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Tag: red blood cells

  • The CRISPR Era Is Here

    The CRISPR Era Is Here

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    When Victoria Gray was still a baby, she started howling so inconsolably during a bath that she was rushed to the emergency room. The diagnosis was sickle-cell disease, a genetic condition that causes bouts of excruciating pain—“worse than a broken leg, worse than childbirth,” one doctor told me. Like lightning crackling in her body is how Gray, now 38, has described the pain. For most of her life, she lived in fear that it could strike at any moment, forcing her to drop everything to rush, once again, to the hospital.

    After a particularly long and debilitating hospitalization in college, Gray was so weak that she had to relearn how to stand, how to use a spoon. She dropped out of school. She gave up on her dream of becoming a nurse.

    Four years ago, she joined a groundbreaking clinical trial that would change her life. She became the first sickle-cell patient to be treated with the gene-editing technology CRISPR—and one of the first humans to be treated with CRISPR, period. CRISPR at that point had been hugely hyped, but had largely been used only to tinker with cells in a lab. When Gray got her experimental infusion, scientists did not know whether it would cure her disease or go terribly awry inside her. The therapy worked—better than anyone dared to hope. With her gene-edited cells, Gray now lives virtually symptom-free. Twenty-nine of 30 eligible patients in the trial went from multiple pain crises every year to zero in 12 months following treatment.

    The results are so astounding that this therapy, from Vertex Pharmaceuticals and CRISPR Therapeutics, became the first CRISPR medicine ever approved, with U.K. regulators giving the green light earlier this month; the FDA appears prepared to follow suit in the next two weeks. No one yet knows the long-term effects of the therapy, but today Gray is healthy enough to work full-time and take care of her four children. “Now I’ll be there to help my daughters pick out their wedding dresses. And we’ll be able to take family vacations,” she told NPR a year after her treatment. “And they’ll have their mom every step of the way.”

    The approval is a landmark for CRISPR gene editing, which was just an idea in an academic paper a little more than a decade ago—albeit one already expected to cure incurable diseases and change the world. But how, specifically? Not long after publishing her seminal research, Jennifer Doudna, who won the Nobel Prize in Chemistry with Emmanuelle Charpentier for their pioneering CRISPR work, met with a doctor on a trip to Boston. CRISPR could cure sickle-cell disease, he told her. On his computer, he scrolled through DNA sequences of cells from a sickle-cell patient that his lab had already edited with CRISPR. “That, for me, personally, was one of those watershed moments,” Doudna told me. “Okay, this is going to happen.” And now, it has happened. Gray and patients like her are living proof of gene-editing power. Sickle-cell disease is the first disease—and unlikely the last—to be transformed by CRISPR.

    All of sickle-cell disease’s debilitating and ultimately deadly effects originate from a single genetic typo. A small misspelling in Gray’s DNA—an A that erroneously became a T—caused the oxygen-binding hemoglobin protein in her blood to clump together. This in turn made her red blood cells rigid, sticky, and characteristically sickle shaped, prone to obstructing blood vessels. Where oxygen cannot reach, tissue begins to die. Imagine “if you put a tourniquet on and walked away, or if you were having a heart attack all the time,” says Lewis Hsu, a pediatric hematologist at the University of Illinois at Chicago. These obstructions are immensely painful, and repeated bouts cause cumulative damage to the body, which is why people with sickle cell die some 20 years younger on average.

    Not everyone with the sickle-cell mutation gets quite so sick. As far back as the 1940s, a doctor noticed that the blood of newborns with sickle-cell disease did not, surprisingly, sickle very much. Babies in the womb actually make a fetal version of the hemoglobin protein, whose higher affinity for oxygen pulls the molecule out of their mother’s blood. At birth, a gene that encodes fetal hemoglobin begins to turn off. But adults do sometimes still make varying amounts of fetal hemoglobin, and the more they make, scientists observed, the milder their sickle-cell disease, as though fetal hemoglobin had stepped in to replace the faulty adult version. Geneticists eventually figured out the exact series of switches our cells use to turn fetal hemoglobin on and off. But there, they remained stuck: They had no way to flip the switch themselves.

    Then came CRISPR. The basic technology is a pair of genetic scissors that makes fairly precise cuts to DNA. CRISPR is not currently capable of fixing the A-to-T typo responsible for sickle cell, but it can be programmed to disable the switch suppressing fetal hemoglobin, turning it back on. Snip snip snip in billions of blood cells, and the result is blood that behaves like typical blood.

    Sickle cell was a “very obvious” target for CRISPR from the start, says Haydar Frangoul, a hematologist at the Sarah Cannon Research Institute in Nashville, who treated Gray in the trial. Scientists already knew the genetic edits necessary to reverse the disease. Sickle cell also has the advantage of affecting blood cells, which can be selectively removed from the body and gene-edited in the controlled environment of a lab. Patients, meanwhile, receive chemotherapy to kill the blood-producing cells in their bone marrow before the CRISPR-edited ones are infused back into their body, where they slowly take root and replicate over many months.

    It is a long, grueling process, akin to a bone-marrow transplant with one’s own edited cells. A bone-marrow transplant from a donor is the one way doctors can currently cure sickle-cell disease, but it comes with the challenge of finding a matched donor and the risks of an immune complication called graft-versus-host disease. Using CRISPR to edit a patient’s own cells eliminates both obstacles. (A second gene-based therapy, using a more traditional engineered-virus technique to insert a modified adult hemoglobin gene into DNA semi-randomly, is also expected to receive FDA approval  for sickle-cell disease soon. It seems to be equally effective at preventing pain crises so far, but development of the CRISPR therapy took much less time.)

    In another way, though, sickle-cell disease is an unexpected front-runner in the race to commercialize CRISPR. Despite being one of the most common genetic diseases in the world, it has long been overlooked because of whom it affects: Globally, the overwhelming majority of sickle-cell patients live in sub-Saharan Africa. In the U.S., about 90 percent are of African descent, a group that faces discrimination in health care. When Gray, who is Black, needed powerful painkillers, she would be dismissed as an addict seeking drugs rather than a patient in crisis—a common story among sickle-cell patients.

    For decades, treatment for the disease lagged too. Sickle-cell disease has been known to Western medicine since 1910, but the first drug did not become available until 1998, points out Vence Bonham, a researcher at the National Human Genome Research Institute who studies health disparities. In 2017, Bonham began convening focus groups to ask sickle-cell patients about CRISPR. Many were hopeful, but some had misgivings because of the history of experimentation on Black people in the U.S. Gray, for her part, has said she never would have agreed to the experimental protocol had she been offered it at one of the hospitals that had treated her poorly. Several researchers told me they hoped the sickle-cell therapy would make a different kind of history: A community that has been marginalized in medicine is the first in line to benefit from CRISPR.

    Doctors aren’t willing to call it an outright “cure” yet. The long-term durability and safety of gene editing are still unknown, and although the therapy virtually eliminated pain crises, Hsu says that organ damage can accumulate even without acute pain. Does gene editing prevent all that organ damage too? Vertex, the company that makes the therapy, plans to monitor patients for 15 years.

    Still, the short-term impact on patients’ lives is profound. “We wouldn’t have dreamed about this even five, 10 years ago,” says Martin Steinberg, a hematologist at Boston University who also sits on the steering committee for Vertex. He thought it might ameliorate the pain crises, but to eliminate them almost entirely? It looks pretty damn close to a cure.

    In the future, however, Steinberg suspects that this currently cutting-edge therapy will seem like only a “crude attempt.” The long, painful process necessary to kill unedited blood cells makes it inaccessible for patients who cannot take months out of their life to move near the limited number of transplant centers in the U.S.—and inaccessible to patients living with sickle-cell disease in developing countries. The field is already looking at techniques that can edit cells right inside the body, a milestone recently achieved in the liver during a CRISPR trial to lower cholesterol. Scientists are also developing versions of CRISPR that are more sophisticated than a pair of genetic scissors—for example, ones that can paste sequences of DNA or edit a single letter at a time. Doctors could one day correct the underlying mutation that causes sickle-cell disease directly.

    Such breakthroughs would open CRISPR up to treating diseases that are out of reach today, either because we can’t get CRISPR into the necessary cells or because the edit is too complex. “I get emails now daily from families all over the world asking, ‘My son or my loved one has this disease. Can CRISPR fix it?’” says Frangoul, who has become known as the first doctor to infuse a sickle-cell patient in a CRISPR trial. The answer, usually, is not yet. But clinical trials are already under way to test CRISPR in treating cancer, diabetes, HIV, urinary tract infections, hereditary angioedema, and more. We have opened the book on CRISPR gene editing, Frangoul told me, but this is not the final chapter. We may still be writing the very first.

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    Sarah Zhang

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  • Someday, You Might Be Able to Eat Your Way Out of a Cold

    Someday, You Might Be Able to Eat Your Way Out of a Cold

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    When it comes to treating disease with food, the quackery stretches back far. Through the centuries, raw garlic has been touted as a home treatment for everything from chlamydia to the common cold; Renaissance remedies for the plague included figs soaked in hyssop oil. During the 1918 flu pandemic, Americans wolfed down onions or chugged “fluid beef” gravy to keep the deadly virus at bay.

    Even in modern times, the internet abounds with dubious culinary cure-alls: apple-cider vinegar for gonorrhea; orange juice for malaria; mint, milk, and pineapple for tuberculosis. It all has a way of making real science sound like garbage. Research on nutrition and immunity “has been ruined a bit by all the writing out there on Eat this to cure cancer,” Lydia Lynch, an immunologist and a cancer biologist at Harvard, told me.

    In recent years, though, plenty of legit studies have confirmed that our diets really can affect our ability to fight off invaders—down to the fine-scale functioning of individual immune cells. Those studies belong to a new subfield of immunology sometimes referred to as immunometabolism. Researchers are still a long way off from being able to confidently recommend specific foods or dietary supplements for colds, flus, STIs, and other infectious illnesses. But someday, knowledge of how nutrients fuel the fight against disease could influence the way that infections are treated in hospitals, in clinics, and maybe at home—not just with antimicrobials and steroids but with dietary supplements, metabolic drugs, or whole foods.

    Although major breakthroughs in immunometabolism are just now arriving, the concepts that underlie them have been around for at least as long as the quackery. People have known for millennia that in the hours after we fall ill, our appetite dwindles; our body feels heavy and sluggish; we lose our thirst drive. In the 1980s, the veterinarian Benjamin Hart argued that those changes were a package deal—just some of many sickness behaviors, as he called them, that are evolutionarily hardwired into all sorts of creatures. The goal, Hart told me recently, is to “help the animal stay in one place and conserve energy”—especially as the body devotes a large proportion of its limited resources to igniting microbe-fighting fevers.

    The notion of illness-induced anorexia (not to be confused with the eating disorder anorexia nervosa) might seem, at first, like “a bit of a paradox,” says Zuri Sullivan, an immunologist at Harvard. Fighting pathogenic microbes is energetically costly—which makes eating less a very counterintuitive choice. But researchers have long posited that cutting down on calories could serve a strategic purpose: to deprive certain pathogens of essential nutrients. (Because viruses do not eat to acquire energy, this notion is limited to cell-based organisms such as bacteria, fungi, and parasites.) A team led by Miguel Soares, an immunologist at the Instituto Gulbenkian de Ciência, in Portugal, recently showed that this exact scenario might be playing out with malaria. As the parasites burst out of the red blood cells where they replicate, the resulting spray of heme (an oxygen-transporting molecule) prompts the liver to stop making glucose. The halt seems to deprive the parasites of nutrition, weakening them and tempering the infection’s worst effects.

    Read: Why science can be so indecisive about nutrition

    Cutting down on sugar can be a dangerous race to the bottom: Animals that forgo food while they’re sick are trying to starve out an invader before they themselves run out of energy. Let the glucose boycott stretch on too long, and the dieter might develop dangerously low blood sugar —a common complication of severe malaria—which can turn deadly if untreated. At the same time, though, a paucity of glucose might have beneficial effects on individual tissues and cells during certain immune fights. For example, low-carbohydrate, high-fat ketogenic diets seem to enhance the protective powers of certain types of immune cells in mice, making it tougher for particular pathogens to infiltrate airway tissue.

    Those findings are still far from potential human applications. But Andrew Wang, an immunologist and a rheumatologist at Yale, hopes that this sort of research could someday yield better clinical treatments for sepsis, an often fatal condition in which an infection spreads throughout the body, infiltrating the blood. “It’s still not understood exactly what you’re supposed to feed folks with sepsis,” Wang told me. He and his former mentor at Yale, Ruslan Medzhitov, are now running a clinical trial to see whether shifting the balance of carbohydrates and lipids in their diet speeds recovery for people ill with sepsis. If the team is able to suss out clear patterns, doctors might eventually be able to flip the body’s metabolic switches with carefully timed doses of drugs, giving immune cells a bigger edge against their enemies.

    But the rules of these food-illness interactions, to the extent that anyone understands them, are devilishly complex. Sepsis can be caused by a whole slew of different pathogens. And context really, really matters. In 2016, Wang, Medzhitov, and their colleagues discovered that feeding mice glucose during infections created starkly different effects depending on the nature of the pathogen driving disease. When the mice were pumped full of glucose while infected with the bacterium Listeria, all of them died—whereas about half of the rodents that were allowed to give in to their infection-induced anorexia lived. Meanwhile, the same sugary menu increased survival rates for mice with the flu.

    In this case, the difference doesn’t seem to boil down to what the microbe was eating. Instead, the mice’s diet changed the nature of the immune response they were able to marshal—and how much collateral damage that response was able to inflict on the body, as James Hamblin wrote for The Atlantic at the time. The type of inflammation that mice ignited against Listeria, the team found, could imperil fragile brain cells when the rodents were well fed. But when the mice went off sugar, their starved livers started producing an alternate fuel source called ketone bodies—the same compounds people make when on a ketogenic diet—that helped steel their neurons. Even as the mice fought off their bacterial infections, their brain stayed resilient to the inflammatory burn. The opposite played out when the researchers subbed in influenza, a virus that sparks a different type of inflammation: Glucose pushed brain cells into better shielding themselves against the immune system’s fiery response.

    Read: Feed a cold, don’t starve it

    There’s not yet one unifying principle to explain these differences. But they are a reminder of an underappreciated aspect of immunity. Surviving disease, after all, isn’t just about purging a pathogen from the body; our tissues also have to guard themselves from shrapnel as immune cells and microbes wage all-out war. It’s now becoming clear, Soares told me, that “metabolic reprogramming is a big component of that protection.” The tactics that thwart a bacterium like Listeria might not also shield us from a virus, a parasite, or a fungus; they may not be ideal during peacetime. Which means our bodies must constantly toggle between metabolic states.

    In the same way that the types of infections likely matter, so do the specific types of nutrients: animal fats, plant fats, starches, simple sugars, proteins. Like glucose, fats can be boons in some contexts but detrimental in others, as Lynch has found. In people with obesity or other metabolic conditions, immune cells appear to reconfigure themselves to rely more heavily on fats as they perform their day-to-day functions. They can also be more sluggish when they attack. That’s the case for a class of cells called natural killers: “They still recognize cancer or a virally infected cell and go to it as something that needs to be killed,” Lynch told me. “But they lack the energy to actually kill it.” Timing, too, almost certainly has an effect. The immune defenses that help someone expunge a virus in the first few days of an infection might not be the ones that are ideal later on in the course of disease.

    Even starving out bacterial enemies isn’t a surefire strategy. A few years ago, Janelle Ayres, an immunologist at the Salk Institute for Biological Studies, and her colleagues found that when they infected mice with Salmonella and didn’t allow the rodents to eat, the hungry microbes in their guts began to spread outside of the intestines, likely in search of food. The migration ended up killing tons of their tiny mammal hosts. Mice that ate normally, meanwhile, fared far better—though the Salmonella inside of them also had an easier time transmitting to new hosts. The microbes, too, were responding to the metabolic milieu, and trying to adapt. “It would be great if it was as simple as ‘If you have a bacterial infection, reduce glucose,’” Ayres said. “But I think we just don’t know.”

    All of this leaves immunometabolism in a somewhat chaotic state. “We don’t have simple recommendations” on how to eat your way to better immunity, Medzhitov told me. And any that eventually emerge will likely have to be tempered by caveats: Factors such as age, sex, infection and vaccination history, underlying medical conditions, and more can all alter people’s immunometabolic needs. After Medzhitov’s 2016 study on glucose and viral infections was published, he recalls being dismayed by a piece from a foreign outlet circulating online claiming that “a scientist from the USA says that during flu, you should eat candy,” he told me with a sigh. “That was bad.”

    Read: You can’t “starve” cancer, but you might help treat it with food

    But considering how chaotic, individualistic, and messy nutrition is for humans, it shouldn’t be a surprise that the dietary principles governing our individual cells can get pretty complicated too. For now, Medzhitov said, we may be able to follow our instincts. Our bodies, after all, have been navigating this mess for millennia, and have probably picked up some sense of what they need along the way. It may not be a coincidence that during viral infections, “something sweet like honey and tea can really feel good,” Medzhitov said. There may even be some immunological value in downing the sick-day classic, chicken soup: It’s chock-full of fluid and salts, helpful things to ingest when the body’s electrolyte balance has been thrown out of whack by disease.

    The science around sickness cravings is far from settled. Still, Sullivan, who trained with Medzhitov, jokes that she now feels better about indulging in Talenti mango sorbet when she’s feeling under the weather with something viral, thanks to her colleagues’ 2016 finds. Maybe the sugar helps her body battle the virus without harming itself; then again, maybe not. For now, she figures it can’t hurt to dig in.

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    Katherine J. Wu

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  • Is Cord-Blood Banking Worth It?

    Is Cord-Blood Banking Worth It?

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    In the fall of 1988, Matthew Farrow, a 5-year-old boy with a rare blood disorder, received the world’s first transplant of umbilical-cord blood from a newborn sibling. It worked: Farrow was cured. This miraculous outcome broke open a whole new field in medicine—and, not long after, a whole new industry aimed at getting expecting parents to bank their baby’s umbilical-cord blood, just in case.

    These days, in fact, being pregnant means being bombarded at the doctor’s office and on Instagram with ads touting cord blood as too precious to waste. For several hundred dollars upfront, plus a storage fee of $100 to $200 every year, the banks’ ads proclaim, you could save your child’s life. Cord-blood banking has been likened to a “biological insurance policy.”

    In the U.S., the two biggest private cord blood banks are Cord Blood Registry and ViaCord. Together, they have collected more than 1 million units. But only a few hundred units of this privately banked cord blood have ever been used in transplant, the great majority by families who chose to bank because they already had a child with a specific and rare disorder treatable with transplant. For everyone else, the odds of using privately banked cord blood are minuscule—so minuscule that the American Academy of Pediatrics (AAP) recommends against private banking. It does make an exception for families with that disease history. “But that’s a rare circumstance,” says Steve Joffe, a pediatric oncologist and ethicist at the University of Pennsylvania, “and not one that anybody is going to build a successful business model around.”

    ViaCord and Cord Blood Registry do offer free services for families in which someone has already been diagnosed with a condition treatable with cord blood. In general, the companies reiterated to me, cord blood does save lives and they are simply providing an option for families who want it.

    But the marketing also gives the impression of much more expansive uses for cord blood. The private banks’ websites list nearly 80 diseases treatable with transplant—an impressive number, though many are extremely uncommon or closely related to one another. (For example: refractory anemia, refractory anemia with ringed sideroblasts, refractory anemia with excess blasts, refractory anemia with excess blasts in transformation.) They have also recently taken to highlighting the promise of still-unproven treatments: Temporary infusions of cord blood, they say, could eventually treat more common conditions such as cerebral palsy and autism. Video testimonials feature parents talking excitedly about the potential of cord blood for their children. But the evidence isn’t there yet—and may never appear. Nonetheless, says Paul Knoepfler, a stem-cell scientist at UC Davis, “the cord-blood companies seem to be trying to expand their base of potential customers.”

    The initial exuberance around cord blood came from a real place. The blood left over in umbilical cords is replete with cells that have the special ability to turn into any kind of blood, including red blood cells, which carry oxygen, and white blood cells, which make up the immune system. Adults have stem cells in their bone marrow and blood—which can also be used for transplant—but those in a baby’s umbilical cord are more immunologically naive. That means they are less likely to go awry and attack a recipient’s body. “They don’t cause as much havoc,” says Karen Ballen, an oncologist at the University of Virginia. This allows doctors to use cord blood that matches only four out of six immunological markers.

    Because cord blood is so valuable, publicly run banks have been collecting donations since the 1990s. Despite amassing fewer units overall, public banks worldwide have provided 30 times as many units of blood for treatment—and saved more lives—than private ones, because they are accessible by any patient in need. Although the AAP recommends against private banking, it does recommend donating to public banks.

    One appeal of private banking, though, as the companies highlight, is that the cells in a baby’s umbilical cord are a perfect match for them in later childhood or adulthood. But this is usually irrelevant: In most of the diseases that can be cured by a cord-blood transplant, doctors would, for medical reasons, not use the patient’s own cells. In cases of inherited disorders such as sickle cell anemia, for example, a child’s own cord-blood stems have the same problematic mutation. For children with one of many types of leukemia, the concern is that cord blood could contain leukemia-precursor cells that cause the cancer to reappear; in addition, donor blood-stem cells are better because they can mop up remaining leukemia cells. Doctors would “never” use banked cord blood from a child with these types of leukemia, says Joanne Kurtzberg, a pediatrician and cord-blood pioneer at Duke University, who helped treat Farrow when he was a young boy.

    When privately banked cord blood is used in transplants, it is more likely to go to a sibling. Genetically, siblings have about a 25 percent chance of being perfect matches for each other. The chances of finding a suitable match among unrelated bone-marrow or cord-blood donors from a public bank, on the other hand, range from 29 to 79 percent, depending on one’s ethnic background. (The majority of donors are white, so it’s highest for white patients.) In any case, not banking a matched sibling’s cord blood doesn’t foreclose the possibility of a transplant, because that sibling can still donate bone marrow. “I often encounter families who have some guilt around not storing the cord blood, and I will point out, ‘Well, your donor child that matches our patient is still here,’” says Ann Haight, a pediatric hematologist and oncologist at Emory University.

    Even if a baby’s cord blood is banked, there’s no guarantee that it will contain enough cells for transplant. In fact, most may not: Public banks only keep 5 to 40 percent of their donations, as the rest don’t meet their standards. Private banks will save much smaller samples, which they argue serve a different purpose. Whereas public banks are looking for large samples that are mostly likely to be used for transplant, says Kate Giradi, the director of medical and scientific affairs at ViaCord, “when families are banking with us, this is that child’s only cord, so our threshold is way lower.”

    Another reason to bank these smaller samples, a spokesperson for Cord Blood Registry pointed out, is that they can still be used for experimental infusions treating conditions such as cerebral palsy and autism. (About 80 percent of units released by CBR have been used this way, as have about half from ViaCord.) The private banks partner with researchers, such as Kurtzberg at Duke, who are running clinical trials to test these treatments. The theory goes that cells from cord blood can make it to the brain, where they might have some neuroprotective role—but the mechanism remains unknown, and the effects are not entirely clear. As Kurtzberg told me, “The therapy is not proven.”

    The current state of cord-blood science might be summed up thus: Proven uses are very uncommon, and unproven uses are, well, unproven. Of course, a future discovery could lead to a real breakthrough in the use of stem cells from cord blood—an idea private banks trade on. Who knows what might be in store for cord blood later, when your baby is 30, 50, 70 years old? In a recent Cord Blood Registry survey of new parents, a spokesperson told me by email, 45 percent named “belief in future treatments” as the primary reason for banking their child’s cord blood and tissue. Knoepfler, the stem-cell scientist, notes that scientists have been excited for decades about the promise of stem cells. But translating interesting results in the lab to a doctor’s office, he says, “​​is really much harder than many of us realized. I include myself in that.”

    Medical discoveries have actually changed the ways cord blood is used over years, but they have so far resulted in less use of cord blood. In the past several years, doctors have refined a protocol to use half-matched donors in transplants. Doctors generally get more cells from these donors than from an infant’s banked cord blood, which means the transplants “take” more quickly and the patient spends less time in the hospital. For this reason, cord blood has been falling out of favor. Public banks have started scaling down their collections; the New York Blood Center, which had launched the world’s first public bank, recently stopped collecting new donations. How cord blood gets used in the future is still unknown.

    More than 30 years ago after Kurtzberg first treated Farrow, she is still in touch with him. He’s 39 now, and doing well. Having watched cord banking grow and evolve over the years, she remains a proponent of public banking and the possibilities ahead. When it comes to private banks, however, she says, “I don’t think it’s a necessity. I think it’s nice to have if you can do it.” There isn’t much harm in private banking, after all, as long as parents can afford the several thousand dollars over their child’s lifetime.

    Afford might be the key word here. The ads for cord-blood banking feel a lot like those for any number of “nice to have” baby products aimed at anxious parents, be they organic diapers or BPA-free wooden toys tailored to your child’s age and cognitive development. If anything, the stakes of cord-blood banking are higher than anything else you might choose to buy. The opportunity only comes around “once in a lifetime,” and it could literally save your child’s life—even if the chances of that are very, very small. “It’s playing to parental guilt and the desire for parents to have healthy children and do whatever they can for their kids,” says Timothy Caulfield, a health-law professor at the University of Alberta who has studied cord-blood banks. “There’s a huge market based on exactly that.”

    It’s telling, perhaps, that Cord Blood Registry ran a giveaway of $20,000 worth of baby products this summer. The curated package of luxury “baby essentials” resembled the registry of parents who want the best for their kid, and can afford it. Included were a Snoo smart bassinet ($1,695), an Uppababy stroller and car seat ($1,400), Coterie diapers ($100 for a month’s supply, guaranteed to be “free of fragrance, lotion, latex, rubber, dyes, alcohol, heavy metals, parabens, phthalates, chlorine bleaching, VOCs, and optical brighteners”), and, of course, a lifetime of cord-blood and tissue banking ($11,860).

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    Sarah Zhang

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