Breasts (9 page)

How do we convince our daughters not to join the legion of women who feel they have such limited avenues to happiness? Unfortunately, that challenge seems to be only growing. Double-D breasts on skinny women are not all that common in nature. (Barbie’s proportions are naturally found in one out of one hundred thousand women, according to researchers from the University of South Australia; Ken’s bod, by contrast, is found in one in fifty men.) Big, fake breasts have so thoroughly saturated mainstream entertainment and media that they’ve created a new standard by which boys judge girls and girls judge themselves.

Thanks to the alliance of two kinds of silica-based technologies—breasts and computer chips—most young people learn about bodies and sex from the Internet; they have seen many more factorymade breasts than real ones. In this crowd anyway, natural breasts just keep losing traction.

THE PATIENTS IN DR. C’S SURGICAL SUITE KNEW AS MUCH. THE
first patient I met was a twenty-nine-year-old named Gloria who weighs ninety-nine pounds. A recent college graduate, she has a two-year-old. When Dr. C came in for a pre-op review, she took off her robe to reveal breasts that are quite fantastic: firm and nicely rounded, probably a B cup. A delicate butterfly tattoo lay between them, and her back sported a geisha surrounded by cascading pink blossoms. She would be getting 275-cubic-centimeter implants, for “a full C.” I asked her what made her decide to do this. “I just want to put back what I had before my son was born,” she said.

Gloria was, explained Ciaravino later, ideal for surgery. “You want the little skinny ones,” he said, reflecting a truism among all surgeons. “The ideal patient, she’s had a couple of kids, she’s good looking to start out with. If you have funky breasts to begin with, they’re going to be funky after. It’s not going to be picture perfect. It’s all a relative improvement.”

As Gloria went off to meet the anesthesiologist, Dr. C strode to OR1 to place saline implants in a forty-one-year-old Filipina nurse. I watched as he rolled up the silicone shell like a pirouette cookie and then pushed it through the incision. After he flattened it out with his fingers inside her breast, he connected some tubing to its valve. He talked as he went. “With silicone, you have to push it in. You can get a little wear and tear. And you can see her filling up here before your eyes. She’s blowing up like we’re filling up a balloon here.” A machine was pumping in 340 cubic centimeters of saline fluid through the tube and into her breast. When she was fully inflated, Ciaravino stuffed some escaping yellow breast tissue and fat back into the incision, and then he and a nurse took turns sewing her up. She moaned and thrashed a bit. The anesthesiologist by her head adjusted her dose.

Next we went to have a pre-op with Courtney. As always, Ciaravino had a half-dozen patients rolling through the surgical suite in a conveyor belt of calm efficiency. Courtney was sitting with her husband, who wore a T-shirt and baseball cap. They were both in their mid-twenties, from a small town not far away. Courtney, a former cheerleader, now owns a tanning salon. She has dark shoulder-length hair and strenuously plucked brows. A mother of two small kids, she was eager for a better body. In a Texas accent, she explained what brought her here. “I’m a very small B or A, prob
ably A. When I was in high school, I probably had a small C. My sister, she didn’t have big boobs, but after her daughter was born, hers stayed big. But mine, they got smaller every time. My sister-in-law used him,” she said of Dr. C. “Some of my good friends and customers have implants. I just want a full C. I don’t have to look good for anybody else, just for myself, I guess to help me feel better about myself.”

When I next saw Courtney, she was lying asleep on the surgery table. Her uncovered breasts had been marked with a blue pen. The ink made dotted lines along the contours of her flesh like rivers on a topographical map. Her torso had an orange-tinted tan, and her breasts were indeed small. She’d be getting 350-cubic-centimeter Mentor MemoryGel implants, bigger than the old-fashioned Burlesque. Dr. C explained that Courtney was a bit of a challenging case. “The issues here,” he said, “are that she doesn’t really have a defined fold at all so we’re going to have to sort of create that. It puts her at a little bit of a risk for the implant moving down. So when I close it I’m going to have to tack it in place.” He went to work on her, cutting and singeing below her pectoral muscle. He pulled the space open with an instrument resembling a shoehorn. It’s called a Biggs Retractor, named after the Houston surgeon who trained with Cronin. Ciaravino motioned me over to catch a glimpse of Courtney’s heart beating between her ribs. The wound smelled of burning flesh.

When I’d seen enough, I stepped out to chat with the next patient in line, an insurance agent named Katie. She was thirty, a brown-haired mother of two, from Orange, Texas. She said she’s never been under anesthesia before, and she’s nervous. She wanted to go from a size A to just a small C because “we’re conservative people,” Katie explained. “It’s not like all my life, I said, ‘Oh my
God, I want boobs, I want fake boobs.’ I just want my clothes to fit better without having to buy an extra padded bra.” Not having implants, she said, “I’m like the minority, I think, in our circle of friends.” She laughs, patting down her hospital gown. “It’s peer pressure.”

I tell people I come from a different planet because the planet I arrived on is so unlike the planet of the 21st century. There were no plastics; there was less carbon dioxide. There were more fish in the sea. I come from the pre-Plasticozoic era.

— SYLVIA EARLE,
National Geographic
explorer-in-residence

T
HE SAME YEAR THAT TIMMIE JEAN WAS EXCHANGING
an ear tuck for a boob job, Rachel Carson published a book about the destructive power of pesticides. These two events had more in common than it might appear, for both heralded a new era of synthetic compounds that would forever alter breasts. In 1958, the nature writer and biologist had received a disturbing letter from Olga Huckins, a gardener in Duxbury, Massachusetts. It described how the local authorities had sprayed fuel oil and DDT (dichlorodiphenyltrichloroethane) to kill mosquitos, leaving scores of songbirds dead in her neighborhood and in her very backyard. Huckins wrote that birds fell from the sky. Others perished in grotesque postures around her birdbath, their claws splayed, their bills gaping open.

Carson was already known as a voice for nature. The first female biologist hired by the U.S. Bureau of Fisheries, she’d written several odes to the sea, including the wildly popular best seller
The Sea around Us.
It won a National Book Award in 1952.

Inspired by Olga’s letter,
Silent Spring
was a measured and eloquent argument against the indiscriminate use of synthetic pesticides, which Rachel Carson called “elixirs of death.” She described the little-known work of scientists showing how DDT and its ilk caused damage beyond their target insects, affecting birds, fish, and other vertebrates. She got a couple of things wrong in the book, such as the statement that few carcinogens exist in nature (in fact, there are many, including the sun, wood smoke, and numerous viruses and fungi). She could be melodramatic, describing a future lifeless world and quoting Keats (“The sedge is wither’d from the lake, / And no birds sing”). But history would prove her correct about the unanticipated effects of widely used neurotoxins in the environment. She introduced a nation to the idea that human actions and the natural world were inextricably linked, and that people had some obligation to protect that world. The United States’ seminal environmental legislation of the 1970s can be traced back to the wide constituency she built.

Carson made
ecology
a household word. Moreover, she placed the human body squarely within that ecology. She described the rising rates of cancer since World War II, which launched a new era of synthetic organic chemicals. She pointed out that we are now living with persistent industrial chemicals in a way our ancestors never did. “For the first time in the history of the world, every human being is now subjected to contact with dangerous chemicals, from the moment of conception until death,” she wrote. Or
as The Who put it in 1966, “I was born with a plastic spoon in my mouth.”

Carson didn’t know that many of these compounds have the ability to alter human hormone systems, but she presciently described chemicals accumulating in the sex organs of birds and mammals and corresponding drops in sperm levels. She was struck by reports that roosters were losing their wattles and that sperm counts were found to be low in pilots who sprayed pesticides from the sky.

The term
endocrine disruptor
wouldn’t be coined for another thirty years, when a concerned group of wildlife biologists gathered to exchange research on everything from intersex fish to birds that refused to act like parents. To the scientists, the evidence was mounting that synthetic compounds in polluted areas, notably the Great Lakes, were altering the cells, bodies, and behavior of these animals in ways not seen before.

Until that time, most people thought synthetic estrogens showed up only where we intended them to, namely, in medication. But hormones are famously sneaky. They do their work in our bodies in infinitesimally small quantities. One molecule of a hormone fits into one receptor on a cell like a key in a lock, unleashing a chain of biochemical events. These are the keys that govern everything from cell division to metabolism to hair and breast growth to cognitive performance on spatial tasks. Hormonal changes during women’s monthly cycles affect how they smell things, how they perceive the faces and bodies of the opposite sex, and even how they think. Some studies show that when estrogen levels peak midmenstrual cycle, women reportedly get better at verbal and finemotor skills.

If a foreign imposter shows up on the receptor, however, the body’s responses become all but impossible to predict. Some foreign estrogens, called xenoestrogens, occupy the receptors so native estrogens can’t do their jobs. Others pass the security test and turn on estrogenic responses. Some seem to mess with the body’s feedback loops, causing the brain to release more or less hormone than it otherwise would.

It is now known that some imposters occur naturally, like estrogenic substances in plants. Why would plants bother to make estrogen mimics? For the same reason they make acids, poisons, and thorns. Plants are smart, or at least evolutionarily successful. One jaunty example is marijuana, which figured out how to make THC (tetrahydrocannabinol), a compound that happens to fit perfectly into pleasure receptors in the human brain, all but ensuring its spread around the world. Which begs the question, do humans cultivate marijuana, or is the plant actually cultivating its human growers? Marijuana also releases compounds that inhibit testosterone in people who consume it. Long-term male stoners are known to sometimes grow small breasts, and they also face increased risk of breast cancer. Is this a coincidence, or is the plant somehow benefiting from having less aggressive users who giggle easily and croon folk songs?

A couple of dozen plants are known to produce high levels of phytoestrogens, which essentially act as oral contraceptives, in order to knock back their predators. When sheep eat a particular strain of clover, they can’t reproduce. Humans have long taken advantage of these plant properties, using certain herbs and fruits to prevent pregnancy or induce miscarriage. Hippocrates knew that the seed of Queen Anne’s lace, when eaten, worked as a contraceptive and morning-after pill, as did an infusion of pennyroyal. Giant fennel,
found by the Greeks in the seventh century BC, was so coveted for the contraceptive trade that it was harvested to extinction.

ALL OF THIS WAS FAR FROM THE MIND OF PATRICIA HUNT IN 1998,
when she was working in her lab at Case Western Reserve University in Ohio. She is an experimental biologist with a fascination for aneuploidy, the chromosomal abnormalities that cause miscarriages or birth defects (like an extra copy of chromosome 21, which causes Down syndrome). These are the things that can go wrong in the earliest moments of conception and fetal development. Humans are supposed to have twenty-three pairs of chromosomes, but sometimes there’s a little, or big, miscalculation, especially in the eggs of older women. Hunt wanted to know why. She hoped studying mice would yield clues.

As was typical, she was working with mutant mice and some control, or normal, mice. One day, she noticed that her control mice, which were supposed to have healthy eggs, were producing a high rate—40 percent—of abnormal eggs, when the usual rate is 1 to 2 percent. Something had gone terribly wrong. “We checked everything,” she told me, “the air in the facility, were there pesticides coming in? It took us weeks. We finally noticed some wear and tear on the animals’ plastic cages.” It turned out a temporary worker was using the wrong detergent to clean the cages, and it was degrading the cage walls, causing a substance called bisphenol A to leach into the mice’s food and water.

Bisphenol A, or BPA, was an artificial estrogen developed in the 1930s as a possible drug to prevent miscarriages in women. It didn’t work for that, but the compound soon found other uses, like making polycarbonate plastic. BPA’s molecular structure is simple
and elegant: two joined hexagons, each made up of six bonded carbons. When these are neatly stacked to make a long-chain polymer, the material is incredibly strong. You can drive over a polycarbonate water bottle and it won’t break. It’s also cheap, derived as a byproduct of refining petroleum. Unfortunately, BPA’s versatile ring structure bears a close resemblance to estrogen. Now produced in mind-boggling quantities of two million pounds per year in the United States, for annual profits in excess of $6 billion, it’s in everything from the lining of canned food to dental sealants, to consumer products like CDs, cellphones, and bike helmets, to the shiny paper receipts we get from the grocery store. It was also in lab equipment at Case Western Reserve.

“I don’t think anybody in the aneuploidy field really believed in environmental effects. I know I didn’t,” said Hunt, who’s petite and trim, with short, tousled hair. “That fad came and went in the 1970s.” That was when, spurred by the connections suggested in
Silent Spring,
scientists realized that it was much harder to attribute disease to pollution than anyone expected. “We knew that maternal age was the huge, main event [for abnormal eggs], and that trying to see any other effect would be like trying to see a snowball fight in the midst of an avalanche. That’s why this really caught our attention,” she said.

Another, much more personal, endocrine effect caught her attention five years after the leaching-cage problem. Hunt was diagnosed with breast cancer. She knew she was a so-called DES daughter (her mother had taken diethylstilbestrol while pregnant) ever since she’d received abnormal pap-smear results in college. In other words, in the earliest beginnings of her own life, she was exposed to a potent hormone that wasn’t supposed to be there. Ironically, the drug that replaced BPA in the 1930s to prevent miscarriage was
DES, a more powerful estrogen (but alas, no better in hindsight at preventing miscarriage). Because of their early-life exposures, some DES daughters are known to suffer from rare, devastating reproductive cancers, malformed uteri, and higher-than-normal rates of breast cancer. When they’ve been able to bear children, their daughters are also more prone to breast cancer. DES sons have lower sperm counts and higher rates of genital birth defects. DES was not discontinued in pregnant women until 1971, nearly three decades after it was introduced. An estimated five million people were exposed through pregnancy, and many millions more consumed DES-tainted beef and poultry. Because of DES, scientists learned that chemicals can and do cross the placenta, which they once didn’t believe was possible.

Hunt has described these events as being twice struck by lightning. Two artificial estrogens were now determining her destiny. She’s since devoted her career to studying the strange and ominous effects of BPA in her mice. Hunt and numerous other researchers around the world have found that early-in-life exposures to BPA can cause early puberty, lower sperm counts, changes in mating behavior, predisposition to obesity, increased rates of breast and prostate cancers, and increased rates of miscarriages. All these troubles were observed in rodents, many of which were exposed while in their mothers’ wombs.

“The long-term ability to reproduce is my focus,” she explained from her immaculate lab, now housed in a spanking new building at Washington State University in Pullman. Her office is filled with “chromosome art,” prints and ceramics showing the spindly wormlike forms of the substance that begins all life. Her husband’s office down the hall sports a wooden lamp with a sperm-shaped pull cord.

Hunt showed me the basement “vivarium” where her strains of
mice live, the breeders, the studs, and the babies. She no longer uses cages made with BPA. She saves that for her experiments.

When she doses her mice with BPA, she sees abnormal behavior or cells in the mother, the pup, and, later, the pup’s children, for what she terms a “grandmaternal effect.” One dose effectively damages three generations, just as some researchers are seeing with DES and humans. Hunt’s studies are controversial because sometimes the results haven’t been replicated. Hunt has a reasonable explanation for this: the effects depend precisely on when the mice are exposed. “The developing fetus is exquisitely sensitive to environmental factors,” said Hunt. “There are critical windows, sometimes just one or two days long, in which a tiny dose of chemical can send the wrong message to cells, and other days when the window has shut and the mouse will develop normally.”

Depending on that timing, in the mama mouse ovaries she often sees eggs in which the chromosomes aren’t lining up right. Normally, these eggs shouldn’t even be viable, but for some reason, the body’s quality-control checks aren’t working to destroy them. “We want to see the earliest possible defects, and here it is,
bam.
It means we can see things in the early stages of making an egg that should lead to mistakes, and they do.” She showed me a magnified image of scattered red wormlike chromosomes, the confounding mistakes in germ-cell scaffolding caused by BPA—a “funny little beast,” as she calls it. Pointing to the worm pattern, she noted, “The chromosomes are completely disorganized. I wouldn’t want my eggs looking like that spaghetti.”

Looking at the images, I could almost feel my ovaries twisting up. But these were mouse eggs. Did her work have relevance for us?

“That [multigenerational effect] for me was huge,” said Hunt. “It would be a fifty-year problem in humans. We think these effects
are at doses that are environmentally relevant.” She was saying that people today are exposed to similar levels per body weight as her mice. “How would we see this in humans?” she asked. “Increasing rates of miscarriages, low sperm counts, testicular problems. We already do see that. How long will it be before we say, ‘Holy cow, are we crippling both sexes at once?’ “ Hunt is frustrated—passionate, even—that U.S. and many international agencies still have not taken a strong stance against BPA. (As of this writing, though, ten states have banned it for use in baby products. France has banned the substance from water bottles, and Denmark has banned it from food packaging meant for children under age three.) She reminded me of the once-staid climate scientists who have become some of the most outspoken critics of U.S. climate and energy policy. They know too much to keep quiet.