This fall, millions of Americans might be lining up for yet another kind of COVID vaccine:  their first-ever dose that lacks the strain that ignited the pandemic more than three and a half years ago. Unlike the current, bivalent vaccine, which guards against two variants at once, the next one could, like the first version of the shot, have only one main ingredient—the spike protein of the XBB.1 lineage of the Omicron variant, the globe’s current dominant clade.

That plan isn’t yet set. The FDA still has to convene a panel of experts, then is expected to make a final call on autumn’s recipe next month. But several experts told me they hope the agency follows the recent recommendation of a World Health Organization advisory group and focuses the next vaccine only on the strains now circulating.

The switch in strategy—from two variants to one, from original SARS-CoV-2 plus Omicron to XBB.1 alone—would be momentous but wise, experts told me, reflecting the world’s updated understanding of the virus’s evolution and the immune system’s quirks. “It just makes a lot of sense,” said Melanie Ott, the director of the Gladstone Institute of Virology, in San Francisco. XBB.1 is the main coronavirus group circulating today; neither the original variant nor BA.5, the two coronavirus flavors in the bivalent shot, is meaningfully around anymore. And an XBB.1-focused vaccine may give the global population a particularly good shot at broadening immunity.

At the same time, COVID vaccines are still in a sort of beta-testing stage. In the past three-plus years, the virus has spawned countless iterations, many of which have been extremely good at outsmarting us; we humans, meanwhile, are only on our third-ish attempt at designing a vaccine that can keep pace with the pathogen’s evolutionary sprints. And we’re very much still learning about the coronavirus’s capacity for flexibility and change, says Rafi Ahmed, an immunologist at Emory University. By now, it’s long been clear that vaccines are essential for preventing severe disease and death, and that some cadence of boosting is probably necessary to keep the shots’ effectiveness high. But when the virus alters its evolutionary tactics, our vaccination strategy must follow—and experts are still puzzling out how to account for those changes as they select the shots for each year.

In the spring and summer of 2022, the last time the U.S. was mulling on a new vaccine formula, Omicron was still relatively new, and the coronavirus’s evolution seemed very much in flux. The pathogen had spent more than two years erratically slingshotting out Greek-letter variants without an obvious succession plan. Instead of accumulating genetic changes within a single lineage—a more iterative form of evolution, roughly akin to what flu strains do—the coronavirus produced a bunch of distantly related variants that jockeyed for control. Delta was not a direct descendant of Alpha; Omicron was not a Delta offshoot; no one could say with any certainty what would arise next, or when. “We didn’t understand the trajectory,” says Kanta Subbarao, the head of the WHO advisory group convened to make recommendations on COVID vaccines.

And so the experts played it safe. Including an Omicron variant in the shot felt essential, because of how much the virus had changed. But going all in on Omicron seemed too risky—some experts worried that “the virus would flip back,” Subbarao told me, to a variant more similar to Alpha or Delta or something else. As a compromise, several countries, including the United States, went with a combination: half original, half Omicron, in an attempt to reinvigorate OG immunity while laying down new defenses against the circulating strains du jour.

And those shots did bolster preexisting immunity, as boosters should. But they didn’t rouse a fresh set of responses against Omicron to the degree that some experts had hoped they would, Ott told me. Already trained on the ancestral version of the virus, people’s bodies seemed to have gotten a bit myopic—repeatedly reawakening defenses against past variants, at the expense of new ones that might have more potently attacked Omicron. The outcome was never thought to be damaging, Subbarao told me: The bivalent, for instance, still broadened people’s immune responses against SARS-CoV-2 compared with, say, another dose of the original-recipe shot, and was effective at tamping down hospitalization rates. But Ahmed told me that, in retrospect, he thinks an Omicron-only boost might have further revved that already powerful effect.

Going full bore on XBB.1 now could keep the world from falling into that same trap twice. People who get an updated shot with that strain alone would receive only the new, unfamiliar ingredient, allowing the immune system to focus on the fresh material and potentially break out of an ancestral-strain rut. XBB.1’s spike protein also would not be diluted with one from an older variant—a concern Ahmed has with the current bivalent shot. When researchers added Omicron to their vaccine recipes, they didn’t double the total amount of spike protein; they subbed out half of what was there before. That left vaccine recipients with just half the Omicron-focused mRNA they might have gotten had the shot been monovalent, and probably a more lackluster antibody response.

Recent work from the lab of Vineet Menachery, a virologist at the University of Texas Medical Branch, suggests another reason the Omicron half of the shot didn’t pack enough of an immunizing punch. Subvariants from this lineage, including BA.5 and XBB.1, carry at least one mutation that makes their spike protein unstable—to the point where it seems less likely than other versions of the spike protein to stick around for long enough to sufficiently school immune cells. In a bivalent vaccine, in particular, the immune response could end up biased toward non-Omicron ingredients, exacerbating the tendencies of already immunized people to focus their energy on the ancestral strain. For the same reason, a monovalent XBB.1, too, might not deliver the anticipated immunizing dose, Menachery told me. But if people take it (still a big if), and hospitalizations remain low among those up-to-date on their shots, a once-a-year total-strain switch-out might be the choice for next year’s vaccine too.

Dropping the ancestral strain from the vaccine isn’t without risk. The virus could still produce a variant totally different from XBB.1, though that does, at this point, seem unlikely. For a year and a half now, Omicron has endured, and it now has the longest tenure of a single Greek-letter variant since the pandemic’s start. Even the subvariants within the Omicron family seem to be sprouting off each other more predictably; after a long stint of inconsistency, the virus’s shape-shifting now seems “less jumpy,” says Leo Poon, a virologist at the University of Hong Kong. It may be a sign that humans and the virus have reached a détente now that the population is blanketed in a relatively stable layer of immunity. Plus, even if a stray Alpha or Delta descendant were to rise up, the world wouldn’t be caught entirely off guard: So many people have banked protection against those and other past variants that they’d probably still be well buffered against COVID’s worst acute outcomes. (That reassurance doesn’t hold, though, for people who still need primary-series shots, including the kids being born into the world every day. An XBB.1 boost might be a great option for people with preexisting immunity. But a bivalent that can offer more breadth might still be the more risk-averse choice for someone whose immunological slate is blank.)

More vaccination-strategy shifts will undoubtedly come. SARS-CoV-2 is still new to us; so are our shots. But the virus’s evolution, as of late, has been getting a shade more flu-like, and its transmission patterns a touch more seasonal. Regulators in the U.S. have already announced that COVID vaccines will probably be offered each year in the fall—as annual flu shots are. The viruses aren’t at all the same. But as the years progress, the comparison between COVID and flu shots could get more apt still—if, say, the coronavirus also starts to produce multiple, genetically distinct strains that simultaneously circulate. In that case, vaccinating against multiple versions of the virus at once might be the most effective defense.

Flu shots could be a useful template in another way: Although those shots have followed roughly the same guidelines for many years, with experts meeting twice a year to decide whether and how to update each autumn’s vaccine ingredients, they, too, have needed some flexibility. Until 2012, the vaccines were trivalent, containing ingredients that would immunize people against three separate strains at once; now many, including all of the U.S.’s, are quadrivalent—and soon, based on new evidence, researchers may push for those to return to a three-strain recipe. At the same time, flu and COVID vaccines share a major drawback. Our shots’ ingredients are still selected months ahead of when the injections actually reach us—leaving immune systems lagging behind a virus that has, in the interim, sprinted ahead. Until the world has something more universal, our vaccination strategies will have to be reactive, scrambling to play catch-up with these pathogens’ evolutionary whims.

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Three and a half years since the start of a pandemic that has killed millions of people and debilitated countless more, the world is still stuck at the start of the COVID-19 crisis in one maddening way: No one can say with any certainty how, exactly, the outbreak began. Many scientists think the new virus spilled over directly from a wild animal, perhaps at a Chinese wet market; some posit that the pathogen leaked accidentally from a local laboratory in Wuhan, China, the pandemic’s likely epicenter. All of them lack the slam-dunk evidence to prove one hypothesis and rule out the rest.

That’s not to say nothing has changed. Those embroiled in the origins fracas now have much more data to scrutinize, debate, and re-debate. In March, I reported that the case for a zoonotic origin had acquired a consequential new piece of support: An international team of scientists had uncovered genetic data, collected from a wet market in Wuhan in the weeks after the venue was closed on January 1, 2020, that linked the coronavirus to wild animals. This evidence, they said, indicated that one of those creatures could have been shedding SARS-CoV-2, the virus that causes COVID-19; one of the most intriguing bits of data pointed to raccoon dogs, a foxlike creature that was already known to be vulnerable to the virus. The finding wasn’t direct evidence of an animal infection, but, stacked alongside other clues, ​​“this really strengthens the case for a natural origin,” Seema Lakdawala, a virologist at Emory University who wasn’t involved in the research, told me at the time.

Not everyone agreed that the finding counted as a substantial new insight. When the researchers who originally collected the samples, many of them from the Chinese Center for Disease Control and Prevention, published their own analysis of the data in April—a revision of an earlier report—they emphasized that there was no clear evidence that the virus had been introduced to the market by a wild animal. Then, this month, Jesse Bloom, a computational biologist at Fred Hutchinson Cancer Center, in Seattle, posted a third analysis of the market data, inspired in part, he told me, by his concern that the public discussion of the initial findings, and their connection to raccoon dogs, had overinflated their worth. The international team’s report, he argued, hardly moved the needle on the origins debate at all—certainly not “much beyond where it was before,” he told me.

Bloom’s analysis, too, set off a wave of fervor—including a fresh spate of claims that he told me were “exaggerated,” or even outright wrong; some even asserted, for instance, that his preprint proves that raccoon dogs “weren’t infected, which is not an accurate summary,” he said. All the while, researchers have been squabbling on social media over the minutiae of statistical methodology, and what constitutes a meaningful amount of viral RNA; some have even come to loggerheads publicly at conferences.

At the crux of this particular fight is a difference of interpretation, with one camp of researchers contending that the recent data matter a lot, and another asserting that they matter much less, or perhaps not even a little bit at all. Under most other circumstances, a scientific scuffle this deep in the weeds might hold the attention of a few dozen people for a few months at best. Here, though, the central topic is one of the most consequential in recent memory—a virus that’s left its mark on the world’s entire population, and will continue to do so. Which has made it easy for pitched battles over differences in scientific opinion to become a public spectacle—and difficult, maybe even impossible, for the debate to ever end, no matter what evidence might emerge next.

The genetic sequences analyzed in the March report contained evidence of a zoonotic origin that is more circumstantial than direct. Researchers extracted them from swabs taken from surfaces in and around Wuhan’s Huanan Seafood Wholesale Market from January to March of 2020, weeks after the first known COVID cases were documented in Wuhan. That makes these environmental samples “a useful part of the story,” Alice Hughes, a conservation biologist at the University of Hong Kong, told me. Though, by themselves, “they are limited in what they are able to tell us.”

By the time the swabs were collected by China CDC researchers, Chinese officials had hastily closed Huanan; many vendors had likely disappeared with their animals, or culled them en masse. The swabs could show only where the virus had once been, or which animals the venue had sold—more akin to dusting a crime scene for fingerprints than catching a vagrant in the act. And although they could show where animal and viral genetic material had mixed, they couldn’t guarantee that those two types of genetic material had been deposited at the same time. Nor could they distinguish between, say, a sick creature sneezing on the bars of its cage and an infected human coughing on an enclosure housing healthy wildlife. Those answers could have come from swabs taken directly from the noses or mouths of live animals for sale at Huanan in late November or early December of 2019. But as far as researchers know, those swabs don’t exist—or at least, the public has no record of them.

The sequences from these environmental samples, then, are “what we have,” says Katherine Xue, a computational virologist at Stanford who previously worked with Jesse Bloom, the author of the May preprint, but was not involved in any of the new reports. And “we want to do what we can with what we have.” When the international team behind the March analysis found that several market samples contained genetic material from both the virus and a wild animal known to be susceptible to it—including the common raccoon dog—they said that the best explanation for this commingling was an infection.

As I reported at the time, the data don’t constitute direct evidence of an infected raccoon dog at the market. “But this is exactly what we would observe if infected raccoon dogs were in fact present in this location,” says Kristian Andersen, a computational biologist and virologist at the Scripps Research Institute and one of the authors of the March analysis. Which, they wrote in their analysis, “identifies these species, particularly the common raccoon dog, as the most likely conduits for the emergence of SARS-CoV-2 in late 2019.”

Other researchers, though, think that calling the evidence even supportive of an animal origin for the outbreak is a stretch. The samples were taken too long after the outbreak’s start to be meaningful, some said; the data were too shaky to even hint at the idea of an infected raccoon dog, others insisted, much less one that might have passed the virus to us.

Bloom, too, was unswayed. The swabs contained genetic material from many creatures at the market—some of them alive, some dead; some that we now know can host the virus, others that almost certainly do not. In Bloom’s analysis, he explains that the species repeatedly highlighted as potential hosts weren’t the animals that were most frequently and notably commingled with the virus in the market swabs. “If you’re trying to figure out if there is a meaningful association between raccoon dog and viral genetic material,” he told me, there should be a lot of raccoon-dog genetic material in the places where the virus was found, and far less where the virus was not.

But that wasn’t the case for raccoon dogs—or “any of the animals that could conceivably have been infected,” Bloom told me. Instead, in his analysis he saw the virus most closely linked to several kinds of fish, which aren’t known to be viable hosts for it. People, Bloom told me, were the probable source of SARS-CoV-2 in those spots. All of that “probably just suggests that it had been spread around the market by humans by the time” the swabs were taken, diminishing the samples’ usefulness.

Several other scientists not involved in Bloom’s preprint were quick to point out the limits and flaws in his approach. To draw meaningful conclusions from this type of analysis, researchers would need samples amassed at about the same time, with the same collection goals in mind. That wasn’t the case for these samples, Zach Hensel, a biophysicist who has been publicly critical of Bloom’s report, told me. Researchers took them over the course of many weeks after Huanan’s closure, altering their tactics as more intel came to light. A first foray into the market, for instance, targeted the parts of the venue where COVID cases had been identified, a strategy that would, by design, turn up more virus-positive samples; another, conducted days later, focused on stalls that had been discovered to have housed wildlife, regardless of their proximity to sick people. Many samples in the latter set, then, would be expected to be virus-negative—and were. Sloshing them together with the first set of swabs and trying to pull patterns out could end up masking actual associations between the virus and any wild animal hosts.

Bloom also points out that many of the swabs that turned up mammalian DNA, including one containing raccoon-dog genetic sequences that some members of the international team initially emphasized, had relatively little material from the virus on them. But genetic material, especially RNA—the basis of SARS-CoV-2’s genome—degrades fast; a difference of even a few days could artificially deflate how important a particular swab looked. Alice Hughes also pointed out that certain market locales highlighted in Bloom’s preprint, including surfaces around duck or fish tanks, might have better preserved viral RNA simply because they were cold or damp. When I brought up these concerns with Bloom, he admitted “there are certainly a lot of confounders” that could have skewed his results. His main goal, he said, was just to show that “the samples are not sufficient to answer whether or not there were infected animals.”

Bloom’s re-analysis doesn’t mark a major shift in thinking for Hughes, who told me she thinks “there is reasonable support for a zoonotic origin.” Felicia Goodrum, a virologist and an immunologist at the University of Arizona who has written repeatedly on the origins debate but was not involved in the team’s analysis, agrees. The Huanan market is “most likely where the spillover occurred,” she told me. “I really, truly believe that, based on the accumulation of the evidence.”

Data never sit alone in a vacuum: They’re amassed, interpreted, and reinterpreted alongside the totality of evidence that precedes them. By themselves, the sequences from the Huanan market couldn’t say much. But they fit a broader, more detailed scenario that researchers on the team behind the March analysis had been exploring for years.

History has always supported a zoonotic scenario: A wet-market spillover is what researchers are fairly certain started the SARS outbreak in China in 2002, potentially via infected masked palm civets. In this latest outbreak, the Huanan Market was one of only four wet markets in all of Wuhan that has consistently been documented selling an array of live, coronavirus-susceptible wildlife; the earliest known COVID cases were detected near the venue, centering “on it like a bull’s-eye,” says Michael Worobey, an evolutionary biologist at the University of Arizona and one of the authors of the March report. Scientists analyzing genetic sequences collected from the venue have also detected two distinct coronavirus lineages from the outbreak’s earliest days—a likely indication, some researchers have argued, that the pathogen spilled over from animals into humans twice.

The missing clincher for them is which creature might have initially carried the virus into the market. The raccoon-dog swab was particularly compelling to the team not only because it contained gobs of animal genetic sequences, and very few human ones—but also because it had been plucked from a stall where Eddie Holmes, one of the report’s authors, had snapped a photo of a raccoon dog in a cage years before. The clues to a possible animal host, Worobey told me, were “right in the very stall we said they would be.”

But data are also amassed, interpreted, and reinterpreted by humans, who have their own biases. The experts now quarreling over the importance of the recent data approached the new evidence having already drawn tentative conclusions and made their opinions known. Kristian Andersen was an early proponent of a zoonotic origin, and has repeatedly denounced the notion of a lab leak; Worobey was later to voice his support for the zoonotic hypothesis, but is now no less enthusiastic. And long before they and their colleagues stumbled across the data that yielded their March analysis, which didn’t become publicly available until recently, the researchers had been hoping that such sequences would appear—noting in a 2022 paper that this sort of intel could constitute an essential and still missing puzzle piece. Now that the evidence has emerged, and fits with their established thinking, it feels validating, Worobey told me.

Bloom, by contrast, has long positioned himself as an agnostic moderate, and isn’t yet budging from his neutral territory. Others who have come out vocally in favor of a lab-leak scenario have cast their own doubts on the international team’s analysis. In a landscape so sparsely populated by data, it gets all too easy for people to fill in the gaps with speculation; “what starts off as a weak preference,” Hughes told me, “becomes almost like a religion.” I’ve been reporting now for three years on many controversial COVID stories, along the way interviewing hundreds of opinionated scientists about dozens of thorny questions. Through it all, this debate has stood out for being so ignitable. Individual data points have become catalysts; single statements have been endlessly scrutinized. And experts have staked out territory and stuck to it almost dogmatically—many of them to the point of avoiding admitting past mistakes. COVID’s origins are now shrouded in combustible gas, with matches scattered everywhere: Lighting up a single point, normally harmless enough, inevitably sets off a conflagration.

All of this leaves the world trying to peer through the smoke. “All hypotheses are on the table,” Maria Van Kerkhove, the World Health Organization’s technical lead on COVID-19, told me. “We can’t take any off.” To her mind, though, “there’s much more evidence to support a zoonotic origin.”

More evidence could still emerge. The international team isn’t yet done analyzing the Chinese researchers’ original data set, which was recently released in fuller form. They’re eager to mine the sequences to tease out the subspecies of some of the market’s potential SARS-CoV-2 hosts, which could inform searches for the virus out in nature or on animal farms; other experiments, analyzing how degraded certain genetic samples are, could hint at how much time passed between the moment the biological material was dropped and the moment it was picked up. Van Kerkhove has also separately been pressing the Chinese researchers for more information on how these and other samples might have been collected, and any intel on where the market’s animals might have been sourced from—which could guide searches for evidence of the virus or its relatives on farms or in the wild. These bits of data, too, would all be incremental,with no single shred of evidence acting as total proof or disproof. But each could constitute a clue, Van Kerkhove told me, to continue nudging the conversation along.

In the grand scheme of things, though, the world probably won’t ever get data that will conclusively end the debate. Even if scientists were to turn up virus-positive samples from a live creature from the market—direct evidence of an infected animal—it would remain technically possible that a human caught the virus first, then passed it on to the venue’s wildlife. But data that aren’t debate-ending can still be notable. And the recent sequences from the market swabs could easily, and frustratingly, end up being one of the best clues to the pandemic’s roots that the world is likely to get.

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The extent of the mental-health crisis in the United States today—especially among young adults—is undeniable. The problem started well before the coronavirus pandemic. A survey conducted from 2005 to 2018 of more than 86,000 adolescents found a startling increase in symptoms of depression after 2010. According to an analysis of Pew Research Center data, the most dramatic rise has been among young, liberal white women, more than 50 percent of whom reported having been told they have a mental-health condition.

Among the competing explanations for this pattern is the assertion that all the contentious issues around us—climate change, racism, gun violence—are leading young adults into depression and anxiety. But it may not be the crises themselves that are causing despair so much as young people’s typical responses to them. Protest and political activism have exploded among Gen Z and younger Millennials. Although these may seem like productive ways to address negative emotions from these social problems, activism itself can increase unhappiness. It can provoke anger and hatred toward others, and create a win-lose mentality that leads to disappointment.

The right conclusion is not to become apathetic about the world’s ills to protect one’s mental health and well-being. It is to change one’s perspective about how to help alleviate those ills.

The tendency of many Gen Z and younger Millennials—people born from the 1990s onward—to choose protest as a first resort has given rise to the label “activist generation.” A 2021 survey of some 10,000 Gen Zers showed that 70 percent are involved in a political or social cause; in another study that year, only 19 percent said they would work for a company that doesn’t share their values. This age cohort is also among those most likely to boycott a product or company.

Some would argue that today’s problems merit greater activism than those of previous generations, but my Gen Z daughter offered a different view: “We have been conscripted as child soldiers in the Baby Boomers’ culture war.” Touché.

Whatever accounts for the rise in activism, research shows that it’s connected to this generation’s psychological distress. Last year, scholars studying climate-change activists found an association between their activism and short-term depressive symptoms. Obviously, the causality could run in either direction: The activism may lead to depression, or the depression to activism. Or, in fact, they may be mutually reinforcing.

The best available answer comes from activists themselves. For a 2021 study in the Journal of Adolescent Research, researchers interviewed college students about the effects of their activism on their well-being. Although nearly a third of the students believed that their advocacy work improved their well-being, 60 percent reported harm to their mental health. “There’s been times that at the end of the day, I’ll come to bed and I’ll just cry,” one interviewee said, “because I really don’t know what I’ve gotten myself into.”

Several mechanisms may be at work here. One is that the nature of much activism involves anger and contempt for people on the “wrong side” of the issue; that sort of hostility toward others can be psychologically harmful for those who feel it. Today’s activism tends to encourage us to see people in a binary way: good or bad, right or wrong. Scholars have observed that this leads people to show disgust or moral condemnation toward opponents, or engage in othering behaviors.

Psychologists have demonstrated how these attitudes can lead to guilt, shame, and anxiety. And this is hardly a new idea: The fifth-century Indian Buddhist sage Buddhaghosa argued that one who hates is “like a man who wants to hit another and picks up a burning ember … and so first burns himself.”

Even for those who manage to disagree with others without hating them (and thus hurting themselves), political activism commonly leads to a sense of futility. Researchers studying prodemocracy demonstrators in Hong Kong found that during periods of protest, people involved had elevated states of psychological and social well-being. But a year later, after protesters had failed in their goals, their well-being was, on average, lower than that of their non-activist peers. A good deal of social and political activism is zero-sum, and admits only two possible outcomes: winning or losing. When these causes become an uphill battle, as commonly happens, losing is likely. Then the disappointment can be crushing.

None of this is to say that activism is a mistake; that is for each person to decide. But much of the data present a challenge for people who want to stay engaged without sacrificing their mental health—as well as for people in positions of political leadership and in academia, who often encourage young people to be involved in important causes.

A compromise might be available through minimizing activism’s most psychologically harmful elements: hatred and defeat. A shift in perspective—from winning to helping—can address both problems. This could mean a switch from protesting homelessness to providing services for people experiencing homelessness—for instance, by volunteering at a shelter or soup kitchen—or from marching against the president to giving people a ride to the polling station. Focus on what you can do to ameliorate a situation rather than simply demonstrating your opposition to it.

An enormous body of evidence shows that the right sort of volunteering leads unambiguously to greater happiness. A 2022 paper in the Journal of Happiness Studies found that older adults who volunteered reported greater life satisfaction—but with an important qualification that would certainly have a bearing on younger people’s mental health. These adults found that their morale improved after they performed more frequent nonpolitical volunteer work (such as helping with social services), but that it was lower after more frequent political activity (such as party work).

Another study of a 2004 Texas survey showed that participants who had volunteered even once to help others—again, in nonpolitical causes—experienced improvements in mental health, physical health, life satisfaction, and social well-being. The type of voluntary work can take many forms depending on one’s concerns: tutoring kids, helping build homes, visiting people in prison. The important thing to note is that the benefactor benefits too.

I’m not arguing that people should abandon politics and lapse into apathy. But at the very least, we need to balance fighting with loving, including loving more indiscriminately. In contrast to the way activism can divide “us” from “them” and allies from adversaries, volunteering tends to expand the allies by connecting us to those who need us, regardless of their views and beliefs. And by helping the people who are right in front of us, we succeed in the goal of helping make a better world. In the Mishnah Sanhedrin of the Jewish Talmud, it is written that “he who saves a single soul saves a whole world.” The profound truth of this for our lives is revealed when our actions affect another person in ways that show us how connected we are to one another, and perhaps even to the divine.

No amount of sharing rage at the state of the world can make us happy. But any amount of sharing love with someone who needs it may help us find the happiness we seek.