Breasts

by Florence Williams

  Puberty is like an orchestra. The ovaries are the violins. Fat cells are the oboes. We have some sort of internal conductor that tells the parts when to make their music. Some call it a gonadostat— literally, a thermostat for our sex gonads—and it sets our pubertal tempo. Whatever it is, it’s regulated by the hypothalamus in the brain, the director of the symphony, and that in turn responds to all sorts of internal and external cues in the forms of enzymes and hormones.

  The BCERC researchers are devoting a lot of time to studying diet and exercise, regularly asking the 1,500 girls what they’re eating and how often they visit playgrounds, play sports, and walk to school. So far, there appears to be some relationship between the amount of fiber in their diet and the age at which they get breasts. The more fiber and vegetables they eat, the later they enter puberty. Another study out of Britain in 2010 found that girls who reached puberty earlier ate more meat than their peers, with the biggest carnivores maturing earliest.

  Said Dr. Frank Biro, a pediatrician and coinvestigator of the BCERC study from the University of Cincinnati, “The nutritional factor consistently associated with timing of puberty, in those societies where there are sufficient calories for all members, is fiber. Higher fiber equals later maturation.” This is probably because of the way some genes interact with fat, he says.

  Fair enough, but as Biro himself acknowledges, diet alone doesn’t seem to explain the puberty clock. I never totally bought the simplistic fat-triggers-puberty argument. I went through puberty a good year earlier than all of my friends, and I was skinny as a rail and always had been. Doctors and cancer scientists know that plenty of thin girls fall on the early side of the puberty curve.

  It turns out that while fat may trigger one pathway to puberty, there are other pathways as well. Some girls get breast buds as their first sign of puberty. It may be months or years before they grow pubic hair or get their periods. Other girls grow pubic hair first, with nary a breast in sight. Pubic hair is influenced more by adrenal hormones than by estrogens. So you might think this means you’re off the hook for breast cancer if you were thin, but, maddeningly, it doesn’t. In fact, thin girls who menstruate early are at slightly higher risk of breast cancer later on than their pudgy peers. In a recent Swedish study, researchers found that women who had fatter bodies during childhood were 27 percent less likely to have breast cancer than women who were leaner as children. I was tall and thin as a fourteen-year-old, and it turns out both of those traits are linked to higher breast cancer risk.

  Because of the holes in the obesity theory, I was curious to visit the lab of pediatric endocrinologist Lise Aksglaede in Denmark. Her office at the Rigshospitalet of the University of Copenhagen looks out over the west side of the city and its lakes. She was late for our appointment and came bounding in, breathless, from her hurried bike ride across town. Like nearly one-third of all workers in the city, she bikes to the office every day. And like nearly everyone here, she’s fit, blonde, and peppy. I suspect the fit and peppy parts come from all the biking. According to various happiness indices, the Danes are among the happiest people on earth, despite terrible North Sea weather and a crippling tax code. In her mid-thirties, Aksglaede is still breast-feeding her one-year-old son, chalking her up as another statistical norm; breast-feeding rates in Denmark are double those in the United States.

  Wondering whether the American puberty data were really so unusual, she decided to take a closer look at her hometown. She and her colleagues examined almost one thousand girls in 2006 using the exact same protocols as a similar study in 1991. It turned out that the girls—all white and middle class—started budding breasts a full year earlier than they had just fifteen years ago. (The age of menstruation had advanced only about four months.) But the real head-scratcher was that the change in the girls’ body weight was minimal and couldn’t account for the difference. Nearly all the girls were relatively thin, said Aksglaede.

  So if fat isn’t setting the puberty clock for these girls, what is?

  There are three other leading theories: artificial light, divorce, and highly sexualized media. The light theory hinges on melatonin, a hormone that flows from our pineal gland at the center of our brain to our hypothalamus, telling it to quiet down (the hypothalamus, remember, regulates our gonadostat). We make melatonin in darkness. Women who are blind make more of it, and guess what? They have a lower risk of breast cancer. By contrast, women who work under lights on the night shift at work have a higher risk.

  Nighttime light—in the form of computer and TV screens, electric overhead lights, and the ubiquitous hallway night-light—is clearly not something we evolved with. Some researchers speculate these girlhood light exposures could be suppressing natural melatonin levels, and in turn speeding up the gonadostat. Studies have found that girls with precocious puberty have unusually low levels of melatonin, while female athletes have high levels. (Note to self: remove the nightlight from Annabel’s bedroom.) The problem, though, with the light theory is it doesn’t totally explain the difference in just fifteen years in girls in Copenhagen. Presumably, even with their crippling tax code, Danes had plenty of electric lights in 1991.

  Let’s look at the divorce theory: it’s been documented that girls not living with a biological father tend to mature earlier. Female elephants do something similar in the absence of a parent. It makes some survival sense that populations under stress would be more desperate to reproduce, even if they can’t raise the next generation in an optimal environment. The absent-father theory could account for my early age at puberty. My parents divorced when I was two. But it couldn’t explain all of today’s girls, because families are actually slightly more stable now than they were two decades ago.

  Which leaves us with the boobs-and-sex-all-over-the-media theory. It sounds reasonable, but if girls are becoming more sexualized from a constant stream of media images, their hormone levels would also be rising, and oddly, that’s not happening. While the Copenhagen girls are growing breasts earlier, their bodies are not making any more estrogen than they were in 1991. To Aksglaede, this indicates that the source of estrogen—needed for breast development—must lie somewhere else.

  “Our best suggestion is that [the source] is something from outside,” said Aksglaede. “The main discussion is environmental factors.” Specifically, chemicals that mimic hormones, many of which girls are exposed to every day, even in Europe, which is only now just starting to regulate them. Endocrine-disrupting compounds, as we saw in the last chapter, include the much-publicized baby-bottle ingredient BPA, as well as other ingredients in plastics, pesticides, and compounds in cigarettes, among many others.

  The BCERC’s Biro agrees, to a point. “Heavier girls are more likely to enter puberty first,” he said, “but something above and beyond that is going on and that’s where it gets really interesting. There are lots of others who believe that chemicals are the major cause. I believe that they are clearly contributing.”

  Not all experts are convinced. Dr. Paul Kaplowitz is the man behind revising the clinical age of “precocious puberty” after Herman-Giddens’s groundbreaking study came out in the 1990s. “The environmental puberty hypothesis is interesting,” said Kaplowitz, the chief of endocrinology and diabetes at Children’s National Medical Center in Washington, D.C. “But my position is that we need more information on environmental exposures. I’ve gotten into the habit of asking my patients with early puberty if they’re using hair care products, essential oils, lavender, tea tree oils, and so on. It’s pretty rare for them to say yes. The phthalates and the BPA are plausible. But if external estrogens were really affecting girls, you’d think you’d see more breast development in boys as well. We do see some of that, but I haven’t seen a big increase,” he said.

  Biro counters this argument by pointing to studies suggesting that boys are indeed showing signs of unusual estrogen and antiandrogen exposure, such as smaller penis sizes, decreased sperm counts, and shorter distances between the genitals and anus, all o
f which are considered markers of “feminization.” By some estimates, the once-rare birth defect of undescended testicles in baby boys is increasing in the United States and parts of Europe. In a study of 1,600 babies born between 1997 and 2001, Danes had smaller testicles than the Finns. Scientists know this because they expertly measured “ellipsoidal volume” and found the Danish package lagging at birth. The differences were even more pronounced after three months, with the Finns averaging three times more testicular growth. Researchers went back and tested samples from the babies’ stored blood and their mothers’ breast milk in each country. Danes are known to smoke and drink during pregnancy, but that didn’t seem to explain the genital effects. Then other hormone-monkeying suspects turned up at relevant levels: certain industrial chemicals. As researcher Katharina Main, who works across the hall from Lise Aksglaede at the University of Copenhagen, told me, “It’s higher here. The higher your [chemical] burden … the higher the risk of undescended testes.”

  IT’S BEEN WELL DOCUMENTED THAT PUBERTY CAN BE SWAYED BY chemical exposures. Lead and dioxin (a by-product of combustion), for example, are known to delay puberty in both animals and people. The pesticide DDT has been associated with earlier puberty in girls, and PCBs (polychlorinated biphenyls, used as industrial greasers) have been alternately linked in separate studies with both delayed and advanced puberty.

  But external culprits are hard to pinpoint. Consider the weird epidemic of precocious puberty in Puerto Rico during the 1980s and 1990s. So many very young girls (under age five) were developing breasts that the government there established the world’s only “early sexual development registry” to record it. The incidence there turned out to be eight out of every thousand girls between 1984 and 1993, eighteen and a half times higher than the incidence in the United States. Why would Puerto Rico be the world’s hot spot for toddler breasts? The cause appeared more geographic than genetic, because Puerto Ricans in the mainland United States had normal development, and the problem was afflicting other ethnic groups living in Puerto Rico as well.

  Journalist Orville Schell describes interviewing a Puerto Rican pediatrician and seeing Polaroids of some of these children in 1982:

  In the first photo, a four-and-a-half-year-old girl with delicate coffee-colored skin, doelike brown eyes and almost fully developed breasts lies on an examining table. She smiles with a sweet innocence at the camera, seemingly unaware of the dramatic changes that have gone on in her body.

  “She had an ovarian cyst,” says Dr. Saenz [de Rodriguez] tersely.

  A twelve-year-old boy stands against a white wall looking with blank bewilderment into the camera. He wears a silver crucifix around his neck, which dangles down between two grossly swollen breasts.

  “We’ve had to schedule him for surgery,” says Dr. Saenz matter-of-factly. “The emotional stress on him is incredible.”

  The children had reportedly eaten school-lunch chicken contaminated with high levels of DES, the same hormone Pat Hunt’s mother took to prevent miscarriage, as we learned in the last chapter. At the time, DES was given to farm animals to make them plumper. When many of Dr. Saenz’s patients stopped eating meat and milk, their symptoms improved. But an investigation—conducted after a considerable delay—turned up only average levels of the growth hormone in more than eight hundred subsequent food samples. Investigators also considered pharmaceutical wastes and agricultural pesticides, both widespread there, but again, there was no obvious evidence. One study did find unusually high levels of phthalates in the blood of girls with early breasts, but there is the lingering possibility that those samples were accidentally cross-contaminated by plastics in the testing laboratory.

  Phthalates are a family of molecules used as scent stabilizers in lotions and shampoos, and as common additives in plastics. Concerned over their health effects, the European Union will soon be restricting three types of phthalates from general use in commercial products. California recently banned several phthalates in products sold to the under-three set. Known endocrine disruptors, they’ve been recently linked to genital abnormalities in baby boys and increased “girl play” in toddler boys. It’s possible they may be turbocharging the future breast tissue of young or even unborn girls. One way to find out is to compare the urinary levels of phthalates in girls and see who gets the earliest breasts. (Unfortunately, it’s not enough to simply ask the girls which toys and personal care products they’ve used; companies are not required to list ingredients on their labels. The only reliable way to test exposures is to ask the girls for body fluids.)

  The BCERC researchers are measuring girls’ blood and urine for fifty-one chemical substances, including phthalates, BPA, organochlorine pesticides, heavy metals, industrial solvents such as PCBs, and naturally occurring plant-based estrogens such as soy. Nearly all the girls have these substances in their bodies, sometimes in much larger concentrations than what is found in adults. There are also some geographical ticks: Girls in California are endowed with the highest recorded levels of flame-retardants, probably due to that state’s strict flammability standards. Girls in New York City carry more cotinine, a molecule found in cigarettes and secondhand smoke, as well as more 2,5-dichlorophenol, used in mothballs and room deodorizers, while girls in Cincinnati carry more PFOA, a chemical used in making products with Teflon.

  The Centers for Disease Control and Prevention (CDC) releases measures of the so-called body burdens of girls every two years as part of its National Health and Nutrition Examination Survey. When the BCERC researchers in Cincinnati studied the values measured in their girls, they found that fully 40 percent of them carried levels of PFOA above the CDC’s last measured ninety-fifth percentile. The researchers are currently trying to determine why the girls had unusually high levels and whether PFOA is linked to early breast development, particularly in thinner girls.

  African-American girls in the study bore considerably higher levels of phthalates (the fragrance stabilizer) and parabens (a preservative in personal care products), four times the level found in white and Asian girls. Could this possibly help explain why the proportion of African-American girls who reach puberty at age eight is four times greater than the proportion of white girls? Or why African-American women in their twenties have a nearly 50 percent higher rate of breast cancer than white women of the same age (above age forty, though, the white rate surpasses the African-American rate). Researchers would like to know.

  AS I FOUND OUT FROM OUR HOME EXPERIMENT, PHTHALATES ARE everywhere. Since they bind fragrances, they’re often present in our shampoos, soaps, and moisturizers. They are an important ingredient in softening polyvinylchloride (PVC), so they waft out of things like shower curtains, plastic toys, and fake leather. (There’s more fake leather lying around than you think. I had to throw out one of my daughter’s play wallets because it smelled so strongly of chemicals. My son has a belt made out of it, and it’s also common in sneakers. Now I have a radar for “pleather” when I go into box retail stores, and I steer clear.) Phthalates may also be present in sandwich bags and plastic wrap, but it’s hard to know for sure since manufacturers aren’t saying.

  A newspaper in Taiwan recently reported that phthalates had been found in food such as baked goods. Apparently it makes them smell good even after many days on the shelf. This put officials in the absurd position of warning consumers not to buy food that smelled fresh.

  For the before—or tox—phase of our experiment, I indulged in some very American habits, and Annabel joined me in some of them. For three days, we ate a couple of meals out of cans. (One out of every five U.S. dinners includes a can, according to the Canned Food Alliance.) Refried beans were a favorite. I drank a can of ginger ale at lunch and dinner. I indulged in a professional pedicure (pearly pink), the better for sitting briefly in a cloud of chemicals. We both shampooed and conditioned with “fresh” floral fragrances and used a perfume-y bar of soap. I wore brand-name deodorant, moisturized my body in “deep healing” lotion. I topped it off with a swath
of coral lipstick. I felt like a beauty contestant.

  As anyone on Celebrity Rehab can attest, detox isn’t nearly as fun as what precedes it. It was very hard to avoid food that had never touched plastic. Coffee beans? Nope. Grapes? Sorry. I rode my bike (because my car interior off-gasses phthalates as well as flame-retardants) to the farmers’ market. Even my bike had plastic handle grips, but there was no helping that. I also wore a helmet made of shatter-proof polycarbonate, rife with BPA. (Yes, there are plenty of beneficial uses for BPA.) My prescription sunglasses are made out of the same, another product that was hard to avoid considering I left my metal frames behind in about 1999. At the market, I perused the farmers’ offerings. Some, like the tomatoes, were displayed in plastic. No tomatoes for me. But beautiful artisanal breads were wrapped in paper bags. I asked the seller where the flour had come from, and if it had touched plastic. This being Boulder, he didn’t look at me like I was a freak. He assured me the flour came straight from the mill in large cloth sacks, the old-fashioned way. I stocked up. I also bought some ridiculously expensive quinoa that came packaged in paper. I eyed some greens, but noticed the seller was serving them with rubber gloves (PVC) and stuffing them into plastic bags (phthalates). I asked him if I could handle my own greens and put them in my own cloth bag. He said sure. Boulder is apparently full of chemically sensitive plastophobes.

  I had a good excuse not to do any other shopping: BPA is used to coat thermal paper, the kind used for store receipts and airline boarding passes. Unlike the BPA in polycarbonate water bottles, the BPA in paper isn’t “bound” to other molecules, so it rubs off in relatively high amounts. Although we don’t generally go around eating receipts, Sonya Lunder says the substance easily ends up on dollar bills and our hands.