Breasts (12 page)

Okay, so now we know the age of puberty naturally fluctuates. That doesn’t mean we should shrug it off. The Herman-Giddens data suggest that between the 1970s and the 1990s, the age of puberty dropped much faster than expected. Perhaps the latest oscillation isn’t so “natural” after all.

There’s no doubt modern society, with its overnutrition and better medicine (as well as perhaps its industrial pollutants), has caused the age of sexual maturation to fall. Ironically, though, this same complex modern world means we need
more
time for what experts call “psycho-social maturation,” or time to figure things out. The human brain takes two decades to mature, especially the prefrontal cortex, which governs self-concept and the control of impulses and reward-seeking. It’s arguably a lot harder to be a young mother now—with all our social and familial fragmentation—than ever
before. Evolutionary biologists call this a “mismatch.” Our bodies are responding to one set of determinants, but our brains don’t appear to be catching up.

Our Paleolithic legacy has left us with other mismatches, such as obesity and diabetes. It’s becoming increasingly obvious that our bodies weren’t designed to handle modern, industrial diets. While metabolic diseases have received a lot of attention, the changing age of puberty hasn’t. But it should. Peter Gluckman is a biologist at the University of Auckland in New Zealand and a pioneer in a field known as evolutionary medicine. As he puts it, “For the first time in our evolutionary history, biological puberty in females significantly precedes, rather than being matched to, the age of successful functioning as an adult.”

WHAT EXACTLY IS IT ABOUT OUR MODERN ENVIRONMENT THAT’S
driving the age of puberty toward toddlerhood at an ever-increasing pace? The government’s BCERC study posits the broad hypothesis that “chemical, physical and social factors interact with genes” to set breasts on their inflationary course. Many of those factors are new in our human life history. The research is divided into three areas: animal studies, human breast cell studies, and real-life, whole-person studies. It may be our best hope for understanding some of the key unanswered questions behind the mysteries of puberty and breasts.

Although it’s tempting—for both the researchers and people like me—to try to identify a single culprit for early ballooning bosoms, we won’t be easily gratified. One thing seems clear: many factors lead to the complex, multistaged “event” of puberty.

Obesity has long been the leading contender in the earlypuberty sweepstakes. Everyone in the field knows that the percentage
of American girls aged six to eleven who are obese more than tripled, to 16 percent, between 1974 and 2006. Nearly a third of girls are now labeled overweight. Although the exact timing of puberty remains wrapped in mystery, the role of fat is partly known. Where there’s fat, there’s also the enzyme aromatase. Aromatase helps convert the building blocks of steroids—cholesterol—into estrogen. Fat has been called “the third ovary” because of its ability to make estrogen. The crude equation is more fat equals more estrogen, and this is true even in men, witness man boobs. Fat also increases levels of leptin, a hormone that tells us when we’re hungry, and also seems to fire up the puberty engine. Leptin levels have been found to be higher in African Americans than in other groups. But fat is not the whole story, not by a long shot. Otherwise, fat babies would be oozing in estrogen, and they’re not. And obese women often have
less
circulating sex hormones because they don’t ovulate regularly.

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 of
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: