NAGOYA, Japan--Vegetables, vegetables, vegetables. I am sitting in a cardboard cubicle at a counter inside a ramen shop here in Nagoya, Japan, rehearsing my order in my head over and over again. My sister is in the next cubicle over—all I can see is the top of her head—and later I will learn that she is doing the exact same thing. Small paper signs pasted to the partitions ask us customers to tell the chef what toppings we’d like (garlic, vegetables, soy sauce, or pork drippings) in a loud, clear voice with good tempo. The kitchen is loud and the restaurant is full, so it helps if patrons can communicate in one efficient go. Like an enthusiastic movie extra delivering a single line, I really want to get it right. That’s because it is the only thing I will say during the entire hour I spend here. My sister and I are at Rekishi wo Kizame, a wildly popular ramen restaurant where customers are asked to refrain from basically all chatter. The silence is not a regular aspect of eating ramen here, but is instead a more recent rule because of COVID-19. Usually, both the restaurant and the line of soon-to-be diners waiting outside are raucous and noisy. But Takeshi Kitagawa, the restaurant’s owner, told me that at the beginning of the pandemic, the restaurant received several complaints from people in the neighborhood that the line was a potential spot for people to cluster and spread the coronavirus. So Kitagawa implemented a strict mask mandate, as well as the practice of mokushoku, or silent dining, to help make things a little safer. (And there’s evidence that silence actually works.) Besides specifying your toppings, only one other interaction is allowed. While we wait in line, an employee comes to ask us how many people are in our party (just two). Other than that, no one is supposed to speak—and, at least when I was there, that’s exactly what happened. No conferring with your lunch-mates about what type of ramen you’ll get. No delighted exclamations when your food comes. No asking what the time is or seeing whether your friend wants to get coffee afterward. Even the initial order itself requires no speech: Like lots of other restaurants, Rekishi wo Kizame has a vending machine nestled inside, where customers insert cash and receive a ramen ticket corresponding to their order. Inside the restaurant, there are several blue-and-white posters with a face, its eyes closed and one hand raised in front of its mouth in a universal shh gesture. It must be mass-produced, because I’ve seen the same poster at other restaurants and coffee shops in town with the same policy. I couldn’t find any official numbers on how many restaurants in Japan are implementing a form of mokushoku, but silent dining seems to have really caught on in early 2021, when a curry restaurant in Fukuoka made the news for its policy. One March survey of restaurant customers in Japan found that 22 percent of diners planned to practice mokushoku regardless of restaurant rules, in an effort to help stop the spread of the coronavirus. After snaking through the line outside—we spent the time making excited eyes at each other over our masks—my sister and I are ushered into the small storefront, to the counter that rings the kitchen. The distinctly homemade dining booths we are cordoned off into make it virtually impossible to have a conversation with anyone. I sit on a stool between my cardboard partitions and reach over to clip my ramen ticket (a regular bowl of the restaurant’s house noodles) onto a clothespin attached to the counter. I look again at the instructions on how to order toppings. Vegetables, vegetables, vegetables! A loud crack interrupts my concentration. The three men next to us have apparently ordered an egg on the side. Or at least that’s what I deduce, since I can’t eavesdrop on their orders. I understand what just happened only when I see another customer receive a shining, white egg that he proceeds to whack against the counter. Though there is no chatter, the shop still feels fairly loud. There is the backbeat of cars whizzing down the busy street outside, the blare of J-rock over the speaker, and the constant whirring of several industrial fans. Water roils on a stove, metal sieves clang against bowls, soup splashes. It’s a comfortable, cheery din that makes me feel even more hungry for my ramen. [Read: The pandemic really did change how we tip] Kitagawa finally asks me what toppings I want, and in a practiced shout I say, “Vegetables and garlic.” The garlic is a last-minute decision, and for a split second I am nervous that I have butchered my one and only utterance. I didn’t, and from over the counter descends a bowl heaped with cabbage, bean sprouts, and two slabs of glistening roast pork. Under the meat rests a nest of thick-cut ramen noodles swimming in a dark broth. I push the minced garlic into the soup and crack apart my chopsticks, breathing in the scent of alliums, soy sauce, and rich pork-bone broth. For a moment, I am almost apathetic about the restaurant’s mokushoku policy. Maybe it doesn’t matter at all that people can’t talk with one another—especially here. Americans might eat ramen like it’s dinner-party food, lingering over their bowl for what seems like hours as the noodles languish and bloat. But from a Japanese standpoint, ramen is a food to eat quickly, to slurp down before the heat of the broth causes the noodles to swell up and lose their chew. Sure, it’s nice to chat with a fellow diner or remark upon how savory the broth is, how impressive a slab of char siu teetering on a pile of bean sprouts appears. But sitting in the whirlwind of ambient restaurant noise, the forced silence gives me no choice but to inhale my noodles quickly, exactly how they should be eaten. Still, I want more than anything to poke my head over the barrier and make a quick comment to my sister, to marvel with her at this steaming mountain of ramen we are about to devour. But there is just me and the ramen in our little cardboard confessional, staring each other in the face. I know the clock is ticking, that I need to suck down my noodles before they become heavy with water, but I want to nudge my sister with my knee. I want to clap my hands together and say Itadakimasu!, the traditional Japanese phrase meant to open a meal. Above me, the blue shh-ing icon looks down beatifically, radiating its reminder of quiet. [Read: An extinction event for America’s restaurants] When I spoke with Kitagawa, he said that, generally, most customers have an experience not too different from mine: Even if they might want to speak, they respect his rules and keep quiet. Sometimes he does have to dole out a reminder, but he’s careful to phrase it as a request and not an order—even if it’s really just that. Could you help us out by quieting down? He said that most people have a hard time turning down such a request. Even though more than 60 percent of people in Japan are now fully vaccinated, he’s not sure when he’ll end the policy, but he can’t wait for his restaurant to once again be full of laughter and liveliness. Before the pandemic, boys would visit in groups and compete to see who could eat the most ramen the fastest, leading to cheers and boos. Still, the policy hasn’t been all bad. Before the pandemic, Rekishi wo Kizame was a ramen shop frequented mostly by men. Porky, garlicky, and inelegant to eat, his ramen was somewhat of a tough sell for female customers. But the silence and privacy of the cardboard dividers has led to an uptick in women visiting the shop, Kitagawa said. They no longer have to fend off any unwanted stares or attempts at conversation, and can wolf down their ramen without a thought to decorum or composure. At the end of our meal, I catch my sister’s eye over the partition and wiggle my eyebrows toward the door to ask whether she’s done. She wiggles her eyebrows back, and we (quietly!) place our ramen bowls on the counter, get up, and leave. Outside, faces fully visible, we hop on our bikes and shout to each other across the lane about the food. I spot other patrons doing the same, shrugging off their quiet as they get to the crosswalk. A pair of boys wait for the red light to turn green and wistfully sum up their meal: Rekishi wo Kizame is always good, they say. We’ll be back soon. They keep talking about their meal as they cross the street, walking out of earshot. I guess you can stop people from talking about their food for only so long. from https://ift.tt/3CpXkmi Check out http://natthash.tumblr.com
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Way back in February, when COVID-19 vaccines were still largely restricted to the most vulnerable among us, public-health leaders were determined to send a unified message: Don’t worry about the differences among the vaccines. “All three of them are really quite good, and people should take the one that’s most available to them,” Anthony Fauci said on Meet the Press. Now that hundreds of millions of vaccine doses have been distributed in the United States, we have plenty of reason to doubt that story. A recent (but not yet peer-reviewed) study of more than half a million U.S. veterans showed that the Johnson & Johnson shot’s protection against infection (whether or not that leads to disease or hospitalization) had plummeted from 88 percent to 3 percent by mid-August, while the other vaccines’ effectiveness had declined much less. Research published in the past few months also signals that Moderna’s shot beats out Pfizer’s in terms of both antibody count and hospitalizations prevented, while a National Institutes of Health study released earlier this month found that Moderna’s booster shot lifted participants’ antibody levels a bit more than Pfizer’s, and that both mRNA boosters were miles ahead of J&J’s. In light of all these data, it’s tempting to rank the vaccines by brand name: Moderna is better than Pfizer is better than J&J. But the same numbers hint at a different pattern: Maybe what matters most is not which vaccine you get, but how much of it. Consider how the vaccines differ in their dosing. J&J, the least effective in the studies, has only one shot in its primary series; the mRNA vaccines have two. So anyone who got J&J (and hasn’t yet gotten a booster) received half as many doses total. Comparing Pfizer with Moderna, you see another dose difference: Each shot of Pfizer contains 30 micrograms of mRNA, while each one of Moderna contains 100. (Doses for children could also differ in size: Pfizer has proposed 10-microgram shots, while Moderna is going with 50.) Just how much of the difference in the shots’ performance can be summed up by saying “More vaccine is better”? “More vaccine” is not a simple proposition. For one thing, doses of Pfizer and Moderna are measured in mass of mRNA lipid nanoparticles; J&J doses are measured by counting the number of harmless adenovirus particles that each one contains (about 50 billion). You can’t really compare lipid nanoparticles with viral particles, several experts told me. According to Michael Arand of the University of Zurich’s Institute of Pharmacology and Toxicology, you shouldn’t even assume that each 50-billion-particle dose of J&J will be equivalent in size to the next one, since, depending on the details of production, some particles can be more infectious than others. A better dosage measure for adenovirus-based vaccines, he argued in a recent opinion paper, would be “infectious units.” When I asked him via email whether developing a standard measure that works across different vaccine platforms might be possible, he said, “I do not think so.” Comparing doses of the Pfizer and Moderna vaccines is much easier, since their mechanisms are so similar. Each shot of Moderna delivers more than three times as much of the active ingredient, compared with Pfizer, and seems to induce a higher antibody count and lead to more durable protection against infection and hospitalization. “Over time, that higher dose might be what is driving the difference in protective efficacy,” John Moore, a microbiology and immunology professor at Weill Cornell Medicine, told me. The vaccines have differed in their dosing schedules too. Vaccinated (and un-boosted) Americans have received 60 micrograms of Pfizer over a period of three weeks, 200 micrograms of Moderna over four weeks, or 50 billion particles of J&J in one sitting. It’s apples and oranges, except you have to wolf down the apple all at once, and some of the oranges are tangerines, and you can eat only a few slices at a time. Even the one-week difference between Pfizer’s schedule and Moderna’s could be important. Mark Slifka, an immunologist at Oregon Health and Science University, told me that it could play into Moderna’s slightly longer-lasting protection. Angela Rasmussen, a virologist at the University of Saskatchewan’s Vaccine and Infectious Disease Organization, pointed out that the AstraZeneca vaccine—an adenovirus-vector design like J&J’s—also seems to provide more protection when its doses are spaced further apart. The number of vaccine doses you receive also matters, no matter their specific size and schedule. Slifka thinks that the number of times you get a vaccine is far more important than the amount of it delivered in each syringe. Getting more than one dose “is actually the great equalizer among vaccinations,” he said, because it teaches the immune system that a particular threat should be taken seriously. Having multiple rounds of a moderately sized dose may also be better than taking one megadose, because the more vaccine you get at once, the worse your side effects are likely to be. “With the mRNA vaccines and the adenovirus vectors, there’s an upper limit to how much you can give [in one dose] before it’s just not a good idea,” Slifka said. American public-health agencies haven’t yet come out and said it, but J&J “is really a two-dose vaccine,” Rasmussen told me. Paul Offit, who directs the Vaccine Education Center at the Children’s Hospital of Philadelphia, said that J&J may turn out to be “every bit as good as the mRNA vaccines” when compared two doses to two doses. He also suspects that a single dose of J&J would prevent more hospitalizations and deaths than a single dose of Pfizer or Moderna. But that opinion is far from universal. “I have absolutely no doubt that adenoviruses are inferior technology to the mRNAs,” Moore said. Many fans of J&J’s shot speculate that its protection against hospitalization and death could last longer than the other vaccines’, thanks to the way it tickles a particular set of immune-system actors called T cells, which help prevent infections from progressing into severe disease. “There’s a sort of T-cell mafia around,” Moore said, but some studies have shown that the mRNA vaccines produce T-cell responses with at least as much vigor as J&J’s. He says that antibodies are a better proxy for protection anyway, and the Moderna and Pfizer options consistently produce more of them in the vaccinated. [Read: Delay a shot? Skip one? Vaccine-dosing messaging is a nightmare.] A few experts continue to suspect that all three vaccines are somewhat interchangeable. Slifka, for example, thinks that the differences between the adenovirus and the mRNA formulas—the ways they target our cells, the nature of the immune response they raise in us—might not be particularly relevant to the protection they provide. “Both of them are nanoparticles. One is a virus nanoparticle and the other one is a lipid nanoparticle, but they’re both doing the same thing,” he said: delivering genetic material into human cells so those cells can produce the coronavirus’s distinctive spike protein and give the immune system target practice for when the real invader arrives. We’ll likely never know for sure how much of the difference among vaccines can be chalked up to their formulas, and how much comes from other factors. In theory, researchers could untangle those questions by running enormous randomized controlled trials of slightly larger and smaller doses of each shot, and of different intervals between (same-size) shots. But with half of the world still yet to receive a single dose of any COVID-19 vaccine, and plenty of good-enough regimens already identified, no one is going to devote resources to such fine-grained questions. “If last year hadn’t been such a shitstorm,” Moore said, “all of these issues would have been ironed out.” For now, we’ll have to keep bumbling forward with our clunky toolbox of boosters and waiting periods and half-doses—and count our blessings to live in a country where we have the luxury of asking how much vaccine is the best amount. from https://ift.tt/2Zvqu5v Check out http://natthash.tumblr.com Some good news finally--finally--appears to be on the horizon for roughly 28 million of the United States’ youngest residents. On the heels of an advisory meeting convened yesterday, the FDA is likely on the cusp of green-lighting a kid-size dose of Pfizer’s COVID-19 vaccines for Americans ages 5 to 11, a move that’s been months in the making. After the agency’s expected emergency authorization, Pfizer’s formulation will need a recommendation from CDC Director Rochelle Walensky, who’s expected to weigh in next week, after her own advisory committee holds a vote. But the nation is ready: Already, 15 million pediatric doses of Pfizer’s vaccine—which will be administered at a third of the amount doled out to adults—have become available for states to order in advance. Yesterday’s discussions were tense, understandably so. These immunizations will protect both the kids who get them and the people they mingle with, and they represent one of the few big levers the government has left to pull in the fight against the coronavirus. But as age eligibility for COVID-19 vaccines continues to drop, the risk-benefit calculations get tougher, and more emotional. This age group has been much less likely than others to come down with serious cases of COVID-19. Stacked up alongside that relative resilience are two rare but serious vaccine side effects: myocarditis and pericarditis, or inflammation of the heart and its surrounding tissue, which have appeared more commonly in boys and young men who have received mRNA-based COVID-19 vaccines. Most of the cases have been relatively minor—notedly less severe, for instance, than the heart inflammation that can follow a SARS-CoV-2 infection—but the phenomenon remains poorly understood. The FDA’s own analysis of the (somewhat limited) data on this age group, presented at yesterday’s meeting, came out in favor of giving pediatric shots the official okay. COVID, after all, is now one of the top 10 causes of death among children ages 5 to 11; the disease has also hit Black, Latino, and Native kids especially hard. But a side effect that’s “less risky than COVID” could still be cause for concern. Maybe the vaccine should be given only to a subset of kids, some committee members argued—those who have medical conditions that up their chances of getting seriously sick, for instance. Still, the panel gave a near-unanimous thumbs-up to the vaccine, with one member abstaining. [Read: Vaccine data for kids under 5 are coming “before the end of the year”] Now comes the hard part: actually getting inoculations into little arms, by no means a slam dunk. As shots become available, just in advance of the holidays, parents will have to opt their children in to receive them—two more jabs, on top of the recommended seasonal flu shot, that potentially come with side effects and may confer protection of debated durability. Adopting any new health intervention requires a gamble, but this one might feel especially fraught. There’s still a lot we don’t know about COVID-19 in the youngest among us, and the vaccines we’re using to shield them. To help make sense of what’s next, I caught up with Sallie Permar, the chair of pediatrics at Weill Cornell Medicine and pediatrician in chief at New York–Presbyterian Hospital in New York. Our interview has been lightly edited for length and clarity. Katherine J. Wu: The FDA is probably on track to authorize this vaccine within the next couple of days—before the CDC’s advisory panel, ACIP, meets next week. What’s the greatest impact this could have on the pandemic overall, assuming we successfully convince parents to sign their kids up for shots? Sallie Permar: To me, the most important thing is that this vaccine takes three new diseases that we’re dealing with in children, and seeing consistently in our health systems, and makes them vaccine-preventable. The first is severe COVID-19, the respiratory disease that’s more rare in kids, but still happens, especially in our adolescent populations and those with high risk. The second is MIS-C, an [inflammatory] condition that happens in 1 in every 3,000 or so infections in children, [and is most common] in the 5-to-11-year age group. And the third is long COVID, which children continue to suffer for months after, due to persistent symptoms. The second biggest benefit would be about transmission. Children can be protected by masks, and they probably transmit less often [than adults]. But children can definitely be part of the transmission chain, especially when it comes to households, and even in settings where precautions are being used. Vaccinating our children will make it so we can recapture school as we once knew it, with kids picking who they want to sit at their lunch table, or being able to face any direction in the classroom, and not a certain distance away from their neighbor—maybe even thinking about whether kids can safely go back to school without masks. Masks might still be a good idea when everybody’s indoors and has runny noses during the winter. But we’ll be able to walk back a lot of the restrictions that have been in place. We can’t even think about that until we get high [vaccine] coverage in our children. Wu: That sounds wonderful, but an authorized vaccine doesn’t guarantee an administered vaccine. You’re a practicing pediatrician—what’s been your sense of how parents will receive this news? Permar: I foresee a lot of my time in the next few weeks being devoted to [navigating] that. Parents want to make the best decision for their children. And they want to make a very careful decision, and they want to consider all of the information that’s available. It is scary to think about: If I choose a vaccination and my child is one that has a rare side effect, how am I going to feel about that? That’s definitely going through parents’ minds. The chance that your child will have a severe COVID infection is rare; the chance that your child will have MIS-C is also pretty rare. Not a lot of people know someone who’s had a child in the hospital with COVID. But what’s even more rare is the chance that there will be an ill effect from the vaccine. We have to educate about those numbers. Not vaccinating is still a risk, and it’s a higher risk than giving your child a vaccine. In fact, we don’t even know if myocarditis is going to be a concern [in 5-to-11-year-olds]. There were no cases in that age group in [Pfizer’s efficacy trial]. Myocarditis tends to be more common in older children. So taking what we know, in this younger age group, it’s postulated to be less of a concern. And let me just say, I am so thrilled that there has been all of this work that went into identifying an age-specific dose for this population. We want to achieve the immune response needed for protection, with the smallest dose to reduce side effects. That is what we should be doing for every new vaccine going forward. One question I get often is “I have an 11-year-old who’s turning 12 in three weeks. Should I wait? The higher dose seems better, right?” First of all, don’t wait for the bigger dose—you never know when COVID will enter your life or your child’s life. Secondly, I think I would actually prefer to get them the lower dose. Pediatric immune systems are more well set up to respond to low doses. They may even achieve a better response. We’ve been studying this in the HIV-vaccine world for several years now. A lower dose in a young age group can achieve a better immune response than even a higher dose. I wouldn’t be surprised if we go to an even lower dose with the youngest age groups. [Read: Why is it taking so long to get vaccines for kids?] Wu: That sounds really promising. At the same time, though, we don’t have certainty on side effects yet. Pfizer’s trial was small—too small to pick up a reliable signal of myocarditis, so we’ll need to wait to see what happens when the vaccine rolls out to a much larger group. How should parents weigh the risk of a rare side effect against the risk of COVID-19, which is less common among young kids? And should certain children be prioritized for the vaccine, and others advised to wait? Permar: If you were playing the numbers and reading the data, you would give your child the vaccine every time. [The alternative] would be taking an unknown risk, and making that the reason you’re not going to protect your child against a known risk that you know how to protect against. Severe infections have been unusual in children, which has been a blessing. But we have no idea what predicts who is going to have MIS-C. Hopefully, we’ll go forward and identify those things. We have some idea of who might be at risk for severe respiratory COVID—older adolescents, [kids with] obesity, diabetes. But there are also children where we don’t know what made them at risk for infection. We see this in flu, too. Totally healthy children just get a very severe illness. We see totally healthy children just get very sick, and you can’t put your finger on it. Wu: Will vaccinating kids feel less urgent if transmission rates plummet? Permar: One thing we know will happen is that there will be new variants of this virus. If the pattern holds true, they will be more transmissible. They may even be vaccine resistant. What drove a lot of parents of adolescents to finally get vaccines [this summer] was that the case numbers rose immensely with the more transmissible Delta variant. That’s great, but it was also too late. It takes five to six weeks [from the first dose] to get fully immune. So we have to anticipate there will be other variants that we will deal with. My hope is we get this last segment highly vaccinated, and that will maybe slow down the variants. But we should not count out a new variant, and we have to anticipate that. [Read: Delta is bad news for kids] Wu: Getting vaccines down to young kids took a very long time, and we still haven’t reached the under-5 crowd. What can we learn from this? Did it have to be this way? Permar: We’ve got to do this differently in the future. It is a travesty that we sent kids back to school without this vaccine available to them, while adults were benefiting from vaccine immunity, going to restaurants with our vaccine cards. We should not leave children to the very last. Maybe in the future, we can start testing age groups in parallel. from https://ift.tt/2XNmigi Check out http://natthash.tumblr.com There was a time, at the start of the 20th century, when the field of public health was stronger and more ambitious. A mixed group of physicians, scientists, industrialists, and social activists all saw themselves “as part of this giant social-reform effort that was going to transform the health of the nation,” David Rosner, a public-health historian at Columbia University, told me. They were united by a simple yet radical notion: that some people were more susceptible to disease because of social problems. And they worked to address those foundational ills—dilapidated neighborhoods, crowded housing, unsafe working conditions, poor sanitation—with a “moral certainty regarding the need to act,” Rosner and his colleagues wrote in a 2010 paper. A century and a half later, public health has succeeded marvelously by some measures, lengthening life spans and bringing many diseases to heel. But when the coronavirus pandemic reached the United States, it found a public-health system in disrepair. That system, with its overstretched staff, meager budgets, crumbling buildings, and archaic equipment, could barely cope with sickness as usual, let alone with a new, fast-spreading virus. By one telling, public health was a victim of its own success, its value shrouded by the complacency of good health. By a different account, the competing field of medicine actively suppressed public health, which threatened the financial model of treating illness in (insured) individuals. But these underdog narratives don’t capture the full story of how public health’s strength faded. In fact, “public health has actively participated in its own marginalization,” Daniel Goldberg, a historian of medicine at the University of Colorado, told me. As the 20th century progressed, the field moved away from the idea that social reforms were a necessary part of preventing disease and willingly silenced its own political voice. By swimming along with the changing currents of American ideology, it drowned many of the qualities that made it most effective. Public health’s turning point, according to several historical accounts, came after the discovery that infectious illnesses are the work of microbes. Germ theory offered a seductive new vision for defeating disease: Although the old public health “sought the sources of infectious disease in the surroundings of man; the new finds them in man himself,” wrote Hibbert Hill in The New Public Health in 1913. Or, as William Thompson Sedgwick, a bacteriologist and a former president of the American Public Health Association, put it, “Before 1880 we knew nothing; after 1890 we knew it all.” This revolution in thinking gave public health license to be less revolutionary. Many practitioners no longer felt compelled to deal with sticky, sweeping problems such as poverty, inequity, and racial segregation (or to consider their own role in maintaining the status quo). “They didn’t have to think of themselves as activists,” Rosner said. “It was so much easier to identify individual victims of disease and cure them than it was to rebuild a city.” Public-health leaders even mocked their predecessors’ efforts at social reform, which they saw as inefficient and misguided. Some dismissively billed the impressive work of the sanitarian movement, which had essentially plumbed entire cities, as “a matter of pipes.” As public health moved into the laboratory, a narrow set of professionals associated with new academic schools began to dominate the once-broad field. “It was a way of consolidating power: If you don’t have a degree in public health, you’re not public health,” Amy Fairchild, a historian and the dean of the College of Public Health at Ohio State University, told me. Mastering the new science of bacteriology “became an ideological marker,” sharply differentiating an old generation of amateurs from a new one of scientifically minded professionals, wrote the historian Elizabeth Fee. Hospitals, meanwhile, were becoming the centerpieces of American health care, and medicine was quickly amassing money and prestige by reorienting toward biomedical research. Public-health practitioners thought that by cleaving to the same paradigm, “they could solidify and extend their authority and bring public health up to the same level of esteem and power that medicine was beginning to enjoy,” Fairchild told me. Public health began to self-identify as a field of objective, outside observers of society instead of agents of social change. It assumed a narrower set of responsibilities that included data collection, diagnostic services for clinicians, disease tracing, and health education. Assuming that its science could speak for itself, the field pulled away from allies such as labor unions, housing reformers, and social-welfare organizations that had supported city-scale sanitation projects, workplace reforms, and other ambitious public-health projects. That left public health in a precarious position—still in medicine’s shadow, but without the political base “that had been the source of its power,” Fairchild told me. After World War II, biomedicine lived up to its promise, and American ideology turned strongly toward individualism. Anti-communist sentiment made advocating for social reforms hard—even dangerous—while consumerism fostered the belief that everyone had access to the good life. Seeing poor health as a matter of personal irresponsibility rather than of societal rot became natural. Even public health began to treat people as if they lived in a social vacuum. Epidemiologists now searched for “risk factors,” such as inactivity and alcohol consumption, that made individuals more vulnerable to disease and designed health-promotion campaigns that exhorted people to change their behaviors, tying health to willpower in a way that persists today. This approach appealed, too, to powerful industries with an interest in highlighting individual failings rather than the dangers of their products. Tobacco companies donated to public-health schools at Duke University and other institutions. The lead industry funded lead research at Johns Hopkins and Harvard Universities. In this era, Rosner said, “epidemiology isn’t a field of activists saying, ‘God, asbestos is terrible,’ but of scientists calculating the statistical probability of someone’s death being due to this exposure or that one.” In the late 20th century, some public-health leaders began calling for a change. In 1971, Paul Cornely, then the president of the APHA and the first Black American to earn a Ph.D. in public health, said that “if the health organizations of this country have any concern about the quality of life of its citizens, they would come out of their sterile and scientific atmosphere and jump in the polluted waters of the real world where action is the basis for survival.” Some of that change happened: AIDS activists forced the field to regain part of its crusading spirit, while a new wave of “social epidemiologists” once again turned their attention to racism, poverty, and other structural problems. But, as COVID has revealed, the legacy of the past century has yet to release its hold on public health. The biomedical view of health still dominates, as evidenced by the Biden administration’s focus on vaccines at the expense of masks, rapid tests, and other “nonpharmaceutical interventions”. Public health has often been represented by leaders with backgrounds primarily in clinical medicine, who have repeatedly cast the pandemic in individualist terms: “Your health is in your own hands,” said the CDC’s director, Rochelle Walensky, in May, after announcing that the vaccinated could abandon indoor masking. “Human behavior in this pandemic hasn’t served us very well,” she said this month. If anything, the pandemic has proved what public health’s practitioners understood well in the late 19th and early 20th century: how important the social side of health is. People can’t isolate themselves if they work low-income jobs with no paid sick leave, or if they live in crowded housing or prisons. They can’t access vaccines if they have no nearby pharmacies, no public transportation, or no relationships with primary-care providers. They can’t benefit from effective new drugs if they have no insurance. In earlier incarnations, public health might have been in the thick of these problems, but in its current state, it lacks the resources, mandate, and sometimes even willingness to address them. Public health is now trapped in an unenviable bind. “If it conceives of itself too narrowly, it will be accused of lacking vision … If it conceives of itself too expansively, it will be accused of overreaching,” wrote Lawrence Gostin, of Georgetown University, in 2008. “Public health gains credibility from its adherence to science, and if it strays too far into political advocacy, it may lose the appearance of objectivity,” he argued. But others assert that public health’s attempts at being apolitical push it further toward irrelevance. In truth, public health is inescapably political, not least because it “has to make decisions in the face of rapidly evolving and contested evidence,” Fairchild told me. That evidence almost never speaks for itself, which means the decisions that arise from it must be grounded in values. Those values, Fairchild said, should include equity and the prevention of harm to others, “but in our history, we lost the ability to claim these ethical principles.” This tension has come up over and over again in my reporting. Although the medical establishment has remained an eager and influential participant in policy, public health has become easier than ever to silence. It need not continue in that vein. “Sick-leave policies, health-insurance coverage, the importance of housing … these things are outside the ability of public health to implement, but we should raise our voices about them,” said Mary Bassett, of Harvard, who was recently appointed as New York’s health commissioner. “I think we can get explicit.” Public-health professionals sometimes contend that grand societal problems are beyond the remit of their field. Housing is an urban-planning issue. Poverty is a human-rights issue. The argument goes that “it’s not the job of public health to be leading the revolution,” Goldberg said. But he and others disagree. That attitude emerged because public health moved away from advocacy, and because the professionalization of higher education splintered it off from social work, sociology, and other disciplines. These fragmented fields can more easily treat everyone’s problems as someone else’s problem. The future might lie in reviving the past, and reopening the umbrella of public health to encompass people without a formal degree or a job at a health department. Chronically overstretched workers who can barely deal with STDs or opioid addiction can’t be expected to tackle poverty and racism—but they don’t have to. What if, instead, we thought of the Black Lives Matter movement as a public-health movement, the American Rescue Plan as a public-health bill, or decarceration, as the APHA recently stated, as a public-health goal? In this way of thinking, too, employers who institute policies that protect the health of their workers are themselves public-health advocates. “We need to re-create alliances with others and help them to understand that what they are doing is public health,” Fairchild said. The field in the late 19th century was not a narrow scientific endeavor but one that stretched across much of society. Those same broad networks and wide ambitions are necessary now to deal with the problems that truly define the public’s health. from https://ift.tt/2ZmO1Ft Check out http://natthash.tumblr.com
Last night, CDC Director Rochelle Walensky gave the green light for Moderna and Johnson & Johnson booster shots, the long-awaited follow-up to a similar recommendation given to the Pfizer formulation last month. As the endorsement stands, all who are eligible for an additional jab—which now includes tens of millions more Americans—should be able to pick whatever booster brand they like. But discussions among a panel of experts who advised Walensky hinted at a catch: The agency has yet to issue its final clinical guidance on who, specifically, might want to boost with what—and an early draft of the recommendations suggests that Americans “should” stick with the same brand they got in their first go-round. Switching to a different shot would be allowed, as was authorized by the FDA on Wednesday; per the draft CDC guidance, people may opt to mix and match based on availability or preference, after assessing their individual risks and benefits. (As a reminder, the FDA’s authorizations tell Americans what vaccines they’re allowed to get. The CDC follows that up with advice on what folks should do with those options.) The CDC’s stance on mixing and matching, then, could end up being a relatively soft one, neither extolment nor excoriation. That might also be the most practical course of action for the agency, given the variables involved and the lack of clear-cut evidence that could untangle them. But the wishy-washiness of Pick whatever is confusing as hell. Consider, first, the sheer number of choices now available to booster-eligible Americans (a limited set of mRNA recipients, and all folks who got J&J). With three approved or authorized vaccines, the simplest mix-and-match matrix has nine possible combos. But that’s an underestimate of the absolutely unmanageable number of variations therein. Moderna’s third shots, for instance, come in full doses for immunocompromised people and half doses for everyone else. The timing of additional shots might matter, too: People who get a second injection of J&J half a year after their first seem to churn out more antibodies than people who wait just two months. Clearly, inoculation isn’t just about which vaccines you’re getting. It’s about which vaccines, when, how much, how often, in what order, on and on and on—an absolute multiverse of choices. Add to that the inevitable differences among individual immune systems, and just start to imagine the terror of the resulting flow chart. Against that chaotic-evil backdrop, the CDC’s interim preference for homogeneity has a certain appeal—even if it sets up a slightly judgy juxtaposition between what’s by the book and, essentially, what the mavericks might do, if they feel like it. [Read: Should you mix and match your booster shot?] Then again, maybe what the CDC says is, at this point, kind of moot. Millions of people have already boosted, some of them ahead of eligibility. Now, with even more choices available, “people who care will vote with their feet,” Céline Gounder, an infectious-disease physician at Bellevue Hospital, in New York, told me. That may in the CDC guidance is easy to grab and run with. For anyone who has made up their mind, in any direction, the agency’s relatively hands-off approach isn’t all that useful (or hard to ignore). Cross-vaccine boosting can certainly come with perks. People won’t have to stress about matching brands across doses; individuals in at-risk groups might have the flexibility to avoid rare, shot-specific side effects. The strategy might even be more protective. None of that, though, makes actually selecting a booster any easier. As things stand, the decision requires a small leap of faith, or at least some immunological inference. Data on mixing and matching is still relatively scant, though the early evidence looks promising. A recent National Institutes of Health study found that switching shots seems to juice out antibodies at least as well as, and in some cases quite a bit better than, staying the course with one brand. That seems especially true for the OG J&J crowd: mRNA boosters sent antibody levels soaring, compared with a second helping of J&J. (A caveat: The study boosted with the full Moderna dose, not the half dose that the FDA authorized for non-immunocompromised people.) If that pattern holds, J&J, already the least popular vaccine in the U.S., might become even more of an underdog. That’s not for sure. Gounder is advising caution: The NIH study was small, tracking an imperfect proxy for protection in fewer than 500 people for a very limited period of time. Boghuma Kabisen Titanji, an infectious-disease physician and researcher at Emory University, in Atlanta, is a bit more optimistic, and told me that she finds the mix-and-match data compelling enough to offer the strategy. The trends in the NIH study, she pointed out, seem well in line with the months of data that have come out of places such as the United Kingdom, which adopted a hybrid approach early on, albeit for original doses and with a different set of brands (Pfizer and AstraZeneca). Ideally, mixing and matching could blur the brand boundaries between vaccinated Americans, effectively collapsing more of us into the same pretty-well-protected pool. (Did you get Pfizer or Moderna? J&J? Who cares?) Or, it could splinter us into infinite subgroups that become ever more difficult to compare. Collecting good data on vaccine responses is getting harder as inoculation becomes more bespoke. With so many Americans now poised to choose their own vaccine adventure--you know, as they may—the differences among regimens might get tougher to pin down. We need that data: What we learn now will—hopefully—help us design better, safer, more efficient vaccine regimens for future generations. But if fewer people embark on similar trajectories, they could get more difficult to group together. Studies might have to be more limited in scope, or work harder to combine data from different parts of the country. That’s not impossible, Saad Omer, a vaccine expert and epidemiologist at Yale, told me. But it does make things “more challenging.” Some of this beta-testing vibe harkens back to last winter, when experts heatedly debated the merits of skipping or delaying second doses of the Pfizer and Moderna vaccines. Certain countries, including the U.K., spaced out the shots; the U.S. and others stuck to the very trim gaps prescribed by trials. The delay was a gamble, since it left people partially protected for longer and sent mixed messages to a frustrated public. But now it looks beneficial. Really, we were all guinea pigs—and this mass round of boosting is slating us for a discombobulation redux. We won’t all be winners; someone always has to be in the group that fares worse. Then again, “worse” is always relative. Anyone who’s playing the booster game is already, technically, fully vaccinated, putting them ahead of the billions around the globe who still are not. Titanji pointed out that more Americans have gotten boosters than people have received first doses in Nigeria, a country with some 200 million residents. Even in the U.S., getting more first shots to people remains the bigger priority—that’s how we collectively contain the coronavirus. But the hyper-individualistic American approach to the pandemic is once again nudging each of us to chart our own course. The government has kind of shrugged about mix-and-match boosting, and punted the decision to us: Choose whichever path seems right to you; turn to page 7; hope for the best. Here’s the trick, though—no one’s sure where this chapter ends. Good luck, I guess. from https://ift.tt/3C5NsxS Check out http://natthash.tumblr.com In early March, Deepta Bhattacharya, an immunologist at the University of Arizona, celebrated a milestone: hitting the point of full vaccination, two weeks after getting his second Pfizer shot. Since then, he’s been watching the number of coronavirus antibodies in his blood slowly but surely decline. The drop hasn’t been precipitous, but it’s definitely happening—regular checkups have shown his antibody levels, also known as titers, ticking down, down, down, from spring through summer, now into fall. The downtick fits the narrative that countless reports have been sounding the alarm on for a while now: In the months after vaccination, our antibodies peace out, a trend that’s often been described as a “waning” of immunity, and evidence that we’re all in dire need of boosters to shore our defenses back up. It all sounds, quite frankly, like a tragedy. But as Bhattacharya and others assured me, it’s really, really not. “All we hear about is titers,” says Stephanie Langel, an immunologist at Duke University. That fixation “misses an entire nuance.” Antibodies are supposed to peter out; that’s why they always do. Still, even as our antibodies are dwindling in absolute quantity, these scrappy molecules are enhancing their quality, continuing to replace themselves with new versions that keep improving their ability to bring the virus to heel. Months after vaccination, the average antibody found in the blood simply has higher defensive oomph. “That’s why I hate the word waning,” Jennifer Gommerman, an immunologist at the University of Toronto, told me. “Antibody levels are declining, but something good is happening too: The immune response is evolving.” The focus on antibody counts alone actually does a disservice to our understanding of immunity, experts told me. Like a block of wood being hewn down into a sharper blade, vaccinated immune systems can hone their skills over time. Part of waning certainly does mean fewer. But it can also mean better. [Read: What we actually know about waning immunity.] A couple weeks after vaccination, a group of immune defenders called B cells starts to pump out antibodies en masse. But many of these early antibodies are, as Bhattacharya told me, “really crappy” at their jobs. Their raison d’être is to be clingy—the Y-shaped molecules hook their tips onto a specific hunk of SARS-CoV-2’s anatomy, and hang on for dear life. The better they are at glomming on, the better chance they have of waylaying the threat. Sometimes it’s a solo act: Antibodies alone can grab on so firmly that they block the virus from hacking into a cell, a process called neutralization. Or they’ll use the stems of their Ys to flag down other members of the immune system in a destructive assist. But that’s the best-case scenario. Most of our B cells, or the antibodies they produce, won’t actually react at all to SARS-CoV-2, or a vaccine that resembles it. That’s because our bodies are always churning out B cells at random, repeatedly futzing with their genetics so that they’ll make a diverse array of antibodies--billions or trillions in total—that can collectively recognize just about any microbe they might ever see. This process is haphazard and imprecise, though: When B cells are born, “they don’t have any particular pathogen in mind,” Gabriel Victora, an immunologist at Rockefeller University, told me. Instead of gripping firmly onto the virus’s surface, many antibodies might just “bounce on and off,” giving the pathogen ample time to wrest itself free, Bhattacharya said. It’s the best defense the body can slap together on short notice, having never met the bug before. Early antibodies are sort of the immune system’s best guesses at defense—the immunological equivalent of throwing spaghetti against a wall to see what sticks—which usually means we need a lot of them to truly pen the pathogen in place. They’re also fragile. Most antibodies don’t hang around for more than a few weeks before they degrade. Such flimsy fighters aren’t terribly good investments for the long term. So while the subpar antibodies are duking it out on the front lines, the immune system will shuttle a contingent of young B cells into a boot camp, called a germinal center, where they can study up on the coronavirus. What happens inside these training camps is a battle royal in miniature: The cells crowd together and desperately vie for access to the resources they need to survive. Their weapons are their antibodies, which they wave frantically about, trying to latch on to chunks of dead coronavirus, while a panel of other immune cells judges them from afar. Only the most battle-ready among them—the ones whose antibodies grip most tightly onto the coronavirus—move on to the next round, and the losers perish in defeat. As Gommerman put it, “If they suck, they die.” The harrowing cycle repeats itself over and over, and only gets more grim. Survivor B cells will xerox themselves, deliberately introducing errors into their genetic codes in the hopes that some of the mutations will enhance their antibodies’ chances of gluing themselves to the virus. The entire process is downright “Darwinian,” like a super-sped-up form of natural selection, Victora said. The weaklings are weeded out, leaving just the sharpest and strongest behind. It’s also very prolonged. Researchers such as Ali Ellebedy, of Washington University in St. Louis, have found that these tournaments of culling continue for at least 12 to 15 weeks after people receive their COVID-19 vaccines, perhaps longer. If all of this is getting a little too Squid Game, consider the much rosier upshot: At the end of this process, our bodies are left with some truly primo antibodies, well poised to take up the mantle of protection as the first waves of mediocre defenders start to fall away. This is what is happening in the immune system of those who got vaccinated months ago: An initial burst of antibody activity, followed by a gentle tapering off, as the body goes back to baseline. “Immune responses can’t just stay in your blood forever,” Langel told me. If they didn’t, we’d have no room or resources for the body to mount a different defense, against another threat—and our blood would be nothing more than a useless antibody sludge. There’s another way to think about the post-vaccination dip in antibodies: taking out the trash. Early-acting B cells are, in some cases, so crummy that they’re not all that worth keeping around. Evolution, too, has clued into the perks of this pattern, which might be why the B-cell victors aren’t just higher quality, but also much longer-lived. Whereas the first B cells that rally after vaccination might live just a few days, the cohort that trounced their peers in training can post up in the bone marrow or the blood for months or years. Some will continue to squeeze out antibodies for the long term, while others drift about in quietude, ready to resume their defensive duties when they’re called upon again. “What is seen as a ‘loss’ in antibodies is actually the slow waning of the less-good, short-lived response,” Victora told me. And when antibodies are needed—say, when the actual virus infects us—veteran B cells will produce them again, in gargantuan quantities. Antibodies themselves don’t always linger. But the capacity to create them usually does. There’s definitely a limit to how much quality can compensate for quantity—one antibody, no matter how badass, can’t do the work of hundreds. Experts don’t yet know how many antibodies (good, meh, or “crappy”) people need to have in tow to be considered well-guarded from COVID. Rishi Goel, an immunologist at the University of Pennsylvania, told me that his work has shown that, six months out from vaccination, the number of neutralizing antibodies found in people’s blood tends to drop noticeably from its peak. But he and others have also found that there’s little difference in how much neutralization the body is capable of—a strong hint that superior antibodies have since stepped up to the plate. Again, antibody levels always drop. That doesn’t mean that immune protection (which, by the way, is about more than just antibodies) disappears. [Read: You might want to wait to get a booster shot] The slow trudge toward self-improvement might also be one reason to not rush into nabbing a booster shot. Boosting reminds the immune system of a threat it’s seen before. But offering up that refresher too often or too soon could be pointless, even slightly counterproductive, if active germinal centers are still doing their thing. Waiting a bit longer might help ensure that the best possible B cells are reawakened into action, to manufacture antibodies anew. Immunity, then, is much less about what’s around now, and more about what’s around when it’s needed; it’s no big deal if those defenses aren’t always visible, as long as they kick back into gear when they’re called to the fore. All this means that a slowdown in antibody production could, in a way, be seen as comforting. It’s a sign of an immune system that’s allocating its resources wisely, rather than working itself into a constant panic. Bhattacharya, for one, hasn’t been at all fazed by what’s happening to his antibodies, which, nearly eight months out, still look pretty freaking good, despite the numerical drops—because they still seem to be walloping the virus when he tests them in his lab. Langel says that’s standard. When she sees antibodies “waning,” she shrugs. “I say, ‘Look,’” she told me, “‘that’s the immune system, doing what it does.’” from https://ift.tt/2ZhZXrU Check out http://natthash.tumblr.com Nothing about The Body Keeps the Score screams “best seller.” Written by the psychiatrist Bessel van der Kolk, the book is a graphic account of his decades-long career treating survivors of traumatic experiences such as rape, incest, and war. Page after page, readers are asked to wrestle with van der Kolk’s theory that trauma can sever the connection between the mind, which wants to forget what happened, and the body, which can’t. The book isn’t academic, exactly, but it’s dense and difficult material written with psychology students in mind. Here’s one line: “The elementary self system in the brainstem and limbic system is massively activated when people are faced with the threat of annihilation, which results in an overwhelming sense of fear and terror accompanied by intense physiological arousal.” And yet, since its debut in 2014, The Body Keeps the Score has spent 150 weeks—nearly 3 years—and counting at the top of the New York Times best-seller list and sold almost 2 million copies globally. During the pandemic, it seems more in demand than ever: This year, van der Kolk has appeared as a guest on The Ezra Klein Show, been profiled in The Guardian, and watched his book become a meme. (“Kindly asking my body to stop keeping the score,” goes one viral tweet.) After all the anxiety and social isolation of pandemic life, and now the lingering uncertainty about what comes next, many people are turning to a growing genre of trauma self-help books for relief. The Body Keeps the Score is now joined on the best-seller list by What Happened to You?, a compilation of letters and dialogue between Oprah Winfrey and the psychiatrist Bruce D. Perry. Barnes & Noble, meanwhile, sells about 1,350 other books under the “Anxiety, Stress & Trauma-Related Disorders” tab, including clinical workbooks and mainstream releases. Sometimes, new installments in the genre seem to position themselves as a cheat code to a better life: Fill out the test at the back of the book; try these exercises; narrativize your life. One blurb I read, on the cover of James S. Gordon’s Transforming Trauma, basically said as much: “This book could give you back your life in unimaginable ways, whether you think of yourself as a trauma victim or not.” “You can kind of understand why the sales of these books are going up in this stressful, pressurized situation,” Edgar Jones, a historian of medicine and psychiatry at King’s College London, told me. In a moment of personal and collective crisis, the siren song of a self-help book is strong. There’s just one problem. In spite of their popularity, trauma books may not be all that helpful for the type of suffering that most people are experiencing right now. “The word trauma is very popular these days,” van der Kolk told me. It’s also uselessly vague—a swirl of psychiatric diagnoses, folk wisdom, and popular misconceptions. The pandemic has led to very real suffering, but while these books have one idea of trauma in mind, most readers may have another. [What happens when Americans can finally exhale] The Greek term for “wound,” trauma was initially used to refer to physical wounds. Although today’s best sellers seem to provide all the answers, psychiatrists began to widely embrace the notion of purely psychological trauma only around World War I. But the disorder has evolved since the days of shell shock. The current diagnosis of PTSD dates back to only 1980, applied to the flashbacks experienced by some soldiers who had served in the Vietnam War. In the decades since, trauma has come to signify a range of injuries so broad that the term verges on meaningless. The American Psychological Association, for example, describes trauma as “an emotional response to a terrible event like an accident, rape or natural disaster”--like, but not only. “Like weeds that spread through a space and invasively take over semantic territory from others,” trauma can be used to describe any misfortune, big or small, Nicholas Haslam, a psychology professor at the University of Melbourne, told me. That concept creep is evident on TikTok, where creators use “trauma response” to explain away all kinds of behavior, including doomscrolling and perfectionist tendencies. In the pandemic, trauma has become a catchall in the U.S. for many varied, and even competing, realities. Some people certainly are experiencing PTSD, especially health-care workers who have dealt with the carnage firsthand. For most people, however, a better description of the past 19 months might be “chronic stressor,” or even “extreme adversity,” experts told me—in other words, a source of immense distress, but not necessarily with severe long-term consequences. The whole of human suffering is a lot of ground for one word to cover, and for trauma best sellers to heal. [Read: On top of everything else, the pandemic messed with our morals] Today, a comprehensive shelf of trauma self-help includes the biophysicist Peter Levine’s Waking the Tiger, which argues that a lack of trauma in wild animals can offer insight into how humans might overcome their seemingly unique susceptibility to it; The Deepest Well, by the surgeon general of California, Nadine Burke Harris, who uses personal experience to draw a direct line from childhood stress to a host of physical and social ills; and It Didn’t Start With You, in which the author, Mark Wolynn, makes the controversial claim that trauma can be inherited from distant ancestors. These books tend to follow a reliable arc, using the stories of trauma survivors to advance a central thesis, and then concluding with a few chapters of actionable advice for individual readers. In The Body Keeps the Score, van der Kolk writes about people he refers to as Sherry, a woman who was neglected in childhood and kidnapped and repeatedly raped for five days in college, and Tom, a heavy drinker whose goal was to become “a living memorial” to his friends who had died in Vietnam. For patients like these, van der Kolk eventually turned to yoga, massage therapy, and an intervention called eye-movement desensitization and reprocessing, or EMDR, which specifically treats the traumatic memories that pull people with PTSD back into the past. Those experiences are remarkably different from what most Americans have endured in the pandemic. Although almost everyone has struggled with the risk of contracting a deadly virus and the resulting isolation and potential loneliness, a remote worker’s depressive episode, or an unemployed restaurant worker’s inability to pay their bills, has little in common with stories like Tom’s and Sherry’s. They are no less important—no less deserving of attention—but we need better words to describe them, and other remedies to treat them. Even van der Kolk himself is wary of some of the ways in which trauma is used today. When I asked him whether he thinks The Book Keeps the Score is useful for all the readers turning to it during the pandemic, he objected to the premise of my question: The readers he hears from most, he said, are those who grew up in abusive households, not those who feel traumatized by COVID-19. “When people say the pandemic has been a collective trauma,” van der Kolk said, “I say, absolutely not.” [Read: When PTSD is contagious] Still, the trauma books keep selling. Some lessons they contain are universally applicable, if a little trite. In What Happened to You? Oprah and her co-author dedicate a chapter to their spin on the idea of “post-traumatic growth,” a concept popular again in the pandemic, as people search for a silver lining to what they’ve been through. But sometimes, there is no wisdom to glean or personal growth to uncover—what happened happened, and people move forward anyway. Other recommendations, as with van der Kolk’s emphasis on EMDR, are specific to people with more typical symptoms of PTSD. Most people just don’t need those kinds of interventions, says George Bonanno, a clinical-psychology professor at Columbia University and the author of The End of Trauma. In the aftermath of disasters such as 9/11, Bonanno has found remarkable resilience, despite the odds. Yet people “don’t seem to want to let go of the idea that everybody’s traumatized,” he told me. Surely some people find solace in these books, whatever their reason for reading. And not all trauma books have these pitfalls. In My Grandmother’s Hands, the therapist Resmaa Menakem examines the physical and emotional toll of racism and white supremacy, and his advice charts a different course. When people feel they have experienced a collective trauma, Menakem writes, “our approaches for mending must be collective and communal as well.” When it comes to the challenges Americans now face—as varied as responding to the pandemic and acting on climate change—that’s advice worth taking. Ultimately, talking about trauma isn’t just a semantic matter. “Having a tight, limited idea of what mental illness looks like is a recipe for stigma; it’s a recipe for not seeking help for oneself [and for] not offering help to others,” Haslam said. The desire to validate other people’s suffering “is a good corrective,” he added. “It just happens to be a pretty blunt object in this concept of trauma.” And that is the major lesson you’ll learn if you can make it to the end of this grueling syllabus: We still have so much to understand about trauma. If we want a shot at addressing the real consequences of the pandemic, we will need not only more research but a new language—one that expresses terrible experiences that aren’t strictly traumatic and leads to solutions that are bigger than any one of us in isolation. Until then, trauma books will just keep flying off the shelves. from https://ift.tt/3DP2Pvd Check out http://natthash.tumblr.com In the fall of 2006, law enforcement on the southwest border of the United States seized some crystal methamphetamine. In due course, a five-gram sample of that seizure landed on the desk of a 31-year-old chemist named Joe Bozenko, at the Drug Enforcement Administration lab outside Washington, D.C. Organic chemistry can be endlessly manipulated, with compounds that, like Lego bricks, can be used to build almost anything. The field seems to breed folks whose every waking minute is spent puzzling over chemical reactions. Bozenko, a garrulous man with a wide smile, worked in the DEA lab during the day and taught chemistry at a local university in the evenings. “Chemist by day, chemist by night,” his Twitter bio once read. Bozenko had joined the DEA seven years earlier, just as the global underworld was veering toward synthetic drugs and away from their plant-based cousins. Bozenko’s job was to understand the thinking of black-market chemists, samples of whose work were regularly plopped on his desk. He analyzed what they produced and worked out how they did it. In time, Bozenko began traveling abroad to clandestine labs after they’d been seized. His first foreign assignment was at a lab that had made the stimulant MDMA in Jakarta, Indonesia. He saw the world through the protective goggles of a hazmat suit, sifting through the remains of illegal labs in three dozen countries. Meth was the drug that Bozenko analyzed most in the early years of his job. Large quantities of it were coming up out of Mexico, where traffickers had industrialized production, and into the American Southwest. All of the stuff Bozenko analyzed was made from ephedrine, a natural substance commonly found in decongestants and derived from the ephedra plant, which was used for millennia as a stimulant and an anti-asthmatic. A Japanese researcher had first altered the ephedrine molecule to synthesize crystal methamphetamine in 1919. During World War II, it was marketed in Japan as hiropon, a word that combines the Japanese terms for “fatigue” and “fly away.” Hiropon was given to Japanese soldiers to increase alertness. In the early 1980s, the ephedrine method for making meth was rediscovered by the American criminal world. Ephedrine was the active ingredient in the over-the-counter decongestant Sudafed, and a long boom in meth supply followed. But the sample that arrived on Bozenko’s desk that day in 2006 was not made from ephedrine, which was growing harder to come by as both the U.S. and Mexico clamped down on it. There was another way to make methamphetamine. Before the ephedrine method had been rediscovered, this other method had been used by the Hell’s Angels and other biker gangs, which had dominated a much smaller meth trade into the ’80s. Its essential chemical was a clear liquid called phenyl-2-propanone—P2P. Many combinations of chemicals could be used to make P2P. Most of these chemicals were legal, cheap, and toxic: cyanide, lye, mercury, sulfuric acid, hydrochloric acid, nitrostyrene. The P2P process of making meth was complicated and volatile. The bikers’ cooking method gave off a smell so rank that it could only be done in rural or desert outposts, and the market for their product was limited. Bozenko tinkered with his sample for two or three days. He realized it had been made with the P2P method, which he had not seen employed. Still, that was not the most startling aspect of the sample. There was something else about those few grams that, to Bozenko, heralded a changed world. Among the drawbacks of the P2P method is that it produces two kinds of methamphetamine. One is known as d-methamphetamine, which is the stuff that makes you high. The other is l-methamphetamine, which makes the heart race but does little to the brain; it is waste product. Most cooks would likely want to get rid of the l-meth if they knew what it was. But separating the two is tricky, beyond the skills of most clandestine chemists. And without doing so, the resulting drug is inferior to ephedrine-based meth. It makes your heart hammer without offering as potent a high. Bozenko’s sample contained mostly d-methamphetamine. Someone had removed most of the l-meth. “I’ve taken down labs in several continents,” Bozenko told me years later. No one in the criminal world, as far as he and his colleagues knew, had ever figured out how to separate d-meth from l-meth before. Back in the late ’80s and ’90s, when the ephedrine method had taken over, the market for meth had grown because of ephedrine’s availability—and because the substance could be transformed into meth with ease and efficiency. All you had to do was tweak the ephedrine molecule, and doing that required little more than following a recipe. But you had to have ephedrine. The P2P method offered traffickers one huge advantage: The chemicals that could be used to make it were also used in a wide array of industries—among them racing fuel, tanning, gold mining, perfume, and photography. Law enforcement couldn’t restrict all these chemicals the way it had with ephedrine, not without damaging legitimate sectors of the economy. And a trained organic chemist could make P2P, the essential ingredient, in many ways. It was impossible to say how many methods of making P2P a creative chemist might come up with. Bozenko counted a dozen or so at first. He put them up in a large diagram on his office wall, and kept adding Post-it Notes with new ones as they appeared. As Bozenko dissected that sample in 2006, its implications hit him. Drugs made in a lab were not subject to weather or soil or season, only to chemical availability: With this new method and full access to the world’s chemical markets through Mexican shipping ports, traffickers could ramp up production of P2P meth in quantities that were, effectively, limitless. Even so, Bozenko couldn’t have anticipated just how widely the meth epidemic would reach some 15 years later, or how it would come to interact with the opioid epidemic, which was then gaining force. And he couldn’t know how strongly it would contribute to related scourges now very much evident in America—epidemics of mental illness and homelessness that year by year are growing worse. A few months after Bozenko’s discovery, on December 15, 2006, in a town named Tlajomulco de Zúñiga in the central-Mexican state of Jalisco, a methamphetamine lab exploded. Firefighters responded to the blaze, at a warehouse where plastic dinnerware had once been made. No one was hurt in the fire, nor was anyone arrested. But a fire chief called the local DEA office. Abe Perez supervised the DEA’s Guadalajara office back then. The warehouse stood on a cul-de-sac at the end of a house-lined street, Perez, who is now retired, remembered years later. Residents “knew something was going on; the smells were giving them headaches,” Perez told me. But they were afraid to say anything. So they lived with it as best they could until the warehouse exploded, most likely because of a worker’s carelessness. Perez and his agents urged Mexican police and prosecutors to obtain a search warrant for the building. The process was slow, and the day ended with no warrant. That night another fire erupted, at a warehouse across the street that, the agents learned, contained chemicals in blue plastic barrels and in bags neatly stacked on pallets. “The traffickers came in the middle of the night with gasoline and burned it, burned all the evidence,” Perez said. “But we were able to get photos of the place.” Eduardo Chávez, another DEA agent, flew in from Mexico City the next afternoon. He and Perez stood outside the second smoldering warehouse. Each man had spent the early part of his career busting meth labs in rural California—Chávez in the area around Bakersfield, Perez in northeastern San Diego County. That had been a different era, and each had gotten a rare view into it. Bakersfield was Chávez’s first assignment, in 2000, and to his surprise, it was a hotbed of meth production. Southern California was where the ephedrine-based method had been rediscovered, largely due to the efforts of an ingenious criminal named Donald Stenger. Stenger died in 1988, in custody in San Diego County, after a packet of meth he’d inserted in his rectum broke open. But the ephedrine method had by then become more widely known and adopted by Mexican traffickers moving up and down the coast between Mexico and California. [From the January/February 2016 issue: How DEA agents took down Mexico’s most vicious drug cartel] The Mexican meth industry had been pioneered in that earlier time by two brothers, Luis and Jesús Amezcua. They came to California illegally as kids, and eventually ran an auto shop near San Diego. The story goes that a local meth cook dropped by their shop in about 1988, asking Jesús if he could bring in ephedrine from Mexico. Jesús at the time was smuggling Colombian cocaine. But he brought ephedrine north and, with that, became attuned to the market that had been opened by Stenger’s innovation. Ephedrine was then an unregulated chemical in Mexico. Within a few years, the Amezcuas were importing tons of it. Jesús traveled to India and Thailand, where he set up an office to handle his ephedrine exports. Later, his focus shifted to China and the Czech Republic. The Amezcuas’ meth career lasted about a decade, until cases brought against them landed them in a Mexican prison, where they remain. But the brothers marked a new way of thinking among Mexican traffickers. They were more interested in business deals and alliances than in the vengeance and endless shoot-outs so common to the previous generation of smugglers, who had trafficked mostly in marijuana and cocaine. The Amezcuas were the first Mexican traffickers to understand the profit potential of a synthetic drug, and the first to tap the global economy for chemical connections. At first, the brothers ran labs on both sides of the border. They set up many in California’s rural Central Valley—Eduardo Chávez’s territory—making use of an existing network of traffickers among the truckers and migrant farmworkers that stretched up from San Diego. At one bust, agents found a man in protective garments with an air tank on his back. He turned out to be a veterinarian from Michoacán who said he came up for four-month stints to teach the workers to cook. Hell’s Angels cooks took three days to make five pounds of meth. Mexican crews soon learned to arrive at cook sites like NASCAR pit crews, with premeasured chemicals, large vats, and seasoned workers. They produced 10 to 15 pounds per cook in 24 hours in what came to be known as “super labs.” Soon the biker gangs were buying their meth from the Mexicans. But toward the end of Chávez’s Bakersfield assignment, in 2004, the cooks and workers who’d been coming up from Mexico began to vanish. His informants told him that they were heading home. In California, law enforcement had made things hard; the job was getting too risky, the chemicals too hard to come by. The meth-cook migration would accelerate after Chávez left the state in 2004. Meth-lab seizures in the United States withered—from more than 10,000 that year to some 2,500 in 2008. Today in the United States, they are rare, and “super labs” are practically nonexistent. In Mexico, however, it was a different story. The burned-down lab being surveyed by Chávez and Perez at the end of 2006 had been designed to produce industrial quantities of meth. Like many other labs that had been popping up in Mexico, it reflected the union of substantial capital and little concern for law enforcement. It used expensive equipment and stored large inventories of chemicals awaiting processing. Notes found on the scene suggested that the cooks typically got about 240 pounds per batch. Like Joe Bozenko, the agents standing at the edge of the smoke and the stench that afternoon felt that they were glimpsing a new drug world. What struck them both was what they were not seeing. No ephedrine. The lab was set up exclusively to make P2P meth. What’s more, this lab was not hidden up in the mountains or on a rural ranch. Tlajomulco de Zúñiga lies just 15 miles south of Guadalajara, one of Mexico’s largest cities, and serves as home to the city’s international airport. The area has everything needed to be a center of meth manufacturing: warehouses, transportation hubs, proximity to chemists. Trucks rumble through the area daily from the shipping ports in Lázaro Cárdenas, in the state of Michoacán, and Manzanillo, in the state of Colima. The ephedrine method was still very much in use in 2006; Mexico, which had been reducing legal imports of ephedrine, wouldn’t ban them outright until 2008; even after that, some traffickers relied on illegal shipments for a time. And despite all the advances when it came to making P2P, in at least some respects the traffickers “didn’t know what they were doing yet,” Chávez told me. The explosion showed that. Nonetheless, years later he thought back on that moment and realized that it was almost as if they were witnessing a shift right then, that week. About five years after the Tlajomulco lab exploded, in June 2011, Mexican authorities discovered a massive P2P meth lab in the city of Querétaro, just a few hours north of Mexico City. It was in a warehouse that could have fit a 737, in an industrial park with roads wide enough for 18-wheelers; it made the Tlajomulco lab look tiny. Joe Bozenko and his colleague Steve Toske were called down from Washington to inspect it, and they wandered through it in awe. Bags of chemicals were stacked 30 feet high. Hundreds of those bags contained a substance neither Bozenko nor Toske had ever thought could be used to make P2P. Bozenko often consulted a book that outlined chemicals that might serve as precursors to making methamphetamine, but this particular substance wasn’t in it. Well-trained organic chemists were clearly improvising new ways to make the ingredients, expanding potential supply even further. Working through all the chemicals in the plant, by Bozenko’s estimation, the lab could have produced 900 metric tons of methamphetamine. Against a wall stood three 1,000-liter reactors, two stories tall. Nothing like this had been achieved with ephedrine, nor could it have been; no one could have imagined the accumulation of 900 metric tons of the chemical. Later, Mexican investigators would report that of the 16 workers arrested at the Querétaro lab, 14 died over the next six months from liver failure—presumably caused by exposure to chemicals at the lab. Methamphetamine was having a cultural moment in the U.S.—“meth mouth” had become an object of can’t-look-away fascination on the internet, and Breaking Bad was big. The switch from ephedrine-based labs to ones using the P2P method was even a plot point in the series. But few people outside the DEA really understood the consequences of this shift. Soon, tons of P2P meth were moving north, without any letup, and the price of meth collapsed. But there was more to the story than higher volume. Ephedrine meth tended to damage people gradually, over years. With the switchover to P2P meth, that damage seemed to accelerate, especially damage to the brain. One night in 2009, in Temecula, California, partway between San Diego and L.A., a longtime user of crystal meth named Eric Barrera felt the dope change. Barrera is a stocky ex-Marine who’d grown up in the L.A. area. The meth he had been using for several years by then made him talkative and euphoric, made his scalp tingle. But that night, he was gripped with paranoia. His girlfriend, he was sure, had a man in her apartment. No one was in the apartment, she insisted. Barrera took a kitchen knife and began stabbing a sofa, certain the man was hiding there. Then he stabbed a mattress to tatters, and finally he began stabbing the walls, looking for this man he imagined was hiding inside. “That had never happened before,” he told me when I met him years later. Barrera was hardly alone in noting a change. Gang-member friends from his old neighborhood took to calling the meth that had begun to circulate in the area around that time “weirdo dope.” [Read: A former meth addict talks about his experience with drug court] Barrera had graduated from high school in 1998 and joined the Marine Corps. He was sent to Camp Lejeune, in North Carolina, where he was among the few nonwhite Marines in the platoon. The racism, he felt, was threatening and brazen. He asked for a transfer to Camp Pendleton, in San Diego County, and was denied. Over the next year and a half, he said, it got worse. Two years into his service, he was honorably discharged. After the September 11, 2001, terrorist attacks, Barrera was filled with remorse that he hadn’t stuck it out in the Corps. He was home now, without the heroic story he’d imagined for himself when he joined the Marines. The way he tells it, he drank and used meth to relieve his depression. He’d sometimes stay up on meth for four or five days, and he had to make excuses for missing work. But until that point, he’d held his life together. He worked as a loan processor, then for an insurance company. He had an apartment, a souped-up Acura Integra, a lot of friends. But as the meth changed around 2009, so did Barrera’s life. His cravings for meth continued, but paranoia and delusions began to fill his days. “Those feelings of being chatty and wanting to talk go away,” he told me. “All of a sudden you’re stuck and you’re in your head and you’re there for hours.” He said strange things to people. He couldn’t hold a job. No one tolerated him for long. His girlfriend, then his mother, then his father kicked him out, followed by a string of friends who had welcomed him because he always had drugs. When he described his hallucinations, “my friends were like, ‘I don’t care how much dope you got, you can’t stay here.’ ” By 2012, massive quantities of meth were flowing into Southern California. That same year, 96 percent of the meth samples tested by DEA chemists were made using the P2P method. And, for the first time in more than a decade of meth use, Barrera was homeless. He slept in his car and, for a while, in abandoned houses in Bakersfield. He was hearing voices. A Veterans Affairs psychologist diagnosed him with depression and symptoms of schizophrenia. Even many years later, when I spoke with him, Barrera didn’t know how the drug he was using had changed and spread, or why. But as a resident of Southern California, he was among the first to be affected by it. Over the next half-dozen years or so, the flood of P2P meth would spread east, immersing much of the rest of the country, too. Mention drug-running, and many people will think of cartels. Yet over the past decade, meth’s rising availability did not result from the dictates of some underworld board of directors. Something far more powerful was at work, particularly in the Sinaloa area: a massive, unregulated free market. By the time Eric Barrera’s life began to collapse, something like a Silicon Valley of meth innovation, knowledge, skill, and production had formed in the states along Mexico’s northern Pacific Coast. The deaths of kingpins who had controlled the trade, in the early 2010s, had only accelerated the process. “When the control vanishes, all these regional fiefdoms spring up,” said a DEA supervisor who pursued Mexican trafficking organizations during these years. (He, like some other DEA agents I spoke with, asked that his name not be used, because of the dangerous nature of his work.) “We just started seeing more and more labs springing up everywhere.” The new labs weren’t all as enormous as the Querétaro lab that Bozenko had seen in 2011. But they multiplied quickly. Beginning in about 2013 and continuing for the next several years, meth production expanded geometrically; the labs “just escape all limits,” a member of the Sinaloan drug world told me. “In a five-square-kilometer area outside Culiacán [Sinaloa’s capital city], there were, like, 20 labs. No exaggeration. You go out to 15 kilometers, there’s more than a hundred.” Listening to traffickers on wiretaps, one DEA agent told me, made it clear just how loose the confederations of meth suppliers were by then. The cartels had not vanished, and many of these suppliers were likely paying one or another of them off. But the wires nonetheless revealed a pulsing ecosystem of independent brokers, truckers, packagers, pilots, shrimp-boat captains, mechanics, and tire-shop owners. In the United States, the system included meat-plant workers, money-wiring services, restaurants, farm foremen, drivers, safe houses, and used-car lots. The ecosystem harnessed the self-interest of each of these actors, who got paid only when deals got done. “We’d waste hours listening on the wire,” the agent told me, “to people wasting their time calling around doing the networking as brokers, trying to set up drug deals, because they wanted to make money. There’s a huge layer of brokers who are the driving force [in Mexican drug trafficking]. Maybe they own a business or restaurant in Mexico or in the U.S.—this is something they do to supplement income. A large percentage of drug deals at this level don’t happen. But it’s like salesmen—the more calls you make, the more people you know, the more sales you get. So four or five people will be involved in getting 50 kilos to some city in the United States. This guy knows a guy who knows a guy who has a cousin in Atlanta … And with the independent transporters operating at the border, there’s no cartel allegiance. They’re all just making money.” From 2015 to 2019, the Mexican military raided some 330 meth labs in Sinaloa alone. But arrests were rare, according to a person involved in targeting the labs. Far from being a deterrent, the raids showed that no one would pay a personal price, and more people entered the trade as a result. At one point in 2019, DEA intelligence held that, despite all the raids, at least 70 meth labs were operating in Sinaloa, each with the capacity to make tons of meth with every cook. With labs popping up everywhere, the price of a pound of meth fell to nearly $1,000 for the first time on U.S. streets by the late 2010s—a 90 percent drop from a decade earlier in many areas. Yet traffickers’ response to tumbling prices was to increase production, hoping to make up for lower prices with higher volume. Competition among producers also drove meth purity to record highs. Pot was part of this story too. As some American states legalized marijuana, Mexican pot revenue faltered. Many producers switched to making meth and found it liberating. Marijuana took months to grow, was bulky, and could rot. “But with crystal meth,” the member of the Sinaloan drug world told me, “in 10 days you’ve made it. It’s not as bulky as pot, so in two weeks you’re crossing the border with it. Within two or three months, you’re big.” In the Southwest, the drug quickly became more prevalent than ever. And supply kept flowing east, covering the country in meth all the way to New England, which had almost none before the mid-2010s. Since late 2016, the Midwest and South have seen an especially dramatic shift. Mexican traffickers had never been able to get their hands on enough ephedrine to cover those regions, but now that was no longer an issue. In place after place, they made alliances with local dealers to introduce their product. The Louisville, Kentucky, area is one example. For years, Louisville had a paltry meth market. A pound of it sold for $14,000. Then Wiley Greenhill went to prison. Greenhill was a minor drug dealer in Detroit who had come to Louisville in 1999, attracted by Kentucky’s vibrant street market for pain pills, which were fetching five times what they sold for in Detroit. He eventually landed at the Roederer Correctional Complex, north of Louisville, where he struck up a friendship with an inmate from California. The inmate’s father, a businessman from Southern California named Jose Prieto, had gotten into debt with the wrong people from Sinaloa. The Sinaloans told Prieto that to settle his debt, he had to sell their meth. Greenhill was given the opportunity to buy it. By 2016 Greenhill was out of prison, and the meth began to flow. At first Prieto sent small quantities through the mail. Soon the loads reached 50 to 100 pounds a month, driven east by women Greenhill hired. Prieto proved eager to get his product out. He fronted Greenhill hundreds of thousands of dollars’ worth of meth on the promise that he would be repaid. Tim Fritz, a DEA agent who investigated the Prieto-Greenhill ring, told me, “Jose Prieto would say, ‘Whatever you need, we got it. Whatever you buy, I’ll double it. You want 10 pounds, I’ll give you 20—pay me later.’ ” As months passed, the Louisville meth market expanded beyond anything the region had seen before. The trade spread to southern Indiana and nearby counties in Kentucky as the number of customers grew. Other local traffickers began to import meth as well. The price of a pound of meth fell to about $1,200, less than a tenth of what it had been just a few years earlier. At the MORE Center, a Louisville clinic set up to treat pain-pill and heroin addicts, patients started coming in on meth. Before the Prieto-Greenhill connection, only two of counselor Jennifer Grzesik’s patients were using meth. Within three years, almost 90 percent of new patients coming to the clinic had meth in their drug screen. “I don’t remember having any homeless people in my caseload before 2016,” she told me. But 20 percent of her clients now are homeless. Greenhill and Prieto were arrested in 2018 and 2019, respectively, and are now serving lengthy federal-prison terms. They left behind a transformed market. Primed by the new supply, meth demand has exploded, in turn drawing more dealers who have found their own supply connections. The price of a pound of meth remains low. To compete, some Louisville meth dealers now offer free delivery; others offer syringes already loaded with liquid meth so users can immediately shoot up. Similar partnerships, arrangements, and retail innovations have transformed regional drug markets across the U.S. Habits, once entrenched, are difficult to change. If they weren’t, more Americans would have quit smoking soon after 1964, when the U.S. surgeon general issued his first report on its risks. American nicotine addicts kept smoking because nicotine had changed their brain chemistry, and cigarettes were everywhere. We stopped people from smoking, argues Wendy Wood, a psychologist at the University of Southern California and the author of a book on habituation, by adding “friction” to the activity—making it harder to do or limiting access to supply. We removed cigarette vending machines, banned smoking in public spaces. By adding friction to smoking, we also removed cues that prompted people to smoke: bars where booze, friends, and cigarettes went together, for example. Something like the opposite of that has happened with P2P methamphetamine. “Meth reminds me of what alcoholics go through,” Matt Scharf, the director of recovery programs at Midnight Mission, a Los Angeles treatment center, told me. “There’s alcohol everywhere. Meth is now so readily available. There’s an availability to it that is not the case with heroin or crack. It’s everywhere.” All of that meth has been pushed into a market already softened up by the opioid epidemic. That should not have mattered: Historically, meth and opioid users had been separate groups with different cultures, and the drugs affect the brain’s reward pathways differently. But as large supplies of P2P meth began to arrive, many opioid addicts already feared for their life. Fentanyl, a dangerous synthetic opioid, was also spreading quickly. For many, Suboxone—which blocks opiate receptors and hence eliminates opioid cravings—was a lifesaver. They use it daily, the way a heart patient uses daily blood thinners to stay alive. Yet the counseling and continuum of care required to support the broader life changes necessary for addiction recovery are often absent. [From the May 2019 issue: Sam Quinones on how physicians get addicted too] Thus, as P2P meth spread nationwide, an unprecedented event took place in American drug use: Opioid addicts began to shift, en masse, to meth. Meth overdoses have risen rapidly in recent years, but they are much less common than opioid ODs—you don’t typically overdose and die on meth; you decay. By 2019, in the course of my reporting, I was routinely coming into contact with people in Kentucky, Ohio, Indiana, Tennessee, and West Virginia who were using Suboxone to control their opiate cravings from long-standing addiction to pain pills and heroin, while using methamphetamine to get high. Massive supplies of cheap P2P meth had created demand for a stimulant out of a market for a depressant. In the process, traffickers forged a new population of mentally ill Americans. Over the past year and a half, I’ve talked with meth addicts, counselors, and cops around the country. The people I spoke with told me stories nearly identical to Eric Barrera’s: P2P-meth use was quickly causing steep deterioration in mental health. The symptoms were always similar: violent paranoia, hallucinations, conspiracy theories, isolation, massive memory loss, jumbled speech. Methamphetamine is a neurotoxin—it damages the brain no matter how it is derived. But P2P meth seems to create a higher order of cerebral catastrophe. “I don’t know that I would even call it meth anymore,” Ken Vick, the director of a drug-treatment center in Kansas City, Missouri, told me. Schizophrenia and bipolar disorder are afflictions that begin in the young. Now people in their 30s and 40s with no prior history of mental illness seemed to be going mad. Portland, Oregon, began seeing the flood of meth around 2013. By January 2020, the city had to close its downtown sobering station. The station had opened in 1985 as a place for alcoholics to sober up for six to eight hours, but it was unequipped to handle people addicted to P2P meth. “The degree of mental-health disturbance; the wave of psychosis; the profound, profound disorganization [is something] I’ve never seen before,” Rachel Solotaroff, the CEO of Central City Concern, the social-service nonprofit that ran the station, told me. Solotaroff was among the first people I spoke with. She sounded overwhelmed. “If they’re not raging and agitated, they can be completely noncommunicative. Treating addiction [relies] on your ability to have a connection with someone. But I’ve never experienced something like this—where there’s no way in to that person.” [From the April 2015 issue: The irrationality of Alcoholics Anonymous] On Skid Row in Los Angeles, crack had been the drug of choice for decades. Dislodging it took some time. But by 2014 the new meth was everywhere. When that happened, “it seemed that people were losing their minds faster,” a Los Angeles Police Department beat officer named Deon Joseph told me. Joseph had worked Skid Row for 22 years. “They’d be okay when they were just using crack,” Joseph said. “Then in 2014, with meth, all of a sudden they became mentally ill. They deteriorated into mental illness faster than I ever saw with crack cocaine.” Susan Partovi has been a physician for homeless people in Los Angeles since 2003. She noticed increasing mental illness—schizophrenia, bipolar disorder—at her clinics around the city starting in about 2012. She was soon astonished by “how many severely mentally ill people were out there,” Partovi told me. “Now almost everyone we see when we do homeless outreach on the streets is on meth. Meth may now be causing long-term psychosis, similar to schizophrenia, that lasts even after they’re not using anymore.” I called James Mahoney, a neuropsychologist at West Virginia University who had studied the effects of ephedrine meth on the brain in the early 2000s at UCLA. The psychosis he saw then was bad, he said, but it frequently appeared to be the result of extended sleep deprivation. In 2016, Mahoney took a job as a drug researcher and specialist in WVU’s addiction clinic. Less than a year later, the P2P crystal meth from Mexico started showing up. Mahoney was inundated with meth patients who came in ranting, conversing with phantoms. “I can’t even compare it to what I was seeing at UCLA,” he told me. “Now we’re seeing it instantaneously, within hours, in people who just used: psychotic symptoms, hallucinations, delusions.” In community after community, I heard stories like this. Southwest Virginia hadn’t seen much meth for almost a decade when suddenly, in about 2017, “we started to see people go into the state mental-hospital system who were just grossly psychotic,” Eric Greene, then a drug counselor in the area, told me. “Since then, it’s caused a crisis in our state mental-health hospitals. It’s difficult for the truly mentally ill to get care because the facilities are full of people who are on meth.” Symptoms could fade once users purged the drug, if they did not relapse. But while they were on this new meth, they grew antisocial, all but mute. I spoke with two recovering meth addicts who said they had to relearn how to speak. “It took me a year and a half to recover from the brain damage it had done to me,” one of them said. “I couldn’t hardly form sentences. I couldn’t laugh, smile. I couldn’t think.” I spoke with Jennie Jobe, from rural Morgan County, in eastern Tennessee. Jobe had spent 20 years working in state prisons when she started a drug court and associated residential treatment center in 2013. For its first few years, Jobe’s court handled meth addicts who got their drugs from local “shake and bake” manufacturers— small-batch cooks using Sudafed, and usually producing just a few grams of the drug at a time. These meth users were gaunt, she remembers, and picked at their skin. But they were animated, lucid, with memories and personalities intact when they arrived at her facility, detoxed after months in jail. By 2017, however, people were coming to her treatment center stripped of human energy, even after several months spent detoxing from the drug in jail. “Normal recreational activities where guys talk trash and have fun—there’s none of that. It’s like their brain cannot fire.” Treating them was daunting. Despite years of research, science has found no equivalent of methadone or Suboxone to help subdue meth cravings and allow people addicted to the drug a chance to break from it and begin repairing their life. And, like many others I spoke with, Jobe found that the human connection essential to successful drug treatment was almost impossible to establish. “It takes longer for them to actually be here mentally,” Jobe said. “Before, we didn’t keep anybody more than nine months. Now we’re running up to 14 months, because it’s not until six or nine months that we finally find out who we got.” Some can’t remember their life before jail. “It’s not unusual for them to ask what they were found guilty of and sentenced to,” she said. Why is P2P meth producing such pronounced symptoms of mental illness in so many people? No one I spoke with knew for sure. One theory is that much of the meth contains residue of toxic chemicals used in its production, or other contaminants. Even traces of certain chemicals, in a relatively pure drug, might be devastating. The sheer number of users is up, too, and the abundance and low price of P2P meth may enable more continual use among them. That, combined with the drug’s potency today, might accelerate the mental deterioration that ephedrine-based meth can also produce, though usually over a period of months or years, not weeks. Meth and opioids (or other drugs) might also interact in particularly toxic ways. I don’t know of any study comparing the behavior of users—or rats for that matter—on meth made with ephedrine versus meth made with P2P. This now seems a crucial national question. Once your eyes are open to the scale and human consequences of the P2P-meth epidemic, it’s hard to miss its ramifications in many areas of American public life. Perhaps the most significant is homelessness. In 2012, a Los Angeles Superior Court judge, Craig Mitchell, founded L.A.’s Skid Row Running Club. Every Monday, Thursday, and Saturday, 20 to 50 people—recovering addicts, cops, public defenders, social workers—meet around dawn in front of a local shelter to run for an hour through the greatest concentration of homeless people in the United States. The club’s broader mission is to support the area’s homeless community through mentorship and a focus on wellness. Los Angeles has long been the nation’s homelessness capital, but as in many cities—large and small—the problem has worsened greatly in recent years. In the L.A. area, homelessness more than doubled from 2012 to 2020. Mitchell told me that the most visible homelessness—people sleeping on sidewalks, or in the tents that now crowd many of the city’s neighborhoods—was clearly due to the new meth. “There was a sea change with respect to meth being the main drug of choice beginning in about 2008,” he said. Now “it’s the No. 1 drug.” Remarkably, meth rarely comes up in city discussions on homelessness, or in newspaper articles about it. Mitchell called it “the elephant in the room”—nobody wants to talk about it, he said. “There’s a desire not to stigmatize the homeless as drug users.” Policy makers and advocates instead prefer to focus on L.A.’s cost of housing, which is very high but hardly relevant to people rendered psychotic and unemployable by methamphetamine. Addiction and mental illness have always been contributors to homelessness. P2P meth seems to produce those conditions quickly. “It took me 12 years of using before I was homeless,” Talie Wenick, a counselor in Bend, Oregon, who began using ephedrine-based meth in 1993 and has been clean for 15 years, told me. “Now within a year they’re homeless. So many homeless camps have popped up around Central Oregon—huge camps on Bureau of Land Management land, with tents and campers and roads they’ve cleared themselves. And almost everyone’s using. You’re trying to help someone get clean, and they live in a camp where almost everyone is using.” Eric Barrera is now a member of Judge Mitchell’s running club. Through the VA, he got treatment for his meth addiction and found housing; without meth, he was able to keep it. The voices in his head went away. He volunteered at a treatment center, which eventually hired him as an outreach worker, looking for vets in the encampments. Barrera told me that every story he hears in the course of his work is complex; homelessness, of course, has many roots. Some people he has met were disabled and couldn’t work, or were just out of prison. Others had lost jobs or health insurance and couldn’t pay for both rent and the surgeries or medications they needed. They’d scraped by until a landlord had raised their rent. Some kept their cars to sleep in, or had welcoming families who offered a couch or a bed in a garage. Barrera thought of them as invisible, the hidden homeless, the shredded-safety-net homeless. But Barrera also told me that for a lot of the residents of Skid Row’s tent encampments, meth was a major reason they were there and couldn’t leave. Such was the pull. Some were addicted to other things: crack or heroin, alcohol or gambling. Many of them used any drug available. But what Barrera encountered the most was meth. Tents themselves seem to play a role in this phenomenon. Tents protect many homeless people from the elements. But tents and the new meth seem made for each other. With a tent, the user can retreat not just mentally from the world but physically. Encampments provide a community for users, creating the kinds of environmental cues that the USC psychologist Wendy Wood finds crucial in forming and maintaining habits. They are often places where addicts flee from treatment, where they can find approval for their meth use. In Los Angeles, the city’s unwillingness, or inability under judicial rulings, to remove the tents has allowed encampments to persist for weeks or months, though a recent law allows for more proactive action. In this environment, given the realities of addiction, the worst sorts of exploitation have sometimes followed. In 2020, I spoke with Ariel, a transgender woman then in rehab, who had come to Los Angeles from a small suburb of a midsize American city four years before. She had arrived hoping for gender-confirmation surgery and saddled with a meth habit. She eventually ended up alone on Hollywood’s streets. “There’s these camps in Hollywood, on Vine and other streets—distinct tent camps,” she said, where women on meth are commonly pimped. “A lot of people who aren’t homeless have these tents. They come from out of the area to sell drugs, move guns, prostitute girls out of the tents. The last guy I was getting worked out by, he was charging people $25 a night to use his tents. He would give you girls, me and three other people. He’d take the money and we’d get paid in drugs.” Megan Schabbing, a psychiatrist and the medical director of emergency psychiatric services at OhioHealth, in Columbus, Ohio, later described to me how meth use and this sort of suffering can reinforce each other. Schabbing spends much of her time on the job digging into the underlying causes of drug use among those who end up in the ER. Often there was trauma: beatings, molestation, rape, war deployment, childhood chaos, neglect. For many of these patients, she discovered, the delusions fueled by meth became the point—the drug’s attraction. “Many would tell me, ‘I can stay out of reality on the street’ ” by using meth, she said. “When they come to us, it takes them days to figure out who and where they are. But some patients have told me that’s not a bad thing if you’re on the street.” If P2P meth pushed her patients toward homelessness, it also helped them bear it. How could this crisis emerge so quietly and remain, in many ways, invisible to most Americans? One reason, perhaps, is the national focus on the opioid epidemic, which was itself ignored for a long time. In recent years, the headlines have been about pain-pill or heroin overdoses, then fentanyl overdoses, and the funding has followed. Besides, deaths, however tragic, allow for memorials, a chance to remember the deceased’s better days. Meth doesn’t kill people at nearly the same rate as opioids. It presents, instead, the rawest face of living addiction. That part of addiction, one counselor told me, “people don’t want to touch it.” There is no central villain in the P2P-meth story—no Purdue Pharma, no dominant cartel. There’s no single entity to target, either. So the issue is often enveloped in a willful myopia. Advocates for homeless people seem reluctant to speak out about the drug, for fear that the downtrodden will be blamed for their troubles. The spread of P2P meth is part of a larger narrative—a shift in drug supply from plant-based drugs such as marijuana, cocaine, and heroin to synthetic drugs, which can be made anywhere, quickly, cheaply, and year-round. Underground chemists are continually seeking to develop more potent and addictive varieties of them. The use of mind-altering substances by humans is age-old, but we have entered a new era. Drug demand is important in this new era. People need to understand what these drugs will ultimately do to them, and those who are using will need substantial help getting off them. But it must be said: The story of the meth epidemic (like the opioid epidemic before it) begins with supply. In a previous era, most Vietnam vets kicked heroin when they got home and were far from war and the potent supplies they were used to in Southeast Asia. Today, supplies of meth are vast and cheap throughout much of the country. Crystal meth is in some ways a metaphor for our times—times of anomie and isolation, of paranoia and delusion, of communities coming apart. Meth is not responsible for these much wider social problems, of course. But the meth epidemic is symptomatic of them, and also contributes to them. If you spend time among meth users, you’ll notice certain habits and tics: fixations on flashlights, for instance, and on bicycles, which are endlessly disassembled and assembled again. Hoodies are everywhere. The hoodie is versatile—cheap, warm, functional. But as opioids, then meth, spread across America, the hoodie also became, for many, a hiding place from a harsh world. “When we put up that hood,” one recovering addict told me, “we’re making the choice to separate ourselves from everyone else—instead of someone pushing us out. I think it’s our way to hide from the world that doesn’t accept us. The hood is the refuge. It’s our safe place.” Perhaps the best defense against epidemics like this one lies in choosing to look more closely and more sympathetically at the people in those hoods—to put a higher priority on community than we’ve done in recent years. America has made itself more vulnerable to scourges, even as those scourges grow more potent. But scourges are also an opportunity: They call on us to reexamine how we live. Until we begin to look out for the most vulnerable among us, there’s no reason to expect them to abate. This article is adapted from Sam Quinones’s new book, The Least of Us: True Tales of America and Hope in the Time of Fentanyl and Meth. It appears in the November 2021 print edition with the headline “The New Meth.” When you buy a book using a link on this page, we receive a commission. Thank you for supporting The Atlantic. from https://ift.tt/3AXK476 Check out http://natthash.tumblr.com In this week’s installment of the booster chronicles, the plot is picking up. An advisory committee to the FDA began a two-day meeting today to formulate recommendations for whether the agency should authorize additional doses of the Johnson & Johnson and Moderna COVID-19 vaccines. (The FDA still has to authorize, and the CDC still has to recommend, any new use of boosters before they’ll be readily available.) Committee members have already voted yes on giving boosters to people over 65 and other high-risk adults who received the Moderna vaccine. Meanwhile, the NIH released the results of a long-awaited (and not yet peer-reviewed) clinical trial on the “mix and match” approach to booster shots, in which people receive a dose of a different vaccine from the one they started with. The FDA committee is scheduled to discuss that idea, too, before this meeting ends. The 458-person NIH study showed that mix-and-match—also known as heterologous—boosting is safe and induces an increase in the relevant antibody counts, no matter the combination of vaccines. This isn’t particularly surprising, given the data that have already emerged from countries such as the U.K. and Spain, which have been studying the mix-and-match approach to initial shot regimens for months. In general, these have shown it’s about as good as, and in some cases better than, a homologous regimen. This week’s report expands that finding for the booster age, and adds one more: When boosters were compared head-to-head, the mRNA vaccines blew J&J’s out of the water. When the vaccines first debuted last winter, Americans were told that each one was excellent, so we should all get whichever of the three was most accessible. If mix-and-match boosters are authorized, we might find ourselves with a more bewildering decision: Nine different paths will be available in total, depending on where you started. Assuming that every option will soon be on the table, which one should people take? [Read: You might want to wait to get a booster shot] The NIH study tested and compared every possible combination, and here’s the gist: If you need a booster, don’t take J&J. Two weeks after boosting, people who had followed a J&J → Moderna regimen registered average antibody levels that were 9.8 times higher than those who had gotten two J&J shots; antibody levels among J&J → Pfizer recipients hovered just behind. Overall, the highest antibody levels were found among people for whom all three doses were Moderna; Pfizer → Moderna produced the second-highest levels, then Moderna → Pfizer. Moderna’s boosters seemed to be slightly more effective than Pfizer’s in general, but that doesn’t mean that Americans who have already gotten Pfizer boosters are missing out. The differences between those mRNA regimens were relatively small; more to the point, they’re absolutely dwarfed by the differences between either mRNA option and the J&J → J&J approach. Saad Omer, who directs Yale’s Institute for Global Health, told me that “we can’t be too precise” in interpreting these data, given the study’s small size. (There were only about 50 people in each of the nine trial groups.) But the apparent advantage of using the mRNA vaccines as boosters, compared with J&J’s, is so large, he said, that it’s unlikely to be an error. [Read: Fully vaccinated is suddenly a much less useful phrase] Other factors might also limit the significance of the apparent Moderna-Pfizer divide. In a paper published earlier this week, a team including Omer and led by his colleague Akiko Iwasaki found that those who have recovered from a COVID-19 infection and been vaccinated might be approaching a plateau of immune protection after which “the juice [of a booster shot] is not worth the squeeze,” Omer said. That suggests that the differences between the mix-and-match combinations could be even less meaningful for that population (though Omer said he’d have to see clinical data to be certain). Moderna’s edge might also be dulled given today’s recommendation from the committee for the use of a half-dose booster. (The NIH study tested full-dose boosters of Moderna.) Still, prior research suggests that a half dose of Moderna for the first or second shots were “generally comparable” in effect to the original regimen. “I’d be very surprised if it didn’t work quite well as a booster,” says Paul Sax, a Harvard professor and the clinical director of Brigham and Women’s Hospital’s infectious-disease division. All the findings described above may be telling just part of the story. Remember, the NIH study used antibody counts, which are a proxy measure of actual immunity. Antibodies represent the body’s first line of defense against the coronavirus, but they’re not our only weapon. Immune cells, such as B and T cells, are also important, especially in the long run. (Sax told me that some researchers guess that J&J might be especially good at inducing the latter, longer-lasting form of immunity.) The best way to determine which of the nine mix-and-match options produces the best protection from disease would be to recruit thousands of volunteers for a randomized controlled trial, and then count how many people on each regimen get sick over an extended period. But short of doing that, antibody levels provide the best and most convenient information that can be garnered quickly from the greatest number of people. [Read: A better name for booster shots] Omer would like to see such long-term data on clinical outcomes, along with more data on mix-and-match strategies’ effects on different age groups and how long booster protection lasts. These sorts of data are missing from plenty of booster studies, not just mix-and-match. Until we get them, we’ll be stuck where we are right now, knowing more than ever about how to boost, but still unsure of when, exactly, it’s most appropriate to do so. from https://ift.tt/3j1f9QQ Check out http://natthash.tumblr.com Perhaps the oddest consolation prize of America’s crushing, protracted battle with the coronavirus is the knowledge that flu season, as we’ve long known it, does not have to exist. It’s easy to think of the flu as an immutable fact of winter life, more inconvenience than calamity. But each year, on average, it sickens roughly 30 million Americans and kills more than 30,000 (though the numbers vary widely season to season). The elderly, the poor, and people of color are all overrepresented among the casualties. By some estimates, the disease’s annual economic cost amounts to nearly $90 billion. We accept this, when we think about it at all, as the way things are. Except that this past year, things were different: During the 2020–21 flu season, the United States recorded only about 2,000 cases, 17,000 times fewer than the 35 million it recorded the season before. That season, the flu killed 199 children; this past season, as far as we know, it killed one. “We’ve looked for flu in communities and doctors’ offices and hospitals, and we’ve gotten almost zero,” says Emily Martin, a University of Michigan epidemiologist who’s part of the CDC’s flu-monitoring network. The same was true of other seasonal respiratory viruses last winter, says Saskia Popescu, an epidemiologist at George Mason University in Virginia, though some have since rebounded. RSV, parainfluenza, rhinovirus, adenovirus—for a while, they all but vanished. [Read: The pandemic broke the flu] For this, perversely, we can thank the pandemic. The coronavirus itself may have played some role—infection could produce a general immune response that would also confer protection against the flu—but most of the epidemiologists I spoke with instead emphasized the importance of the behavioral changes adopted to slow the spread of the coronavirus: masking, distancing, remote learning, working from home, limiting indoor social gatherings. Despite the inconsistency with which America deployed them, these measures helped tamp down the spread of the virus, but they completely crushed influenza, a less transmissible foe to which the population has considerable preexisting immunity. We set out to flatten the curve, and we ended up stamping out the flu. This was one of the few blessings in an otherwise abysmal winter, in which COVID cases and deaths surged to their highest levels ever in the U.S. At least we didn’t face the dreaded “twindemic.” But our triumph over the flu also poses a dilemma, as much ethical as epidemiological. We’ve demonstrated conclusively that saving nearly everyone who dies of the flu is within our power. To do nothing now—to return to the roughly 30,000-deaths-a-year status quo without even trying to save some of those lives—would seem irresponsible. So what do we do? Which measures do we maintain and which do we let go? One thing we’re not going to do is go into lockdown every year (or even go into what passed for lockdown in the United States, which in reality was not). This, the public-health experts I spoke with for this story all agreed, would be neither feasible nor desirable. Broad restrictions on travel and large indoor gatherings, they said, also seem like nonstarters (though Seema Lakdawala, a flu-transmission expert at the University of Pittsburgh, suggested that companies might consider rescheduling their annual holiday party for the summer and moving it outdoors). Even more moderate capacity limitations, though beneficial from a health perspective, Popescu told me, are “tricky for business.” Still, perhaps other, targeted versions of the restrictions deployed during the pandemic could work. Linsey Marr, an environmental engineer at Virginia Tech, proposed a sort of “circuit breaker” system, in which schools and workplaces could go remote for a week or two to slow flu transmission during severe local outbreaks. Before shutdowns kick in, people could keep a close eye on flu cases in their area—just as many have monitored COVID numbers over the past two years—and make their own personal risk assessments. For one person, Lakdawala imagines, that might mean being more efficient in a crowded grocery store; for another, masking at a movie theater. (That said, people tend to be less than perfect at gauging the danger of different situations.) Masks, in theory, are one of the simplest pandemic-times interventions to hold on to. They are “the low-hanging fruit,” says the Emory University immunologist Anice Lowen, since, unlike shutdowns or restrictions on indoor gatherings, they don’t disrupt our daily routines. In an ideal world, several epidemiologists told me, people would mask in crowded indoor spaces during flu season—if not all the time, then at least when case counts are on the rise. If that became the norm, Marr told me, “we would see huge reductions in colds and flus. No question.” [Read: Why are Americans still—still!—wearing cloth masks?] Ours, of course, is not an ideal world, and masking is unlikely to become an uncontroversial American norm anytime soon. Demand too much, warns Angela Rasmussen, a virologist at the Vaccine and Infectious Disease Organization, in Saskatchewan, Canada, and you risk inciting backlash. Even if health officials ask people to mask only during local surges, she worries, “you’re going to have a lot of people who are like, ‘Well, we saw this coming. First you mandated masks for COVID; now you’re mandating masks all the time. It’s all about control! What about my freedom!’” At the very least, both Marr and Rasmussen would like to see the CDC recommend that people wear masks when symptomatic and provide information about how masking in crowded indoor spaces can lower the risk of infection. For now, the CDC isn’t prepared to endorse any new antiflu interventions. David Wentworth, the virology, surveillance, and diagnosis chief within the agency’s influenza division, agrees that pandemic precautions played a major role in reducing flu transmission over the past year. But he told me that the agency needs to see more data on which measures were most effective before it officially recommends any of them. “It sounds like we’re doing nothing, but really we want to understand what factors have the big impact before you start making those kinds of recommendations,” he said. “It’s not that we don’t care about the tens of thousands of people who are impacted by flu.” The agency’s most up-to-date information on masks and the flu is labeled “Interim Guidance” … as it has been since it was published in 2004. It stresses, as several of the experts I spoke with did, that no one intervention can provide total protection, and it even mentions social distancing and school closures as possible “community measures.” But outside of a health-care setting, it recommends masks only for people who either are diagnosed with the flu by a doctor or have a fever and respiratory symptoms during a known local outbreak—and even then, it stops short of an actual prescription. Those people should try to stay home, it says, but if they can’t, “consideration should be given” to masking in public spaces. Like everyone else I spoke with, Wentworth strongly recommended flu shots, which he called “the most important tool” at our disposal for fighting influenza. And while most years flu shots are considerably less effective than the best-performing COVID vaccines, several of the experts I spoke with said that not-so-far-off advances in immunization technology could narrow the gap before long. [Read: The most important vaccine I’ll get this fall] Certainly, methods for knocking out the flu need not be limited to successful pandemic interventions. Many experts advocated for changes they said were long overdue even before the pandemic began, chief among them paid sick leave, which every wealthy country in the world except the U.S guarantees. As a result, nearly a quarter of the American labor force must report to work when ill. Among the bottom quartile of earners, that proportion is more than half. And while many employers have introduced more accommodating policies during the pandemic, there’s no guarantee they’ll outlast it. In schools, perfect-attendance awards encourage a similar dynamic, even if well intentioned, says Sarah Cobey, an evolutionary biologist at the University of Chicago. Giving workers and students the ability to stay home when sick would go a long way toward reducing the flu’s spread. But policy changes alone won’t unravel the problem overnight. “There’s a real culture … that if you’re not on your deathbed or you’re not going to the hospital, that you’re fine to go to work,” Rasmussen told me. “If you’re sick, you should stay home. It seems like a no-brainer, but people are actually really resistant to that.” Whether because of that culture or because they don’t realize they’re contagious, some sick people will still come in to work. That, experts told me, is where overhauled ventilation can help us. For all the advances we’ve made in preventing diseases transmitted via water or insects, my colleague Sarah Zhang has written, we have overlooked air. Until the advent of sewer systems and water treatment, Marr said, people accepted deadly waterborne diseases as a basic fact of life. These days, the idea of drinking dirty water strikes most as repulsive, even as we resign ourselves to breathing filthy air and contracting seasonal respiratory viruses. But now, Marr said, “we’ve seen we don’t have to live that way.” By better ventilating our buildings—which to this point have largely been optimized for energy efficiency, not air quality—she said, we could do for air what we have done for water. That is at least a little ways off, though. To fight the flu right now, flu shots and nonpharmaceutical interventions are all we’ve got. If we’re going to save people, that’s how. We’re unlikely to consistently replicate the nonexistent flu season we just had, but the experts I spoke with said that even the more modest precautions could reduce mortality by 25, 50, even 75 percent, which translates to tens of thousands of lives saved. Those figures, they stressed, are highly speculative. So far, the 2021–22 season is off to a good start, though some experts worry that the flu will be back with a vengeance before long. Whatever happens, there can be no more illusions of inevitability. The flu, it turns out, has always been a choice. Now we have the opportunity to do something about it—and the burden of knowing we can. from https://ift.tt/3DI50kd Check out http://natthash.tumblr.com |
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