Be the Sucker Who Waits to Cross


You’ve seen him before: the poor soul who doesn’t cross the street on a Don’t Walk signal, even when there isn’t a car in sight. Even while other pedestrians are streaming past him, crossing the street and continuing along their merry way. Bottom line: you should try to become that guy.

Think of it as a late New Years resolution. Most resolutions are lofty and hard to carry out. Chances are good that if you made a resolution for 2017, you have already broken it. But waiting for the Walk signal is a resolution that you can keep for life. It would be an easy win, and one with a small but increasing likelihood of saving your life – or someone else’s.

First, a few facts. Pedestrian fatalities and injuries in the U.S. are on the rise. A pedestrian was injured from a traffic accident every eight minutes, on average, in the United States in 2014. One died every two hours. The vast majority of these deaths, more than 70 percent, take place in urban areas. Over half of those who die in traffic accidents in New York City aren’t in a car – they are on foot.

Few among us would advocate jaywalking. Waiting for the signal to cross is great in principle, but in reality we have compelling reasons to disobey that lighted hand. The most obvious is that we are in a hurry. There are a million tasks waiting for us at work, with a million more waiting for us when we get back home.

Unfortunately, our long to-do lists are precisely the problem. In modern life, distraction is the norm – even without handheld distractions. The human mind is simply prone to wander. A study suggests that we may spend as much as half of our waking hours thinking about something other than what we are actually doing. In other words, those million tasks aren’t just waiting for us at work; they travel with us (and distract us) wherever we go. If you’re like me, you get from place to place on autopilot. That’s fine if you’re a plane, but less than ideal if you’re a pedestrian.

Distraction isn’t our only enemy. Our social nature is also to blame. We are descended from a long line of creatures who follow each other automatically. Think of our living relatives in the animal world: herds of wildebeest, swarms of ants, schools of fish, or flying bird formations. Like them, we use cues from the creatures around us to determine how and where we move. In the case of crossing a street, when one pedestrian begins to cross the street, others tend to follow – often without noticing the traffic circumstances until they are standing in the street.

I have been the trailing wildebeest, blindly following the herd, more than once in my life. Nothing rivals the sunny day when a friend and I were riding home from high school on our bicycles and stopped behind a classmate on the sidewalk. We chatted while waiting for the Walk signal and, when our classmate rode out into the intersection, we instinctively followed him. Perhaps on some level we assumed that he was crossing with the light, but he was not someone we would consciously have trusted with our lunches, much less our lives. All the same, my friend and I looked up to find a car barreling towards us. When the car screeched to a stop just shy of my left caIf, I stared through the windshield, feeling as if I was inside the car with the driver and her two young children.


Talk (but Don’t Walk) to the Hand. Photo by DMangus CC BY-NC-ND 2.0

Beyond the social pull of fellow travelers, we are also at the mercy of our own internal states. Extreme moods or physical discomfort can distract us from our surroundings, but there is also the elephant in the proverbial intersection: alcohol. Although there have been campaigns against driving under the influence, we don’t talk about walking under the influence. Yet in an estimated 34% of U.S. pedestrian deaths in 2014, the pedestrian had a blood alcohol concentration at or above the legal limit for driving under the influence. If you have a few drinks and make the very good decision to walk rather than to drive home, you still face risks from your inattention and sluggish reaction times.

So how do we keep from following others or meandering into the street when we are on autopilot, distracted, or impaired? Being aware of one’s surroundings is always best, but you also need a backup plan. You can make one by building a new habit. Wait at all signaled intersections until you see the Walk signal – even if there isn’t a car to be found. Wait that extra minute for the signal every time, just as you would if you were a car waiting at a red light. If waiting for the signal becomes a habit, then you will default to it, even when you are on autopilot.

Now consider a few benefits of this habit. First, if you cross for a Walk signal, then you are crossing at the intersection. This alone greatly reduces your risk of being struck by a car. In 2014, 71% of US pedestrian deaths occurred outside of an intersection. And as a moral bonus, creating this habit for yourself can also protect others. If you don’t cross against the light, your distracted fellow walkers won’t follow you out into traffic. That particularly benefits children and the elderly, who may require more time to cross the street.

Over the past two years, I have been cultivating this habit. I have been that sucker who waits for the Walk signal, even when there isn’t a car to be seen. I had the idea of writing this post on the walk to work one day. I arrived at my office with an outline of it in my head – but no recollection of actually treading the sidewalks and crossing the streets along the way.

Still, I know one thing: I obeyed that lighted hand.

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:

“According to the Surgeon General, women should not drink alcoholic beverages during pregnancy because of the risk of birth defects.”

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

The Trouble with (and without) Fish


This week I’m posting a piece from my archives (August, 2011) that I’ve updated a little. Two things brought this post to mind: 1) the recent EPA report that women have become better informed about mercury and are making better choices at the fish counter and 2) remarkable updates from my scientist friend who is blogging her way through the world’s oceans as she collects water samples to catalog mercury levels around the globe. Both demonstrate that we are making some progress in studying and alerting people to the mercury in our waters and our fish. NB: when I say “now that I’m pregnant,” it’s 2011 me talking.


Once upon a time in a vast ocean, life evolved. And then, over many millions of years, neurons and spinal cords and eyes developed, nourished all the while in a gentle bath of nutrients and algae.

Our brains and eyes are distant descendants of those early nervous systems formed in the sea. And even though our ancestors eventually sprouted legs and waddled out of the ocean, the neural circuitry of modern humans is still dependent on certain nutrients that their water-logged predecessors had in abundance.

This obscure fact about a distant evolution has recently turned into a major annoyance for me now that I’m pregnant. In fact, whether they know it or not, all pregnant women are trapped in a no-win dilemma over what they put into their stomachs. Take, for instance, a popular guidebook for pregnant women. On one page, it advocates eating lots of seafood while pregnant, explaining that fish contain key nutrients that the developing eyes and brain of the fetus will need. A few pages later, however, the author warns that seafood contains methylmercury, a neurotoxic pollutant, and that fish intake should be strictly curtailed. What is a well-meaning pregnant lady to do?

On a visceral level, nothing sounds worse than poisoning your child, so many women reduce their seafood intake while pregnant. I have spoken with women who cut all seafood out of their diet while pregnant, for fear that a little exposure could prove to be too much. They had good reason to be worried. Extreme methylmercury poisoning episodes in Japan and Iraq in past decades have shown that excessive methylmercury intake during pregnancy can cause developmental delays, deafness, blindness, and seizures in the babies exposed.

But what happens if pregnant women eliminate seafood from their diet altogether? Without careful supplementation of vital nutrients found in marine ecosystems, children face neural setbacks or developmental delays on a massive scale. Consider deficiencies in iodine, a key nutrient readily found in seafood. Its scarcity in the modern land-based diet was causing mental retardation in children – and sparked the creation of iodized salt (salt supplemented with iodine) to ensure that the nutritional need was met.


Perhaps the hardest nutrient to get without seafood is an omega-3 fatty acid known as DHA. In recent years, scientists have learned that this particular fatty acid is essential for proper brain development and functioning, yet it is almost impossible to get from non-aquatic dietary sources. At the grocery store, you’ll find vegetarian products that claim to fill those needs by supplying the biochemical precursor to DHA (found in flaxseed, walnuts, and soybean oils), but it’s not clear that the precursor will do the trick. Our bodies take a while to synthesize DHA from its precursor. In fact, we may burn much of the precursor for energy before we manage to convert it to DHA.

The best way for pregnant women to meet the needs of their growing babies is to eat food from marine sources. Yet thanks to global practices of burning coal and disposing of industrial and medical waste, any seafood women eat will expose their offspring to some amount of methylmercury. There’s no simple solution to this problem, although studies suggest that child outcomes are best when women consume ample seafood while avoiding species with higher levels of methylmercury (such as shark, tilefish, walleye, pike, and some types of tuna). It also matters where the fish was caught. Mercury levels will be higher in fish from mercury-polluted waters – one of the reasons that it’s important to catalog mercury levels around the globe.

Unless we start cleaning up our oceans, pregnant women will continue to face this awful decision each time they sit down at the dinner table. Far worse, we may face future generations with lower IQs and developmental delays regardless of which choice their mothers make. Thanks to shoddy environmental oversight, we may be saddling our children with brains that don’t work as well as our own. And that is something I truly can’t swallow.


Photo credits:

Photo 1: by Gideon (malias) on Flickr, used via Creative Commons license

Photo 2: by @Doug88888 on Flickr, used via Creative Commons license

We Got the Beat


It is both amusing and enlightening to hear my 21-month-old daughter sing the alphabet song. The song is her favorite, though she is years from grasping how symbols represent sound, not to mention the concept of alphabetical order. Still, if you start singing the song she will chime in. Before you think that’s impressive, keep in mind that her version of the song is more or less this: “CD . . . G . . . I . . . No P . . . S . . . V . . . Dub X . . . Z.”

Her alphabet song adds up to little more than a Scrabble hand, yet it is a surprising feat of memory all the same. My daughter doesn’t know her last name, can’t read or write, and has been known to mistake stickers for food. It turns out that her memory for the alphabet has far less to do with letters than lyrics. From Wheels on the Bus to Don’t Stop Believin’, she sings along to all of her favorite songs, piping up with every word and vowel she remembers. Her performance has nothing to do with comprehension; she has never seen or heard about a locker, yet she sings the word at just the right time in her rendition of the Glee song Loser like Me. (Go ahead and judge me. I judge myself.)

My daughter’s knack for learning lyrics is not unique to her or to toddlers in general. Adults are also far better at remembering words set to song than other strings of verbal material. That’s why college students have used music to memorize subjects from human anatomy to U.S. presidents. It’s why advertisers inundate you with catchy snippets of song. Who can forget a good jingle? To this day, I remember the phone number for a carpet company I saw advertised decades ago.

But what is it about music that helps us remember? And how does it work?

It turns out that rhythm, rather than melody, is the crucial component to remembering lyrics. In a 2008 study, subjects remembered unfamiliar lyrics far better if they heard them sung to a familiar melody (Scarborough Fair) than if they heard them sung to an unfamiliar song or merely spoken without music. But they remembered the lyrics better still if they heard the lines spoken to a rhythmic drummed arrangement of Scarborough Fair. Even an unfamiliar drummed rhythm boosted later memory for the words. By why should any of these conditions improve memory? According to the prevailing theory, lyrics have a structural framework that helps you learn and recall them. They are set to a particular melody through a process called textsetting that matches the natural beat and meter of the music and words. Composers, lyricists, and musicians do this by aligning the stressed syllables of words with strong beats in the music as much as possible. Music is also comprised of musical phrases; lyrics naturally break down into lines, or “chunks,” based on these phrase boundaries. And just in case you missed those boundaries, lyricists often emphasize the ends of these lines with a rhyming scheme.

Rhythm, along with rhyme and chunking, may be enough to explain the human knack for learning lyrics. Let’s say you begin singing that old classic, Twinkle, Twinkle, Little Star. You make it to “How I wonder,” but what’s next? Since the meter of the song is BUM bah BUM bah and you ended on bah, you know that the next words must have the stress pattern BUM bah. This helps limit your mental search for these words. (Oh yeah: WHAT you!) The final word in the line is a breeze, as it has to rhyme with “star.” And there you have it. Rhythm, along with rhyme and chunking, provide a sturdy scaffold for your memory of words.

For a more personal example of rhythm and memory, consider your own experience when you remember the alphabet. It’s worth noting that the alphabet song is set to a familiar melody (the same as Twinkle, Twinkle, Little Star and Baa, Baa, Black Sheep), a fact that surely helped you learn the alphabet lyrics in the first place. Now that you know them, ask yourself this: which comes first, the letter O or L? If you’re like me, you have to mentally run through the first half of the song to figure it out. Yet this mental rendition lacks a melody. Instead, you list the letters according to the song’s rhythm. Your list probably pauses after G and again after P and V, which each mark the end of a line in the song. The letters L, M, N, and O each last half as long as the average letter, while S sprawls out across twice the average. Centuries ago, a musician managed to squeeze the letters of the alphabet into the rhythm of an old French folk song. Today, the idiosyncratic pairing he devised remains alive – not just in kindergarten classrooms, but in the recesses of your brain. Its longevity, across generations and across the lifespan, illustrates how word and beat can be entwined in human memory.

While a rhythm-and-rhyme framework could explain the human aptitude for learning lyrics, there may be more to the story. As a 2011 study published in the Journal of Neuroscience shows, beat and meter have special representations in the brain. Participants in the study listened to a pure tone with brief beats at a rate of 144 per minute, or 2.4 Hz. Some of the participants were told to imagine one of two meters on top of the beat: either a binary meter (a march: BUM bah BUM bah BUM) or a ternary meter (a waltz: BUM bah bah BUM bah bah BUM). These meters divided the interval between beats into two or three evenly spaced intervals, respectively. A third group performed a control task that ensured subjects were paying attention to the sound without imagining a meter. All the while, the scientists recorded traces of neural activity that could be detected at the scalp with EEG.

The results were remarkable. Brain waves synchronized with the audible beat and with the imagined meters. This figure from the paper shows the combined and averaged data from the three experimental groups. The subjects in the control group (blue) heard the beat without imagining a meter; their EEGs showed strong brain waves at the frequency of the beat, 2.4 Hz. Both the march (red) and waltz (green) groups showed this 2.4 Hz rhythm plus increased brain waves at the frequency of their imagined meters (1.2 Hz and 0.8 Hz, respectively). The waltz group also showed another small peak of waves at 1.6 Hz, or twice the frequency of their imagined meter, a curiosity that may have as much to do with the mechanics of brain waves as the perception of meter and beat.

Screen Shot 2013-08-21 at 1.15.47 PMIn essence, these results show that beat and meter have a profound effect on the brain. They alter the waves of activity that are constantly circulating through your brain, but more remarkably, they do so in a way that syncs activity with sound (be it real or imagined). This phenomenon, called neural entrainment, may help you perceive rhythm by making you more receptive to sounds at the very moment when the next beat is due. It can also be a powerful tool for learning and memory. So far, only one group has tried to link brain waves to the benefits of learning words with music. Their papers have been flawed and inconclusive. Hopefully some intrepid scientist will forge ahead with this line of research. Until then, stay tuned. (Or should I say metered?)

Whatever the ultimate explanation, the cozy relationship between rhythm and memory may have left its mark on our cultural inheritance. Poetry predated the written word and once served the purpose of conveying epic tales across distances and generations. Singer-poets had to memorize a harrowing amount of verbal material. (Just imagine: the Iliad and Odyssey began as oral recitations and were only written down centuries later.) Scholars think poetic conventions like meter and rhyme arose out of necessity; how else could a person remember hours of text? The conventions persisted in poetry, song, and theater even after the written word became more widespread. No one can say why. But whatever the reason, Shakespeare’s actors would have learned their lines more quickly because of his clever rhymes and iambic pentameter. Mozart’s opera stars would have learned their libretti more easily because of his remarkable music. And centuries later you can sing along to Cyndi Lauper or locate Fifty Shades of Grey in the library stacks – all thanks to the rhythms of music and speech.


Photo credits: David Martyn Hunt on Flickr and Nozaradan, Peretz, Missal & Mouraux via The Journal of Neuroscience

Nozaradan, S., Peretz, I., Missal, M., & Mouraux, A. (2011). Tagging the Neuronal Entrainment to Beat and Meter The Journal of Neuroscience DOI: 10.1523/JNEUROSCI.0411-11.2011

Mother’s Ruin, Moralists, and the Circuitous Path of Science


Update: Since posting this piece, I’ve come across a paper that questions ancient knowledge about the effects of prenatal alcohol exposure. In particular, the author makes a compelling argument that the biblical story mentioned below has nothing to do with the safety of drinking wine while pregnant. Another paper (sorry, paywall) suggests that the “rhetoric of rediscovery” about the potential harm of alcohol during pregnancy was part of a coordinated attempt by “moral entrepreneurs” to sell a moralist concept to the American public in the late 1970s. All of which goes to show: when science involves controversial topics, its tortuous path just keeps on twisting.

If you ask someone to draw you a roadmap of science, you’re likely to get something linear and orderly: a one-way highway, perhaps, with new ideas and discoveries converging upon it like so many on-ramps. We like to think of science as something that slowly and deliberately moves in the right direction. It doesn’t seem like a proper place for off-ramps, not to mention detours, dead-ends, or roundabouts.

In reality, science is messy and more than a little fickle. As I mentioned in the last post, research is not immune to fads. Ideas fall in and out of fashion based on the political, financial, and social winds of the time. I’m not just talking about wacky ideas either. Even the idea that drinking during pregnancy can harm a developing fetus has had its share of rises and falls.

The belief that drinking while pregnant is harmful has been around since antiquity, popping up among the Ancient Greeks and even appearing in the Old Testament when an angel instructs Samson’s mother to abstain from alcohol while pregnant. Yet the belief was far from universal across different epochs and different peoples. In fact, it took a special kind of disaster for England and, in turn, America to rediscover this idea in the 18th century. The disaster was an epidemic . . . of people drunk on gin.

By the close of the 17th century, bickering between England and France caused the British to restrict the import of French brandy and encourage the local production of gin. Soon gin was cheap and freely available to even the poor and working classes. The Gin Epidemic was underway. Rampant drunkenness became a fact of life in England by 1720 and would persist for several decades after. During this time, gin was particularly popular among the ladies – a fact that earned it the nickname “Mother’s Ruin.”

Soon after the start of the Gin Epidemic, a new constellation of abnormalities became common in newborns. Physicians wondered if heavy prenatal exposure to alcohol disrupted fetal development. In 1726, England’s College of Physicians argued that gin was “a cause of weak, feeble and distempered children.” Other physicians noted the rise in miscarriages, stillbirths, and early infant mortality. And by the end of this gin-drenched era, Britain’s scientific community had little doubt that prenatal alcohol could irreversibly harm a developing fetus.

The notion eventually trickled across the Atlantic Ocean and took hold in America. By the early 19th century, American physicians like Benjamin Rush began to discourage the widespread use of alcohol-based treatments for morning sickness and other pregnancy-related ailments. By the middle of the century, research on the effects of prenatal alcohol exposure had become a talking point for the growing temperance movement. Medical temperance journals sprung up with names like Journal of Inebriety and Scientific Temperance Journal. Soon religious and moralistic figures were using the harmful effects of alcohol on fetal development to bolster their claims that all alcohol is evil and should be banned. They often couched the findings in inflammatory language, full of condemnations and reproach. In the end, their tactics worked. The 18th Amendment to the U.S. Constitution was ratified in 1919, outlawing the production, transportation, and sale of alcohol on American soil.

When the nation finally emerged from Prohibition more than thirteen years later, it had fundamentally changed. People were disillusioned with the temperance movement and wary of the moralistic rhetoric that had once seemed so persuasive. They discounted the old familiar lines from teetotal preachers – including those about the harms of drinking while pregnant. Scientists rejected studies published in medical temperance journals and began to deny that alcohol was harmful during pregnancy. In 1942, the prestigious Journal of the American Medical Association published a response to a reader’s question about drinking during pregnancy which said that even large amounts of alcohol had not been shown to be harmful to the developing human fetus. In 1948, an article in The Practitioner recommended that pregnant women drink alcohol with meals to aid digestion. Science was, in essence, back to square one yet again.

It wasn’t until 1973 that physicians rediscovered and named the constellation of features that characterize infants exposed to alcohol in the womb. The disease, fetal alcohol syndrome, is now an accepted medical phenomenon. Modern doctors and medical journals now caution women to avoid alcohol while pregnant. After a few political and religious detours, we’ve finally made it back to where we were in 1900. That’s the funny thing about science: it isn’t always fast or direct or immune to its cultural milieu. But if we all just have faith and keep driving, we’re bound to get there eventually. I’m almost sure of it.


Photo Credit: Gin Lane by William Hogarth 1751 (re-engraving by Samuel Davenport circa 1806). Image in public domain and obtained from Wikipedia.

A New America of Mutts?

8687286808_ce53c853e7_oI recently wrote about my biracial daughter and public assumptions about inheritance for the blog DoubleXScience. Nearly the same day, columnist David Brooks’ op-ed piece, “A Nation of Mutts,” appeared in The New York Times. As you might imagine, I read it with interest.

In his column, Brooks writes about how the long-European roots of America are becoming outnumbered by those of immigrants from elsewhere in the world.  Add to that racial intermarriage and mixed-race offspring and you’re left with what Brooks calls the coming New America. What will this New America look like? Brooks is happy to venture guesses, predicting how the complex forces of socioeconomics, education, ethnicity and heritage may play out in coming generations. Among these predictions: that America will become “a nation of mutts, a nation with hundreds of fluid ethnicities from around the world, intermarrying and intermingling.” The piece sparked an outcry from readers and an online conversation via social media, much of it over his use of the term mutt. While it was obviously an unwise and insensitive word for him to use, I think this was the lesser of the problems with his piece.

According to New York Times public editor Margaret Sullivan, columnists are supposed to stir things up. But in “A Nation of Mutts,” Brooks merely takes a centuries-old argument, injects it with Botox, squeezes it into skinny jeans, and calls it something new.

He begins by telling us that “American society has been transformed” as increasing numbers of immigrants have come to the U.S. in recent decades. He adds that, “up until now, America was primarily an outpost of European civilization” with immigrants who came from Northern, Western, Southern, or Central Europe (depending on the era) but all “with European ideas and European heritage.” That is now changing. Brooks tells us that European-American five-year-olds are already a minority. We have thirty years, tops, before Caucasians will be the minority in America overall.

What strikes me is Brooks’ simplistic picture of racial and cultural differences. He portrays America’s past immigrants from Europe as a monolithic, homogeneous bunch (against which he will compare the diverse immigrants of today) when of course this is a straw man. Ask anyone at a European soccer championship match or at the Eurozone bailout negotiations whether Europeans all have the same “European ideas and European heritage.” On second thought, probably better you don’t.

Americans haven’t historically thought of all Europeans as similar or even equal. Take the 19th century Nativists, or Know-Nothings, who thought that immigrants were ruining America. What exotic nation supplied these immigrants? The Tropics of Ireland.

Our country’s long history of interracial children aside, Caucasians from all over Europe have been intermarrying in America for centuries. I have American ancestors dating back to colonial times and am part German and part British with at least one Frenchman and one Scot thrown in for good measure. Why does David Brooks consider my daughter a mutt yet doesn’t consider me one? Because my ancestors all had more or less the same skin color while my husband is several shades darker than me.

So what is David Brooks really recounting when he writes about the coming nation of mutts? What’s so different about the immigrants of today? Mostly superficial details of appearance. Brooks’ New America is based on the preponderance of pigments in skin, the shape and slope of eyes, the texture of hair. His seemingly profound comment is about the spread of a handful of genes that create innocuous (but visible) proteins like melanin. Big frickin’ deal.

Ultimately, David Brooks is guilty of recycling the same tired old tune: immigrants are changing America and who knows what it might become when they’re done with it? Of course immigrants change our national demographics and  cultural melange. Each generation has wrestled with this self-evident fact for different reasons and in different ways. But if there is anything constant about America’s history, it is the presence of immigration and continuous change. Which means that Brooks was wrong when he said that a New America is coming. It has been here all along.


Photo credit: Steve Baker on Flickr

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

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