Chapter Twelve

The New Eugenics

Sometimes I wonder if I’m kidding myself. For the past ten years I’ve been searching for meaning, uplift, purpose in Becky’s dwarfism. But though I have couched my search in the language of such modern ideas as the value of diversity and equal treatment for the disabled, what I’m really up to may turn out to be very old-fashioned indeed. Even as I reject the notion that God metes out dwarfism either as punishment or as some murky sign of his favor, is it possible that I’ve been pursuing a false god of science, of progress, of reason? The genetic mutation that causes thanataphoric dwarfism is almost identical to the one that causes achondroplasia. With the former, you die shortly after birth; with the latter, you live and thrive and grow. Maybe the truth is that it’s all just random. My quest has been rewarding at times, frustrating at other times. But I have begun to realize that, like life itself, this quest is a journey with no destination.

For me, the whole notion of meaning was dealt its most lasting and significant setback at a news conference on July 29, 1994. It was on that day that a group of scientists, led by the geneticist John Wasmuth, announced in the journal Cell that they had discovered the mutation that causes achondroplasia. As I noted earlier, Wasmuth — who, tragically, died the following year — recommended that screening be limited to cases in which both the father and mother have achondroplasia and whose baby would thus have a one in four chance of inheriting the mutation from both parents, an invariably fatal condition known as double dominance. Even so, Wasmuth surely knew he had given us a taste of the fruit from the Tree of Knowledge. That knowledge could one day lead to the very disappearance of achondroplasia and other genetic forms of dwarfism, whether it be in five years, fifty years, or five hundred.

Despite this possibility, much of the early debate over the discovery of the achondroplasia mutation had to do with the opposite scenario: whether a dwarf couple might go to extraordinary lengths — including abortion — for the purpose of ensuring that their baby would be a dwarf. I’ve collected articles from publications such as Science News and the Journal of Medical Ethics that discuss the implications of such choices. Yet I’m not sure what those articles prove, except that scientific journals, and scientists themselves, are capable at times of being as sensationalistic as tabloid newspapers. Doctors and scientists I’ve spoken with in the dwarf community say they’re not aware of a dwarf couple’s ever having decided to terminate a pregnancy rather than become the parents of an average-size child. No, it’s not the sort of news that a husband and wife would announce in their hometown newspaper. But if such a thing had ever occurred, the presumption in the dwarfism field is that word would have gotten around.

Still, it could happen, couldn’t it? A study undertaken in 2001 of 186 people with achondroplasia showed that 75 percent believed it was “not at all important” or only “somewhat important” that they learn whether their child would be a dwarf or average-size. Yet 2 percent did report that they would consider abortion if they found out their child would not be a dwarf.

As I discovered one afternoon in Salt Lake City, Dave and Becky O’Hara were intensely familiar with that moral dilemma, even though they are most definitely not among the 2 percent. Both are achondroplastic. Becky was twenty-four when I interviewed them and is three feet nine inches tall. Dave was thirty-one and is four-foot-six. They’re the parents of an average-size son, Bryan, who at the age of eighteen months was already nearly as tall as his mother. The O’Haras learned that Bryan would be average-size through amniocentesis. That was fine with Dave, even good news, since he knew that his son wouldn’t have to experience the sort of dwarfism-related back problems he’d had. But Becky was upset.

“I went through a mourning period. I did,” she told me. “Because you grow up thinking that you’ll have a little person. That you’ll have a little person or a double-dominant. But the average is always just put in the back. Now I notice a lot more people with their average-size kids. But you grew up thinking you’ll have an achon kid. And I got scared. How am I going to control this kid? How am I going to carry him?”

I asked if they had ever considered abortion. “Oh, of course not,” Becky answered. “Never. I still love this baby. Now I wouldn’t change a thing about him.”

There was a certain irony in Becky O’Hara’s angst. The image that Little People of America has done so much to promote is one of normality, of families just like everybody else, dwarf parents, dwarf kids. She had so thoroughly internalized that image that she couldn’t imagine having a child who didn’t conform.

***

The fate of dwarfism is just the tip of this new world, a world of stem cells and cloning, of genetic engineering and designer babies, a world in which every child will fit someone’s definition of perfect. Or else. The promise and threat of this new science have implications that go far beyond the relatively small community of dwarfs and their families.

Indeed, within the disability-rights movement as a whole there are few issues as emotional, and as hotly debated. Having fought so hard and so long for the accommodations and respect and understanding they need to become full and equal participants in society, people with disabilities now face the prospect of elimination at the hands of people who don’t understand that their lives aren’t diminished — just different. Critics have referred to prenatal screening and selective abortion as the “new eugenics,” whose aim, as it was with eugenics in an earlier time, is to eliminate anyone who is different, to do away with diversity before it can arrive in the form of a new-born child. Leading thinkers such as Adrienne Asch, a professor at Wellesley College, argue that it’s morally wrong to use screening and abortion to do away with a whole range of disabilities, such as Down syndrome, hereditary deafness, spina bifida (not a genetic condition but a disability that can often be diagnosed in utero), blindness (Asch’s own disability), and the like. She writes:

As with discrimination more generally, with pre-natal diagnosis, a single trait stands in for the whole, the trait obliterates the whole. With both discrimination and prenatal diagnosis, nobody finds out about the rest. The tests send the message that there’s no need to find out about the rest.

But Asch pushes her argument too far. To an extent, she sounds like the spinal-cord-injury activists who criticize Christopher Reeve for working toward a cure. Well, okay, acceptance is the most important goal, and Reeve may in some small way be contributing to the notion that there’s something wrong with being paralyzed. But come on, the man just wants to walk again. There’s nothing wrong with that.

Asch writes that she opposes “using selective abortion to avoid any traits,” whether the case involves an able-bodied couple wishing to terminate a disabled fetus or a deaf or dwarf couple who want a baby with the same disability as they. Yet she also observes that she and other leading critics of selective abortion are actually pro-choice feminists in other contexts. Thus Asch appears to support abortion rights for any woman except when the decision is based on whether or not the fetus would be born with a disability.

To read Asch is to encounter a disability consciousness lurching toward extremism. At one point she criticizes not just the decision to abort a fetus that carries a disability, but also to discard “an otherwise implantable embryo” in which a genetically based disability has been found. Elsewhere, she expresses her disapproval of scientific literature that refers to the “risk” of having a child with, say, Down syndrome or spina bifida. The proper terminology, she explains, is “possibility” or “likelihood.”

In a sense, Adrienne Asch is the flip side of the ludicrous Princeton University philosopher Peter Singer, who is best known for writing that the parents of a seriously disabled new-born should be able to kill him within the first twenty-eight days of birth. Singer’s position may resonate in the case of some infants with heartbreaking, painful disabilities, and in fact the sort of euthanasia he advocates takes place quietly all the time. But his logic strikes most people, including me, as entirely lacking in any moral sense. He begins by writing about fatal conditions such as anencephaly — the absence of a brain — but then discusses at length cases involving Down syndrome and spina bifida. Talk about the slippery slope. It’s the difference between decisions being made by families and their doctors on the one hand, and enshrining such decisions in law and social policy on the other. As the journalist Michael Specter once wrote in the New Yorker, “Singer has never been afraid to take pure reason and drive it right over a cliff.” Asch, by contrast, takes a position that is highly moral but lacking in logic or, for that matter, any real understanding about how the world works.

Dorothy Wertz, a psychiatrist affiliated with the Eunice Kennedy Shriver Center, in Waltham, Massachusetts, spent considerable time and effort in trying to figure out exactly how the world works. To answer Adrienne Asch’s critique of genetic screening, Dr. Wertz joked that most abortions already take place for genetic reasons: half of the fetus’s genes are from a man with whom the woman does not wish to have a baby. From there, it is a short leap to choosing abortion for genetic reasons such as serious illness, not-so-serious illness, or conditions that simply don’t match the prospective parents’ vision of the perfect child.

I interviewed Wertz on a cold February day in the sunroom of her home on Massachusetts’s South Coast. Her husband was dying of lung cancer. She would die a year later. Nevertheless, she cut a flamboyant figure, tall and with a strong physical presence despite her advanced years, wearing a pillbox hat, turquoise earrings, and an enormous silver-and-turquoise necklace that looked heavy enough to weigh her down. I’d met her years earlier when I took part in a study she’d overseen regarding the attitudes that parents of disabled kids hold toward the medical establishment. I liked her forthright, down-to-earth manner. What I didn’t like so much was what she had learned about attitudes toward disability — including dwarfism.

In the late 1990s Wertz conducted a study of about two thousand people — 1,084 genetics professionals, 499 primary-care physicians, and 476 patients. One of the disabilities that participants were questioned about was achondroplasia. The results were stunning. Among the genetics professionals, 57 percent would choose abortion if it were detected in utero; among physicians, 29 percent; and among patients, 24 percent.

To bracket this, let me pull out two other findings. The first pertains to Down syndrome, certainly a serious genetic condition, but one not incompatible with a good quality of life. Here the proportion of genetics professionals who would abort was 80 percent; physicians, 62 percent; and patients, 36 percent. The second involves a genetic predisposition to severe obesity, which is not a disability at all, or even destiny. After all, parents can teach their kids to eat properly and lead healthy, active lives. Yet even in this instance, 29 percent of genetics professionals would choose to abort, as well as 13 percent of physicians and 8 percent of patients.

What’s frightening about all of this is that we are closer to screening for such conditions on a routine basis than many people realize. Some day — perhaps in a decade, perhaps two or three — it will be possible to lay out a person’s entire DNA on a computer chip, all thirty thousand or so genes, and compare that person’s DNA to the ideal. Such chips could be generated for early-term fetuses just as easily as for those already born. Once the use of such technology becomes routine, it would cost “mere pennies per test,” as Wertz has written, to screen fetuses for thousands of genetic conditions. Including, of course, achondroplasia and several other types of dwarfism.

Wertz’s study points to another potential concern. Across the board, her findings show that ordinary people are far less likely to choose abortion than are medical professionals. (To be sure, one in four ordinary couples would choose abortion if they learned their child would have achondroplasia, which is high by any measure.) Yet it is medical professionals who will counsel couples when they learn that the child they are expecting would have a disability. What kind of pressure will these professionals use to obtain what is, to some of them, the preferable result? If we had learned the fetus Barbara was carrying in the early spring of 1992 would have severe respiratory problems and could have a whole host of other complications as well, what would we have chosen to do? There was no Becky at that point, only a possibility. And the possibility would have sounded more frightening than hopeful.

Little People of America has long argued that prospective parents who learn that their child will have a type of dwarfism should be provided with information about the good lives that most dwarfs lead, and even be given a chance to meet dwarf children and adults. It’s a great idea. But will it happen? And at a time of skyrocketing medical costs, are there too many social pressures against that happening? There’s no doubt that, in many instances, abortion would be in the best interest of insurance companies. Think of all the money they could save if they refused to cover a fetus that has been diagnosed with a potentially expensive genetic condition. Some parents, of course, would not choose abortion because of their religious or moral beliefs. But what about the vast majority of us — the people who regularly tell pollsters that they’re pro-choice, although they may be deeply uncomfortable with abortion personally? Would they be able to resist — would they, should they, even attempt to resist — when faced with the possibility of financial ruin?

And abortion is just one part of this, a crude, archaic approach that will likely fade away with improvements in medical technology — improvements that will raise few of the moral qualms that so divide the culture today. For instance, when you think about it, sex is a really messy, random way of reproducing. Sure, it’s fun. But look at all the things that can and do go wrong. In his book Redesigning Humans, Gregory Stock argues that in vitro fertilization will someday be seen as the only proper way to have children. “With a little marketing by IVF clinics,” he writes, “traditional reproduction may begin to seem antiquated, if not downright irresponsible. One day, people may view sex as essentially recreational, and conception as something best done in the laboratory.”

Even average-size couples who wouldn’t abort a fetus with achondroplasia would, in all likelihood, choose against implanting an embryo with the mutation. You’ve got five embryos in that Petri dish over there, and you can only implant one. This one has the genetic mutation for Down syndrome; that one has the mutation for achondroplasia; the other three are mutation-free. All right, Professor Asch, which one do you think should be implanted?

And thus we will take another step down the road toward the “new eugenics” — a road that, in Stock’s utopian vision, will include artificial chromosomes to include spiffy new designer genes that will protect our descendants from disease, help them to live longer, and make them smarter, better, happier, and just generally imbued with oodles of wonderfulness.

Ultimately Stock posits a world in which we’re going to eliminate achondroplasia and hundreds, if not thousands, of other genetic conditions, predispositions, and tendencies. And we’re going to do it either by eliminating any individual whose genes we don’t like — or we’re going to change the genes.

***

Clair Francomano hunched over a desk in the corner of her office at the National Institutes of Health, in Baltimore, carefully drawing a chart to explain the genetics of dwarfism. Dr. Francomano, a longtime member of LPA’s medical-advisory board, was among the scientists who, along with the late John Wasmuth, helped discover the mutation that causes achondroplasia. Her article on how the mutation works was published in the New England Journal of Medicine about six months after Wasmuth’s article appeared in Cell.

Each of our cells has forty-six chromosomes, half from our mothers, half from our fathers. The achondroplasia mutation occurs on the short arm of chromosome 4, in roughly the same region that is responsible for Huntington’s chorea. In fact, the achondroplasia discovery was an outgrowth of research into Huntington’s. Achondroplasia involves a gene known as fibroblast growth factor receptor 3, or FGFR3. The purpose of FGFR3 is to regulate and, ultimately, to turn off — to shut down — the growth of the skeletal system at the right time in a person’s development. Because of the FGFR3 gene, sometime between the ages of fifteen and twenty we stop growing. Without the gene, our bones would keep getting longer and longer.

On the maps that geneticists use, the achondroplasia mutation can be found at location 380. Each location, also known as a codon, consists of three nucleotides, which in turn make up the twenty amino acids that are found in the cells of animals, including humans. (There are four nucleotides, abbreviated as A, C, G, and T. All amino acids, as well as some other substances, are made up of various three-nucleotide combinations.) Normally an amino acid known as glycine (CAG) is produced at codon 380. In achondroplasia, a single nucleotide is different: CAG becomes CGG, which is arginine. Arginine is a more active amino acid than glycine. So in a person with achondroplasia, the FGFR3 gene is too active — in effect, it’s stuck in the “on” position — and it slows down and distorts bone growth. The long bones of the arms and legs do not grow nearly as much as they would in an average-size person. The skull develops differently. The opening in the spinal column is smaller than it should be. The person is a dwarf.

“It’s operating in a manner that’s independent of the usual regulations, I would say,” Francomano explained. She added: “We don’t understand exactly how this mutation results in the effects that we see. There are a lot of people who have been working on this.”

Achondroplasia is just one of four types of dwarfism that have been traced to mutations of the FGFR3 gene, but the only one found at codon 380. The other three are all at codon 650, where, in an average-size person, the amino acid lysine is produced. If, instead of lysine, the amino acid is asparagine, then the person has hypochondroplasia, the mildest of the skeletal forms of dwarfism. If it’s methianine, the person has SADDAN, a recently discovered form of dwarfism that’s an acronym for “severe achondroplasia with developmental delay and acanthosis nigricans,” that last bit referring to skin discoloration that comes with the condition. If it’s glutanic acid, then the person has thanataphoric dwarfism, which results in death either at birth or shortly thereafter. One location, three different mutations, ranging from the most benign to the most lethal forms of dwarfism.

By understanding the genetic mutations that underlie dwarfism, it’s possible to visualize precisely how it might be treated or even eliminated. But transforming that vision into reality could be extraordinarily difficult. Let’s turn our attention back to achondroplasia. With genetic engineering, the middle “G” in CGG at codon 380 would be knocked out and replaced with an “A,” and the person literally would not have achondroplasia: she would be “cured” and would in all respects be no different from an average-size person. But for this to work, the change would have to be made in each of the body’s billions upon billions of cells, seemingly an impossible task. Francomano told me that performing such a feat at, say, the eight-cell stage, right after a fertilized ovum has developed from zygote to embryo, might be possible; but that presumes in vitro fertilization (IVF). And, as we have already seen, with IVF there is little reason to fix a genetic mutation in an embryo. It’s far easier to discard it and implant another embryo instead.

It would seemingly be more practical to treat the effects of the mutation rather than eliminate the mutation itself — to find a way to stop the FGFR3 gene from being hyperactive, to block the effect of the arginine, to get it to behave more like glycine, which would allow the long bones to grow normally and the spinal canal to open up. Here, too, the prospects of developing an effective treatment are daunting. Francomano told me that such a treatment would still have to get around the problem of modifying the behavior of the FGFR3 gene in each of the body’s cells.

Francomano is not alone in her skepticism. Among the most experienced dwarfism doctors in the world is Charles Scott, a semi-retired geneticist based at the Alfred I. duPont Hospital for Children, in Wilmington, Delaware. Dr. Scott, who chaired LPA’s medical-advisory board from 1969 to 2000, still follows some four hundred patients. I spent a day with him as he made the clinical rounds. Unlike the intense, almost frantic days put in by Michael Ain and Dror Paley, Scott will give an hour or more to each patient, asking questions, listening carefully to the answers, joking, measuring, pulling out an old Polaroid camera to take pictures for his files. Of course, Scott’s job is different: he’s not a surgeon, and he follows his patients over a period of years rather than through one acute surgical episode. Still, watching him examine kids whose needs range from the minimal (such as Abby Trifone, a nine-year-old achon from Connecticut who’s so healthy that she plays lacrosse) to the complicated (such as twelve-year-old Danielle Frank, from Pennsylvania, whose achondroplasia has required several surgeries for spinal compression and who was in a wheelchair when I met her) was to observe someone with unusual empathy and patience.

Like Francomano, Scott was dubious when I asked him about the prospect for treatment either by manipulating the genes or by somehow modifying their behavior. “The actual cure, in my opinion — your great-great-great-grandchildren may benefit from it,” he told me. “It’s a lot of hype by the feds and the people in research. It’s not going to help anyone who has it who’s alive today. Not at all. Because the gene is in every cell, and you’re made up of ten to the twenty-seventh power. How could you fix a gene in that many cells?”

***

And yet there remains the fact that people are trying. A few months ago I received a packet of information from the mother of a baby girl with achondroplasia, a mother with a Ph.D. and a scientific background and a dream that her daughter won’t have to go through life as a dwarf. The information pertained to an Israeli company, ProChon Biotech, founded in 1997 by a scientist named Avner Yayon.

Among the products that ProChon is working on is a treatment for achondroplasia that will slow down the activity of the FGFR3 gene — that will “prevent or decrease the level of signal transmitted through the receptor,” as the company’s Web site (www.prochon.com) puts it. Clinical trials could begin as early as 2003, according to ProChon. Treatment would likely take the form of a drug that would be injected on a regular basis from infancy through adolescence. And despite the skepticism expressed by Dr. Francomano and Dr. Scott, the medication apparently would not have to reach each of the body’s cells: according to an e-mail I received from Myriam Golembo, project manager for skeletal genetics at ProChon, the drug would only need to target FGFR3 activity in the growth plates of the bones. “Although definitely not a trivial task,” she said, “it is somehow less daunting.”

Is this real? Is the end of achondroplasia at hand, at least for those with the money and the ambition to seek treatment? I have to admit that I’m skeptical. American dwarfism specialists whom I interviewed, including Francomano and Scott, were only slightly aware of ProChon. And, as we all know, new medical treatments can have unproven consequences.

The type of dwarfism caused by growth-hormone deficiency, as I noted earlier, has been all but eliminated in the United States through injections of human growth hormone, or hGH. But those who began treatment in the 1960s and 1970s got their hGH from the pituitary glands of cadavers, leading some to develop Creutzfeldt-Jakob disease, a devastating, fatal brain illness that is similar to mad-cow disease. Today’s synthetic hGH is presumably safe. Yet there remain unanswered questions as to whether even synthetic hGH might be associated with a greater likelihood of developing cancer. What once looked like a cure for one type of dwarfism now carries with it unanticipated complications and ethical dilemmas.

Let’s say that, when Becky is twelve or thirteen, ProChon’s treatment for achondroplasia is determined to be safe and effective. (This is merely hypothetical, since it assumes an unimaginably fast review-and-approval process by the Food and Drug Administration.) I’m not sure she could even benefit at that age, coming so late in her growth. And, naturally, I would worry about side effects that might not crop up for decades. But it would be tempting to try and to give her treatments until her mid- to late teens. I don’t much care if she might end up two or three inches taller. But if her spinal canal opened up a little more, if her back straightened out a bit, if her arms grew another inch or so — now those are changes that would give her a healthier, easier, more convenient, more pain-free life.

Little people I’ve talked with understand this. To a person, they vociferously object to limb-lengthening, yet have no such philosophical problems with the idea of a cure or a genetically based treatment. They see one as torture, as a brutal attempt to make dwarfs fit the human-made environment rather than the other way around. But they see the other as a natural product of scientific research, a medical treatment no different from any other medical treatment.

Daniel Margulies, a past president of Little People of America, already knows what it’s like to have seen his form of dwarfism eliminated. Margulies’s is a rare case: he got Crohn’s disease as a child. Combined with familial shortness, he ended up being four-foot-eight. With today’s Crohn’s treatments, though, the disease would have affected him to a much lesser extent. He thinks he probably would have been at least as tall as his brothers, who are five-foot-four and five-foot-six.

“I tell people I had to learn to become a dwarf,” Margulies said. “Up until I was a sophomore in high school or thereabouts, the doctors told me, ‘You will grow. You’re going to get a growth spurt.’ Finally, they said, ‘You’re not going to grow. This is your final height, and you need to learn to accept it.’ And when the quote-unquote experts have been telling you for years that you’re going to grow, and to suddenly be told okay, this is it, learn to deal with it — as a teenager, it’s a huge, huge culture shock.”

Perhaps because of his personal experience, Margulies understands that more traditional forms of dwarfism may some day be cured as well. “Just as a total lay person who reads the news, I would not be surprised if in thirty years, forty years, if not sooner, somebody’s going to say, ‘If your child is born an achon, we can now do this, this, and this,’ and they will manifest none of the orthopedic structures of an achondroplastic dwarf.”

I asked Margulies how popular such a treatment would be. “I would say 95 percent of average-size parents would do this,” he replied. “And speaking only for myself and not the organization by any means, I would understand it and see no problem with it. I suspect a large segment of LPA would feel the same way.”

But would we be losing something? Would the culture be poorer if dwarfism — or at least the most common form of dwarfism — were eliminated? “Well, my opinion is yes,” Margulies said. “You lose diversity, and is diversity good? Yes. Nature has created sex on purpose — half of the genes from each parent, and that creates diversity. Socially, I suspect the same thing. I guess the philosophical question is to what degree is it my responsibility as a parent of a dwarf child to be responsible for that diversity. Why is it put on me? It makes for an interesting philosophical discussion that has no right answer.”

And the truth is that if there had been a safe, effective, proven treatment for achondroplasia when Becky was born, Barbara and I would have chosen it without hesitation. How could we not have? I understand and respect dwarf parents who want their own children to be dwarfs. But for the average-size parents of a baby who’s just been diagnosed with achondroplasia? Frankly, I suspect Margulies’s estimate that 95 percent would seek treatment is approximately 5 percent too low.

Genetic diversity may be what’s best for the human race, but giving Becky the gift of health and normality — of a life free of backaches or even paralysis, of respiratory problems, of hearing loss, of orthopedic surgery . . . hell, of discrimination, of being stared at, pointed to, snickered about — well, what parent wouldn’t do that? The truth is that dwarfism has been a lot better for me than it’s been for Becky. After all, I’ve met a lot of interesting people, broadened my horizons, even got a book contract out of it. I’d like to think it’s taught me to be a better, more sensitive person, more attuned to people who are different, and a more caring, patient father. But how, precisely, has dwarfism benefited her?

That’s harsh. It may seem like a negation of Becky’s place in the dwarf community, as a rebuke to our friends in LPA. I don’t think it is. Certainly they, more than I, understand how difficult it can be to live with dwarfism. I would even go so far as to say that I admire their courage, except that — as Benedict Lambert, the brilliant geneticist with achondroplasia who is the lead character of Simon Mawer’s novel Mendel’s Dwarf, puts it — “In order to be brave, you’ve got to have a choice.”

Barbara and I would have chosen not to be brave and not to have forced our daughter to be brave. We would have sought treatment for the effects of Becky’s mutated gene just as readily as we would for any other medical condition. Diversity may be a good thing, but, as Daniel Margulies observed, I can’t see why the responsibility is ours. Eliminating achondroplasia from the gene pool may have unintended consequences, consequences society will one day regret. But eliminating achondroplasia from the genes of Rebecca Elizabeth Kennedy, or somehow countering the effects of her overactive FGFR3 gene, would have been an entirely good thing.

In the decades to come, such dilemmas will only multiply. Any mother, for instance, would choose to fix her child’s genetic predisposition for bipolar disorder, or manic depression, as it used to be called. It’s a devastating mental illness. Yet if you took away Robert Schumann’s manic depression, he might not have been a musical genius. A non-bipolar Abbie Hoffman might be a living but unknown college professor instead of a dead, wildly creative political iconoclast. Or consider homosexuality, which scientists today regard not as an illness at all but, rather, a normal part of human variation. If a genetic proclivity for same-sex attraction is ever discovered, and indeed there are researchers looking for such a variation, then many parents may opt to edit out that trait as well. Some may do it out of fear or prejudice, but others may simply believe that life as a lesbian or as a gay man is just too hard. Who doesn’t want to make life easier for their kids? But what will we have lost?

I’ve come to realize that my quest for meaning — my goal of attaching some larger significance to Becky’s dwarfism — is every bit as limited by my cultural preconceptions and the era in which I live as those who, in decades past, thought that disability was a sign of God’s displeasure. The quest is worthwhile, but the destination keeps receding, even as I keep moving toward it.

What’s truly meaningful is to be the best parent you can be.

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