studies have helped us understand the physiological and biochemical mechanisms behind fetal alcohol syndrome, but they can’t tell us how much alcohol a pregnant woman can safely drink. Alcohol metabolism rates vary quite a bit between species. The sensitivity of developing neurons to alcohol may differ too. One study used computational modeling to predict that the blood alcohol level of a pregnant rat must be 10 times that of a pregnant human to wreak the same neural havoc on the fetus. Yet computational models are far from foolproof. Scientists simply don’t know precisely how a dose in a rat, monkey, or other animal would translate to a human mother and fetus.

And here’s the clincher: alcohol’s prenatal effects also differ between humans. Thanks to genetic differences, people metabolize alcohol at very different rates. The faster a pregnant woman clears alcohol from her system, the lower the exposure to her fetus. Other factors make a difference, too. Prenatal alcohol exposure seems to take a heavier toll on the fetuses of older mothers. The same goes for poor mothers, probably because of confounding factors like nutrition and stress. Taken together, these differences mean that if two pregnant women drink the same amount of alcohol at the same time, their fetuses might experience very different alcohol exposures and have very different outcomes. In short, there is no single limit to how much a pregnant woman can safely drink because every woman and every pregnancy is different.

As organizations like the CDC point out, the surest way to prevent FASD is to avoid alcohol entirely while pregnant. Ultimately, every expecting mother has to make her own decision about drinking based on her own understanding of the risk. She may hear strong opinions from friends, family, the blogosphere and conventional media. Lots of people will seem sure of many things and those are precisely the people that she should ignore.

When making any important decision, it’s best to know as much as you can – even when that means knowing how much remains unknown.


Photo Credit: Uncalno Tekno on Flickr, used via Creative Commons license

Hurley TD, & Edenberg HJ (2012). Genes encoding enzymes involved in ethanol metabolism. Alcohol research : current reviews, 34 (3), 339-44 PMID: 23134050

Stoler JM, & Holmes LB (1999). Under-recognition of prenatal alcohol effects in infants of known alcohol abusing women. The Journal of Pediatrics, 135 (4), 430-6 PMID: 10518076

Plastic and the Developing Brain


When I was pregnant with my daughter, I had enough on my mind. I didn’t have much time to think much about plastic. I knew vaguely that plastics can release estrogen-mimicking substances like bisphenol A (BPA) into our food and I’d heard that they might cause genital defects in male fetuses. But once my husband and I had the 20-week ultrasound and knew we were having a girl, I thought I could stop searching for products in cardboard or glass. It was just too hard. Everything is packaged in plastic these days.

Apparently I jumped the gun.

Scientific papers warning about the hazards of prenatal exposure to BPA have been coming out in a steady stream, with a string of particularly damning ones appearing over the last 18 months in the Proceedings of the National Academy of Sciences. Last month one in particular caught my eye: a study of how prenatal BPA exposure changes the brain. The results were enough to make this neuroscientist pause.

While we tend to think of estrogens as the sex hormones that manage ovulation and pregnancy, these molecules also have powerful and direct effects on the brain. Many types of neurons have estrogen receptors on their outer surface. While there are several kinds of estrogen receptors in the brain, all bind to estrogens (and other molecules that resemble estrogens) and all trigger changes within their neurons as a result. These small changes can potentially add up to alter how entire neural circuits function. In fact, estrogens influence a wide range of skills and behaviors – from cognitive function to mood regulation and even fine motor control. While we don’t yet know why estrogens have such a broad and powerful influence on the brain, it does appear that we should think twice before mucking around with estrogen levels, particularly in the developing brain.

BPA and other compounds found in plastics resemble estrogens. The similarity is close enough to fool estrogen receptors, which bind to these foreign molecules and interpret them as additional estrogen. Although BPA has been used commercially as a dental sealant and liner for food containers (among many other uses) since the 1960s, the health consequences of this case of mistaken identity are just beginning to be understood.

In the PNAS paper published last month, a group of scientists headed by Dr. Frances Champagne at Columbia report the effect of prenatal BPA exposure on mice. They fed pregnant laboratory mice one of three daily doses of BPA (2, 20, or 200 μg/kg) or a control product without BPA. These are not high doses of BPA. Based on the amount of BPA found in humans, scientists estimate that we are exposed to about 400 μg/kg per day. The U.S. Food and Drug Administration reached their own estimate by testing the amount of BPA in various foods and then approximating how much of these people consume daily. Their calculations put the figure at around 0.19 μg/kg daily for adults. This discrepancy (400 versus 0.19) is one of many points of contention between the FDA, the packaging industry, and the scientific community on the subject of BPA.

Champagne and her colleagues fed their mice BPA on each of the twenty days of mouse gestation. (That’s right, ladies: mouse pregnancies last less than three weeks.) After each mouse pup was born, the scientists either studied its behavior or sacrificed it and examined its brain.

What did they find? Prenatal BPA exposure had a noticeable impact on mouse brains, even at the lowest dose. They found BPA-induced changes in the number of new estrogen receptors being made in all three brain areas they examined: the prefrontal cortex, hypothalamus, and hippocampus. These effects were complex and differed depending on the gender of the animal, the brain area, the BPA dose, and the type of estrogen receptor. Still, in several cases the researchers found a surprising pattern. Without BPA-exposure, female mice typically made more new estrogen receptors than their male counterparts. The same was true for mice given the highest BPA dose. But among pups exposed to the two lowest BPA doses, male mice made more estrogen receptors than females! This sex-difference reversal stemmed from changes in both genders; male mice made more estrogen receptors than normal at these doses while female mice made fewer than their norm.

Champagne and colleagues also observed and recorded several behaviors of the mice in different circumstances. For most behaviors, males and females were naturally different from one another.  Just as human boys tend to chase each other more than girls do, male mouse pups chased more than females. Unexposed male mice sniffed a new mouse more than unexposed females did. They showed more anxiety-like behavior in an open space and were less active in their home cages. Prenatal BPA treatment reversed these natural sex differences. Exposed female mice did more sniffing, acted more anxious, and ran around less than their exposed male counterparts. And at the highest prenatal BPA dose, the male mice chased each other as rarely as the females did. In one case, BPA treatment affected the two genders similarly; both sexes were less aggressive than normal at the two lower doses and more aggressive than normal at the highest dose.

Overall, the results of the study are complex and it might be easy to ignore them because they don’t seem to tell a straightforward tale. Yet their findings can be summed up in a single sentence: BPA exposure in utero has diverse effects on the mouse brain and later behavior. Not only does the BPA ingested by the mom manage to affect the growing fetus, but those effects persist beyond the womb and past the end of the exposure to BPA.

Some will dismiss these results because they come from mice. After all, how much do we really resemble mice? Yet studies in monkeys have also found that BPA affects fetal development. And while mice and monkeys excrete BPA differently, they clear it at a similar rate — to each other and to human women. Results from correlational studies in humans also suggest that BPA exposure during development affects mood, anxiety and aggressiveness to varying degrees (depending on the child’s gender).

Still, there’s a lot we don’t know about the relevance of this study for humans. At the end of the day, mice aren’t humans and no one has agreed on how much BPA pregnant women ingest. Moreover, Champagne and colleagues examined only a small subset of the neural markers and behaviors that BPA might affect in mice. Perhaps the changes they describe are the worst of BPA’s effects, or perhaps they are only the tip of the iceberg. We don’t yet know.

What’s the upshot of all this? You may want to err on the side of caution, particularly if you’re pregnant. Avoid plastics when possible. Be aware of other sources of BPA like canned foods (which have plastic liners) and thermal receipts. Do what you can do and then try not to let it stress you out. If you’re pregnant, you already have enough on your mind.

As for my daughter, she seems to be fine despite her plasticized third trimester. While she doesn’t do much sniffing, she does occasionally slap my husband or me in the face. It could be the BPA making her aggressive. I choose to blame it on her sassy genes instead.


Photo credit: .imelda on Flickr

Kundakovic M, Gudsnuk K, Franks B, Madrid J, Miller RL, Perera FP, & Champagne FA (2013). Sex-specific epigenetic disruption and behavioral changes following low-dose in utero bisphenol A exposure. Proceedings of the National Academy of Sciences of the United States of America, 110 (24), 9956-61 PMID: 23716699

Flipping the Baby Switch

img_2348-1Rewind to last night. It was bedtime. My infant daughter was screaming and struggling in my lap while I tried to rock her to sleep. She pulled and twisted the skin on my face. She sunk her tiny teeth into my shoulder and chest. Exasperated, I rose from the rocker and started pacing around the nursery. Her tense little body instantly relaxed. Within ten seconds she was quiet and still. Within two minutes she was asleep.

The scene was not unusual for our household. Even as a newborn, my daughter was easy to upset and hard to soothe. When nothing else worked and I was about to lose my mind I’d get up and walk with her. Often the results were nothing short of miraculous. Imagine going from 100 miles per hour to zero in a snap. For those who recall the child android Vicki on the ‘80s TV show Small Wonder, think of the times someone flipped the off-switch on her back. That’s what it’s like when I walk with my daughter. Our aimless walking flips a switch somewhere inside of her. But how does the switch work? And why does she have one in the first place? A study published in Current Biology last month helps to explain this curious facet of infant behavior.

The head scientist behind the study was Dr. Kumi Kuroda at the RIKEN Brain Science Institute in Japan. As she described in an interview with ScienceNOW, she became interested in the topic when she noticed that she could calm her own newborn son by carrying him. She later tested 12 other newborns with their mothers and found that they behaved like her son. Overall, the effect was rapid and dramatic. Some babies stopped crying as soon as their mothers began to walk with them. The rest cried less and were less shrill when they did cry. The babies also moved less and had lower heart rates while they were being carried.

To study the biological mechanisms behind this remarkable calming response, Dr. Kuroda and her colleagues turned to mice. They showed that mouse pups have a similar response when carried by their mothers. Mouse moms carry their pups by the scruff of their necks. When carried, mouse pups less than 20 days old stop wriggling. Their heart rate slows and they stop crying out. (Like most mouse vocalizations, baby mouse cries are ultrasonic). They also draw their legs in when carried, making their bodies more compact for toting around.

Kuroda and colleagues investigated several physiological aspects of the calming response in mice. Only a few of these experiments are probably relevant for infants, since human babies don’t assume a compact position like carried mouse pups do. One looked for the triggers that make carried pups stop squirming. The scientists anesthetized the neck skin of baby mice and found that these animals wriggled more than untreated mouse pups when carried. They got the same result when they overdosed pups with vitamin B6 before testing. (Vitamin B6 overdose causes animals and humans to lose the sense of their body position and movement.) The upshot? For a mouse pup to stop wriggling when carried it must 1) sense that it’s being lifted and 2) sense that something is pulling on its neck skin. Take either sense away and the calming response disappears. My daughter may draw on similar senses to trigger her miraculous stillness while carried. (Only if you replace neck pulling with the pressure of my arms around her, of course. I don’t carry her by her neck skin, I swear.)

The scientists also wondered why a baby’s heart rate drops when it’s picked up and carried. To test this in mice, they gave pups a drug that turns down the parasympathetic nervous system (the set of nerves that return the body to a calm state after arousal). Pups treated with the drug still stopped wriggling when lifted, but their heart rates didn’t drop as they do in untreated pups. So while the parasympathetic nervous system slows down the carried pup’s (and possibly infant’s) heartbeat, it can’t take credit for other features of the calming response.

Clearly this calming response is more complicated than it seems. Many of my daughter’s brain areas, neural pathways, and sensory mechanisms were working in concert to soothe her last night as I walked her in circles. But why does she have this complex reaction to carrying in the first place? Grateful parents might imagine that the calming response evolved to keep us from going crazy, but unless going crazy involves committing infanticide, this explanation doesn’t hold water. Evolution doesn’t care whether parents are happy or well rested or have time to watch Game of Thrones. It only cares whether our offspring survive.

Dr. Kuroda and her colleagues propose that the calming response helped parents escape dangerous situations while protecting their young. According to this logic, calmer carried babies meant faster escapes and higher rates of survival. Certainly if you were running from a wild beast or a member of a rival village, holding a struggling infant might slow you down. Of course holding any infant would slow you down and it’s not clear that sprinting with a struggling newborn is much harder than lugging one that’s asleep.  The paper’s authors present little evidence to support their proposal, particularly in the context of human evolution. They point to a minor result with their mice that doesn’t easily translate to human behavior. In effect, the jury’s still out.

There are other possible explanations for the calming response, ones that don’t involve predators outrunning parents. Shushing can calm crying babies too, probably because it simulates an aspect of their environment in the womb (in this case,  physiological noise). The same could be true of walking with infants. The mothers in the Kuroda study held their babies against their chest and abdomen, which is also how I hold my daughter when I walk to soothe her. The type of movement she feels in that position is probably similar to the rocking and jostling she felt as a fetus in utero whenever I walked. If so, the calming response might be a result of early learning and comfort by association – a nice thought when you consider the gory alternative.

Each year at the end of May we find ourselves as far as possible from Thanksgiving Day. It can be something of a thankfulness drought. This May I am thankful for women in science and maternity leaves, computer-generated dragons and ’80s sitcom androids. And like Vicki’s parents, I am profoundly thankful that my daughter came furnished with an off-switch. Whatever the reason why.


Photo credit: Sabin Dang

Esposito G, Yoshida S, Ohnishi R, Tsuneoka Y, Rostagno Mdel C, Yokota S, Okabe S, Kamiya K, Hoshino M, Shimizu M, Venuti P, Kikusui T, Kato T, & Kuroda KO (2013). Infant Calming Responses during Maternal Carrying in Humans and Mice. Current biology : CB, 23 (9), 739-45 PMID: 23602481

At the Gates of Sleep

497736998_45c09a136e_oNow that my daughter is about to reach her first birthday, I’m in the mood to reflect on the year that just passed. Unfortunately, my recollections of it are a little fuzzy, probably because I can count on one hand the number of times I’ve enjoyed a good night’s sleep over the past year. Some people have babies who regularly sleep through the night and I am happy for them. Truly, I am. But clearly I was not meant to be in their ranks.

Still, the never-ending parade of nighttime awakenings has taught me something about my own brain. It is precisely tuned to hear my baby. Although I sleep blithely through my husband’s thunderous snoring and the loud buzz of his alarm clock – multiple times a day, thanks to the snooze button – I awaken at the faintest sound of my daughter’s sighs, coos, or grumbles. When she cries, I am immediately awake while my husband sleeps on beside me, undisturbed.

People are generally able to sleep through minor sounds and sensations thanks to a subcortical structure in the brain called the thalamus. This structure receives incoming signals from our senses and relays them to cortical areas devoted to processing sensory information like sounds or tactile sensations. When we’re awake, the thalamus faithfully relays nearly every sensory signal on to the cortex. But when we’re asleep, neurons in the thalamus participate in strong, synchronized waves of activity that squelch incoming signals. As a result, about 70% of these signals never make it to the cortex. This process, known as sensory-gating, is how we manage to sleep through the roar of rainstorms or the brush of the sheets against our skin each time we turn in bed. It is also how we sleep through our husband’s room-rattling snores.

Yet some sensory information does get through to the rest of the brain during sleep. These signals do get processed and can even wake us up if they are either intense (like a loud noise) or personally relevant. A clever study illustrated the importance of personal relevance by exposing sleeping subjects to a loud presentation (via tape recorder) of their own name spoken aloud. The scientists played the recording either normally or backwards and found that subjects awoke in less than half the time when they heard their names presented in the recognizable form.

So did my daughter, in effect, sleep train me by training my brain to recognize her sounds as personally relevant? It’s a plausible explanation, but one that is ultimately lacking. It cannot explain that first night when I slept beside my baby at the hospital nearly one year ago. Although I had labored through the entire night before and had not slept in the ensuing day, I awoke constantly to every little sound my mewing newborn made, not to mention the cries that told me she wanted to nurse. She’d had no time to train me; I had come pre-trained. Just as my breasts were primed to make milk for her, my brain was primed to wake for her. We seemed to be engineered for one other, mother and child, body and brain. And we spent that first long night discovering how clever a designer Nature can be, while my husband slept peacefully on the couch.


Photo credit: planetchopstick

Tooling Around

tools1There was a time when my daughter used her hands exclusively to shovel things into her mouth. Not so anymore. For the last few months, she has been hard at work banging objects together. This simple action is setting the stage for some pretty cool neural development. She is learning to use tools.

Of course it doesn’t look too impressive right now. She might bang a ball with a block and then switch and strike the block with the ball. In one recent playtime she tore a cardboard flap out of her board book and examined it, trying different grips and holding it from different angles as she watched how it cut the air. Then, brandishing her precious flap, she went to work. She wielded it with a scooping motion to lift other flaps in the book, and later, to turn the book pages themselves. After that, she descended on her toy box with the flap. She used it to wipe her blanket, poke her stuffed animal, and finally scrape its face like she was giving it a close shave.

Although my daughter’s fun with flaps may seem aimless, it had an important purpose. Through experimentation and observation, she was learning how two objects can interact and how such interactions are affected by object shape, configuration, and pliability. Such details are so well known to adults that we forget there was anything to learn. But consider how often we use objects against one another. We hammer nails, rake leaves, and staple pages. When using scissors, we must apply different levels of force to cut through paper versus cardboard or fabric. When lifting a pan with a potholder, we must adjust our grip depending on the weight of the pan and whether we are lifting it by the base, side, or handle. We must know the subtle differences between holding a sponge to wash a glass and using a towel to dry it, and we must do each deftly enough that our glassware comes out clean and intact at the end.

There are also countless tools we create on the fly every day. When you use a magazine to nudge your cell phone within reach or flip a light switch with a book because your hands are full, you are devising novel tools to fit your momentary needs. To do this, our brains must store extensive knowledge about the properties of household objects. Through experimentation, like the kind my daughter is doing, we learned to predict how objects will interact and to capitalize on those predictions.

So far I’ve described the value of tools in terms of what they can do: push, pull, gather, polish, lift, etc. But there is another side to tool use that may play a role in my daughter’s little experiments: sensory information gleaned through the tool. As I watched her probe one object with another, I was reminded of research described in Sandra and Matthew Blakeslee’s book The Body Has a Mind of Its Own. The book discussed neurons in the parietal cortex that are tuned to the sight or feel of objects near a particular body part. For example, cells representing your right hand would fire if something touched your right hand, if you saw an object near your right hand, or both. Neuroscientists have discovered that experience using a tool can change the properties of these cells in monkeys (and therefore likely in us as well). They found that if monkeys used a rake to gather goodies otherwise beyond their reach, the parietal neurons that had responded to objects around the hand now fired for items located anywhere along both the hand and the rake it held. In a sense, object manipulation can temporarily extend certain neural body representations to include the tools we wield. The Blakeslees suggest that this may be how a blind person learns to perceive the contour of items encountered at the tip of his cane. In effect, the cane and the hand are one.

For now, our house is filled with smashing, scraping, banging and bending as our baby descends on toys and her parents’ belongings alike. In the midst of such havoc, it’s good to know that the destruction is part of a crucial learning process. And someday, once it slows down, I can buy her a new board book with all the flaps intact.


Photo credit: zzpza

It’s a Zoo Out There!


Our house is filled with animals. We’ve got animal rattles, animal teethers, stuffed animals and all manner of animal-patterned clothing, towels, and bedding. Then of course there are the board books; those that don’t name animals and list their moos and oinks star bipedal animals that brush their teeth, wear pajamas, and often suffer crushing insecurities. And we’re not talking about your standard cat, dog or hamster. They are usually elephants. Giraffes. Hippopotami. Animals you don’t see cruising down the street on an ordinary day. They are animals you’d probably never see in person if not for your local zoo.

The exotic menagerie that has descended on our house has got me wondering: why do we surround our children with animals that will have no discernible role in their future lives? Why aren’t there more infant toys based on tax returns or grocery lists? Where are the books with titles like The Grumpy Morning Commute or Fruit Salad Makes a Friend? I imagine the reason we supply young children with all-things-animal is because that’s what they like. That’s what fascinates them. And who can blame them? From the elephant’s trunk to the lightning bug’s glow, the odd, diverse traits of other species are just about the neatest show on this planet of ours. It’s a fact we lose sight of as we get older. Giraffes are old news to us now. They’ve got super long necks. So what? Big deal.

This past week, however, I noticed my husband checking his iPhone with unusual glee. Had I heard? The new Mars rover landed without a hitch. Against all odds! And now it’s looking for signs of past or present life on Mars. How cool is that? As a scientist, I have to admit it’s pretty cool. But I can’t get as excited as my husband. It seems odd that we are investing so much to seek out microscopic life on another planet while there are still species here on Earth we have yet to discover. And while our own actions drive other species to extinction.

Clearly, we’ve forgotten how beautiful and strange and remarkable animals are. Perhaps we should re-brand them for adults. Maybe market them as aliens. If we found a cell on Mars (not to mention a roach or a mouse) we would go wild with excitement. Just imagine if the Curiosity rover found something as elegant as a jellyfish, as colorful as a peacock, or as chatty as a wise old humpback. Imagine how cool that would be.

I will have a chance to try this idea out sometime soon, as my new house in Michigan is near a big zoo. My husband and I have been meaning to go there ever since our move, not to see the animals ourselves but to witness our daughter’s reaction to them. Now I have a second reason to go. When we’re there, I’ll try to view the creatures as they might look to my daughter, who will be seeing them for the very first time. I’ll try to think of them as new and fantastic aliens that just so happen to live here on earth.


Photo credit: Doug Kukurudza

Say What?!

Although I grew up outside of Chicago, I’ve spent the last decade split between the East and West Coasts. Now, after 5 years in Los Angeles, my husband and I are settling into life as Michiganders. Aside from the longer days and lower cost of living, the biggest differences I’ve noticed are linguistic. People speak differently here, and for me it’s like coming home. After a decade away, I am back in a state where people drink pop instead of soda. And, at long last, I’ve returned to the land of the Northern City Vowel Shift.

Speech is constantly in flux, whether or not we are aware of it. Regional dialects diverge, giving us the drawls of the South and the dropped r’s of the Northeast. More recently, cities in a large swath of the northern Midwest are reinventing their vowels, especially the short vowels in ben, bin, and ban. From Syracuse to Minneapolis, Green Bay to Cleveland, these vowels have been changing among Caucasian native English speakers. The vowels are now pronounced with a different positioning of the tongue, in some cases dramatically altering the sound of the vowel. A wonderful NPR interview on the subject is available online in audio form and includes examples of these vowel changes.

I must have picked up the Northern City vowels growing up near Chicago. When I arrived in Boston for graduate school, friends poked fun at my subtle accent. They loved to hear me talk about my can-tact lenses. And I can’t blame them for teasing me. The dialect can sound pretty absurd, especially when pushed to the extreme. It was probably best parodied by George Wendt and the SNL cast in the long-running Super Fans sketch.

I have long been in love with the field of phonetics and phonology, or how we produce and perceive speech sounds. Creating and understanding speech are two truly impressive (and often underappreciated) feats. Each time we speak, we must move our tongues, lips, teeth and vocal folds in precise and dynamic ways to produce complex acoustical resonances. And whenever we listen, we must deconstruct the multifaceted spectral signatures of speech sounds to translate them into what we perceive as simple vowels, consonants, syllables. We do all of that without a single conscious thought – leaving our minds free to focus on the informational content of our conversations, be they about astrophysics or Tom and Katie’s breakup.

Experiences in the first couple years of life are critical for our phonetic and phonological development. Details of the local dialect are incorporated into our speech patterns early in life and can be hard to change later on. As a result, everyone’s speech is littered with telltale signs of their regional origins. My mother and aunt spent their early years in a region of Kansas where the vowels in pen and pin were pronounced the same. To this day, they neither say nor hear them as different. Imagine the trouble my mother had when she worked with both a Jenny and Ginny. I’ve noticed major differences between my husband’s dialect and my own as well. My husband, a native Angeleno, pronounces the word dew as dyoo, while I pronounce it as doo because in Chicago the vowels yoo and oo have merged.

These days I’m watching phonetic development from a front-row seat. My baby has been babbling for a while and I’ve watched as she practiced using her new little vocal tract. She would vocalize as she moved her tongue all around her open mouth and presumably learned how the sound changed with it. From shrieks to gasps to blowing raspberries, she tested the range of noises her vocal tract could create.  And as she hones in on the spoken sounds she hears, her babbling has become remarkably speech-like. The consonants and vowels are mixed up in haphazard combinations, but they are English consonants and vowels all right. Through months of experimentation, mimicry, and practice, she has learned where to put her tongue, how far to open her mouth, and how to shape her lips to create the sounds that are the building blocks of our language. And just as she was figuring it out, we went and moved her smack into a different dialect. She will have to muddle through and learn to speak all the same. And once that happens, it will be interesting to see where her sweet little vowels end up.

%d bloggers like this: