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Tag: risk factor

  • Shoveling snow? Over-exertion and cold temps can raise your heart risks

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    Shoveling snow? Over-exertion and cold temps can raise your heart risks

    ON SATURDAY. TIP OFF FOR THAT GAME IS EIGHT. MIGHT HAVE TO DIG OUT IF YOU’RE HEADED TO THAT GAME. THE SNOW STILL FALLING. BUT FOR A LOT OF US MAYBE ALREADY STARTED OR WILL CONTINUE DOING IS THAT TASK OF SHOVELING. AND WHILE IT MAY BE LIGHT SNOW, THERE ARE STILL IMPORTANT HEALTH REMINDERS TO KEEP IN MIND. DOCTOR JORGE PLUTZKY IS THE DIRECTOR OF PREVENTATIVE CARDIOLOGY AT BRIGHAM AND WOMEN’S HOSPITAL. DOCTOR PLUTZKY, THANKS SO MUCH FOR BEING HERE WITH US THIS MORNING. SURE. THANK YOU. WHAT DO YOU WORRY ABOUT MOST WHEN YOU THINK ABOUT PEOPLE WHO ARE HEADING OUT TO MOVE ALL OF THAT SNOW AROUND? WELL, FOR SOME PEOPLE, IT MAY BE THE FIRST TIME THEY’RE EXERTING THEMSELVES TO THAT LEVEL. AND WE KNOW THAT SHOVELING SNOW IS A VERY HIGH LEVEL OF EXERTION. YOU CAN VERY QUICKLY. STUDIES SUGGEST WITHIN TEN MINUTES REACH 100% OF YOUR MAXIMUM HEART RATE. AND SO FOR PEOPLE WITH A HISTORY OF HEART DISEASE OR JUST RISK FACTORS, THAT CAN BE QUITE AN EXERTION. IT’S LIKE SETTLING, DOING A MAXIMAL STRESS TEST AND BRINGING ON ISSUES RELATED TO THAT. DOC, WHAT ARE SOME OF THE WARNING SIGNS THAT FOLKS OUT THERE MIGHT BE? YOU KNOW, WE TOUGH NEW ENGLANDERS WILL SAY, WELL, WE’LL WORK THROUGH IT. BUT, YOU KNOW, THERE ARE SIGNS THAT SOMETHING MAY BE SERIOUSLY HAPPENING AND YOU NEED TO BE ABLE TO TAKE A BREAK, HEAD ON INSIDE FOR A BIT. YES. YOU KNOW, THE CLASSIC SIGNS OF CHEST PAIN AND PERHAPS ASSOCIATED SHORTNESS OF BREATH, NAUSEA, RADIATION DOWN THE ARMS ARE CERTAINLY VERY VALID. BUT WE ALSO WANT PEOPLE TO PAY ATTENTION TO MORE SUBTLE SIGNS LIKE CHEST PRESSURE, ACHING IN THE JAW, JUST THE THE NAUSEA CAN STILL BE RELEVANT. AND SO LISTENING TO YOUR BODY SLOWING DOWN, TAKING BREAKS AND STOPPING IF YOU’RE FEELING ANY OF THOSE IS GOOD ADVICE AND HIGHLY WARRANTED, ESPECIALLY WHEN YOU’RE OUT THERE IN THE COLD, WHICH MAY BE ITS OWN FACTOR FOR WHY THESE ISSUES ARISE. THE COLD CAN CONSTRICT ARTERIES AND MAKE THINGS WORSE, AND THERE REALLY IS NO MESSING AROUND WITH THIS. AND WE KNOW HEART ISSUES PRESENT DIFFERENTLY. BUT ARE THERE? AND MAYBE YOU JUST SPOKE ABOUT THIS MORE SUBTLE SIGNS THAT PEOPLE SHOULD PAY ATTENTION TO DURING THIS KIND OF WEATHER. YEAH, IT’S THINGS LIKE I’M FEELING MORE SHORT OF BREATH THAN I THAN I WOULD EXPECT TO BE. I’M HAVING AN ACHE IN MY JAW OR IN MY NECK THAT IS SURPRISING AND FEELS DIFFERENT. THESE ARE ALL SIGNS TO PAY ATTENTION TO AND TO NOT PUSH IT, TO SORT THAT OUT. THE. THERE ARE VARIOUS STRATEGIES PEOPLE CAN TAKE TO HAVE LESS OF A LOAD, LIKE TAKING BREAKS, COVERING YOUR MOUTH SO YOU WARM THE AIR THAT’S ON ITS WAY IN TO NOT NECESSARILY SHOVEL AND LIFT, BECAUSE USING YOUR ARMS IS MORE OF AN EXERTION, BUT TO PUSH AND TO TO SWIPE. BUT YOU REALLY DO WANT TO LISTEN TO ANY, ANY SENSE YOU HAVE THAT SOMETHING’S OFF. INCLUDING THESE OTHER, YOU KNOW, SOMEWHAT ATYPICAL SYMPTOMS THAT AREN’T CLASSIC CHEST PAIN. EVEN THAT CHEST PRESSURE CAN BE A SIGN. IT’S BEEN FOUR YEARS SINCE WE HAD THIS AMOUNT OF SNOW, SO MAYBE FOLKS HAVEN’T HAD TO FACE IT FOR A WHILE. DOCTOR GEORGE, THANK YOU VERY MUCH. CARDIOLOGIST WITH MASS GENERAL BRIGHAM, WE THANK YOU FOR JOINING US THIS MORNING.

    Digging out from the weekend’s massive snow and ice storm could be hazardous to your heart.Pennsylvania health officials announced three snow-removal-related deaths on Sunday. All were between the ages of 60 and 84. The Lehigh County coroner’s office cautioned people to take breaks and avoid over-exerting themselves.Shoveling snow is heavy, hard work — research has shown that doing it for even a short time can make the heart work as hard as it does during a major workout. Adding to that stress, the cold temperatures cause blood vessels, including those feeding the heart, to constrict. That raises blood pressure, which in turn increases the risk of a heart attack, stroke, or cardiac arrest, according to the American Heart Association.Snow shoveling is especially risky for anyone with known heart disease or who’s already survived a heart attack, as well as older adults and people with risk factors, including high blood pressure or cholesterol. People who think they’re healthy can get in trouble, too, with that combination of heavy exertion in cold weather – especially if they’re generally sedentary until a snowstorm comes along.The heart association advises that if you have to shovel, go slow and try to push the snow instead of lifting and throwing it. It also urges people to learn common warning signs of a heart attack and to call 911 if they experience them.

    Digging out from the weekend’s massive snow and ice storm could be hazardous to your heart.

    Pennsylvania health officials announced three snow-removal-related deaths on Sunday. All were between the ages of 60 and 84. The Lehigh County coroner’s office cautioned people to take breaks and avoid over-exerting themselves.

    Shoveling snow is heavy, hard work — research has shown that doing it for even a short time can make the heart work as hard as it does during a major workout. Adding to that stress, the cold temperatures cause blood vessels, including those feeding the heart, to constrict. That raises blood pressure, which in turn increases the risk of a heart attack, stroke, or cardiac arrest, according to the American Heart Association.

    Snow shoveling is especially risky for anyone with known heart disease or who’s already survived a heart attack, as well as older adults and people with risk factors, including high blood pressure or cholesterol. People who think they’re healthy can get in trouble, too, with that combination of heavy exertion in cold weather – especially if they’re generally sedentary until a snowstorm comes along.

    The heart association advises that if you have to shovel, go slow and try to push the snow instead of lifting and throwing it. It also urges people to learn common warning signs of a heart attack and to call 911 if they experience them.

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  • How Much Less to Worry About Long COVID Now

    How Much Less to Worry About Long COVID Now

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    Compared with the worst days of the pandemic—when vaccines and antivirals were nonexistent or scarce, when more than 10,000 people around the world were dying each day, when long COVID largely went unacknowledged even as countless people fell chronically ill—the prognosis for the average infection with this coronavirus has clearly improved.

    In the past four years, the likelihood of severe COVID has massively dropped. Even now, as the United States barrels through what may be its second-largest wave of SARS-CoV-2 infections, rates of death remain near their all-time low. And although tens of thousands of Americans are still being hospitalized with COVID each week, emergency rooms and intensive-care units are no longer routinely being forced into crisis mode. Long COVID, too, appears to be a less common outcome of new infections than it once was.

    But where the drop in severe-COVID incidence is clear and prominent, the drop in long-COVID cases is neither as certain nor as significant. Plenty of new cases of the chronic condition are still appearing with each passing wave—even as millions of people who developed it in years past continue to suffer its long-term effects.

    In a way, the shrinking of severe disease has made long COVID’s dangers more stark: Nowadays, “long COVID to me still feels like the biggest risk for most people,” Matt Durstenfeld, a cardiologist at UC San Francisco, told me—in part because it does not spare the young and healthy as readily as severe disease does. Acute disease, by definition, eventually comes to a close; as a chronic condition, long COVID means debilitation that, for many people, may never fully end. And that lingering burden, more than any other, may come to define what living with this virus long term will cost.


    Most of the experts I spoke with for this story do think that the average SARS-CoV-2 infection is less likely to unfurl into long COVID than it once was. Several studies and data sets support this idea; physicians running clinics told me that, anecdotally, they’re seeing that pattern play out among their patient rosters too. The number of referrals coming into Alexandra Yonts’s long-COVID clinic at Children’s National, in Washington, D.C., for instance, has been steadily dropping in the past year, and the waitlist to be seen has shortened. The situation is similar, other experts told me, among adult patients at Yale and UCSF. Lisa Sanders, an internal-medicine physician who runs a clinic at Yale, told me that more recent cases of long COVID appear to be less debilitating than ones that manifested in 2020. “People who got the earliest versions definitely got whacked the worst,” she said.

    That’s reflective of how our relationship to COVID has changed overall. In the same way that immunity can guard a body against COVID’s most severe, acute forms, it may also protect against certain kinds of long COVID. (Most experts consider long COVID to be an umbrella term for many related but separate syndromes.) Once wised up to a virus, our defenses become strong and fast-acting, more able to keep infection from spreading and lingering, as it might in some long-COVID cases. Courses of illness also tend to end more quickly, with less viral buildup, giving the immune system less time or reason to launch a campaign of friendly fire on other tissues, another potential trigger of chronic disease.

    In line with that logic, a glut of studies has shown that vaccination—especially recent and repeated vaccination—can reduce a person’s chances of developing long COVID. “There is near universal agreement on that,” Ziyad Al-Aly, an epidemiologist and a clinician at Washington University in St. Louis, told me. Some experts think that antiviral use may be making a dent as well, by decreasing the proportion of COVID cases that progress to severe disease, a risk factor for certain types of long COVID. Others have pointed to the possibility that more recent variants of the virus—some of them maybe less likely to penetrate deeply into the lungs or affect certain especially susceptible organs—may be less apt to trigger chronic illness too.

    But consensus on any of these points is lacking—especially on just how much, if at all, these interventions help. Experts are divided even on the effect of vaccines, which have the most evidence to back their protective punch: Some studies find that they trim risk by 15 percent, others up to about 70 percent. Paxlovid, too, has become a point of contention: While some analyses have shown that taking the antiviral early in infection helps prevent long COVID, others have found no effect at all. Any implication that we’ve tamed long COVID exaggerates how positive the overall picture is. Hannah Davis, one of the leaders of the Patient-Led Research Collaborative, who developed long COVID during the pandemic’s first months, told me that she’s seen how the most optimistic studies get the most attention from the media and the public. With a topic as unwieldy and challenging to understand as this, Davis said, “we still see overreactions to good news, and underreactions to bad news.”

    That findings are all over the place on long COVID isn’t a shock. The condition still lacks a universal definition or a standard method of diagnosis; when recruiting patients into their studies, research groups can rely on distinct sets of criteria, inevitably yielding disparate and seemingly contradictory sets of results. With vaccines, for instance, the more wide-ranging the set of potential long-COVID symptoms a study looks at, the less effective shots may appear—simply because “vaccines don’t work on everything,” Al-Aly told me.

    Studying long COVID has also gotten tougher. The less attention there is on COVID, “the less likely people are to associate long-term symptoms with it,” Priya Duggal, an infectious-disease epidemiologist at Johns Hopkins University, told me. Fewer people are testing for the virus. And some physicians still “don’t believe in long COVID—that’s what I hear a lot,” Sanders told me. The fact that fewer new long-COVID cases are appearing before researchers and clinicians could be in part driven by fewer diagnoses being made. Al-Aly worries that the situation could deteriorate further: Although long-COVID research is still chugging along, “momentum has stalled.” Others share his concern. Continued public disinterest, Duggal told me, could dissuade journals from publishing high-profile papers on the subject—or deter politicians from setting aside funds for future research.


    Even if new cases of long COVID are less likely nowadays, the incidence rates haven’t dropped to zero. And rates of recovery are slow, low, and still murky. At this point, “people are entering this category at a greater rate than people are exiting this category,” Michael Peluso, a long-COVID researcher at UCSF, told me. The CDC’s Household Pulse Survey, for instance, shows that the proportion of American adults reporting that they’re currently dealing with long COVID has held steady—about 5 to 6 percent—for more than a year (though the numbers have dropped since 2021). Long COVID remains one of the most debilitating chronic conditions in today’s world—and full recovery remains uncommon, especially, it seems, for those who have been dealing with the disease for the longest.

    Exact numbers on recovery are tricky to come by, for the same reasons that it’s difficult to pin down how effective preventives are. Some studies report rates far more optimistic than others. David Putrino, a physical therapist who runs a long-COVID clinic at Mount Sinai Health System, where he and his colleagues have seen more than 3,000 long-haulers since the pandemic’s start, told me his best estimates err on the side of the prognosis being poor. About 20 percent of Putrino’s patients fully recover within the first few months, he told me. Beyond that, though, he routinely encounters people who experience only partial symptom relief—as well as a cohort that, “no matter what we think to try,” Putrino told me, “we can’t even seem to stop them from deteriorating.” Reports of higher recovery rates, Putrino and other experts said, might be conflating improvement with a return to baseline, or mistakenly assuming that people who stop responding to follow-ups are better, rather than just done participating.

    Davis also worries that recovery rates could drop. Some researchers and clinicians have noticed that today’s new long-COVID patients are more likely than earlier patients to come in with certain neurological symptoms—among them, brain fog and dizziness—that have been linked to slower recovery trajectories, Lekshmi Santhosh, a pulmonary specialist at UCSF, told me.

    In any case, recovery rates are still modest enough that long-COVID clinics across the country—even ones that have noted a dip in demand—remain very full. Currently, Putrino’s clinic has a waitlist of three to six months. The same is true for clinical trials investigating potential treatments. One, run by Peluso, that is investigating monoclonal-antibody therapy has a waitlist that is “hundreds of people deep,” Peluso told me: “We do not have the problem of not being able to find people who want to participate.”

    Any decrease in long-COVID incidence may not last, either. Viral evolution could always produce a new variant or subvariant with higher risks of chronic issues. The protective effects of vaccination may also be quite temporary, and the fewer people who keep up to date with their shots, the more porous immunity’s safety net may become. In this way, kids—though seemingly less likely to develop long COVID overall—may remain worryingly vulnerable, Yonts told me, because they’re born entirely susceptible, and immunization rates in the youngest age groups remain extremely low. And yet, little kids who get long COVID may need to live with it the longest. Some of Yonts’s patients have barely started grade school and have already been sick for three-plus years—half of their lives so far, or more.

    Long COVID can also manifest after repeat infections of SARS-CoV-2—and although several experts told me they think that each subsequent exposure poses less incremental risk, any additional exposure is worrisome. People all over the world are being exposed, over and over again, as the pathogen spreads with blistering speed, more or less year-round, in populations that have mostly dropped mitigations and are mostly behind on annual shots (where they’re available). Additional infections can worsen the symptoms of people living with long COVID, or yank them out of remission. Long COVID’s inequities may also widen as marginalized populations, less likely to receive vaccines or antivirals and more likely to be exposed to the virus, continue to develop the condition at higher rates.

    There’s no question that COVID-19 has changed. The disease is more familiar; the threat of severe disease, although certainly not vanished, is quantitatively less now. But dismissing the dangers of the virus would be a mistake. Even if rates of new long-COVID cases continue to drop for some time, Yonts pointed out, they will likely stabilize somewhere. These risks will continue to haunt us and incur costs that will keep adding up. Long COVID may not kill as directly as severe, acute COVID has. But people’s lives still depend on avoiding it, Putrino told me—“at least, their life as they know it right now.”

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    Katherine J. Wu

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  • How a Common Stomach Bug Causes Cancer

    How a Common Stomach Bug Causes Cancer

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    At first, doctors didn’t believe that bacteria could live in the stomach at all. Too acidic, they thought. But in 1984, a young Australian physician named Barry Marshall gulped down an infamous concoction of beef broth laced with Helicobacter pylori bacteria. On day eight, he started vomiting. On day 10, an endoscopy revealed that H. pylori had colonized his stomach, their characteristic spiral shape unmistakeable under the microscope.

    Left untreated, H. pylori usually establishes infections that persist for an entire lifetime, and they’re common: Half of the world’s population harbors H. pylori inside their stomach, as do more than one in three Americans. In most cases, the microbe settles into an asymptomatic chronic infection, but in some, it becomes far more troublesome. It can, for example, cause enough damage to the stomach lining to create ulcers. Worse still, H. pylori can lead to cancer. This single bacterium is by far the No. 1 risk factor in stomach cancers worldwide. By one estimate, some 70 percent can be attributed to H. pylori.

    But what still puzzles doctors years later is why H. pylori has such different consequences for different people. Why is it asymptomatic in most but carcinogenic in others? Although the full answer is complex, one key factor seems to be mutations in H. pylori itself. Not every strain is created equal. The presence of select genes intensifies H. pylori’s pathogenicity, and even a single mutation in a single gene, scientists recently found, enhances the link to cancer. A small genetic tweak in a common stomach bug could have profound consequences for us, its unwitting hosts.


    H. pylori has lived inside of us for a long time. Our ancestors who left Africa likely carried it inside them as they crossed continents and oceans, built and felled civilizations. And over the course of what some scientists hypothesize to be more than 100,000 years of co-evolution, H. pylori has exquisitely adapted to the harsh, acidic conditions of the human stomach.

    It survives, for example, by producing “copious amounts” of an enzyme that neutralizes stomach acid, Richard Peek, a gastroenterologist at Vanderbilt, told me. H. pylori can also burrow into the mucus-gel lining of the stomach using powerful, whiplike flagella. The mucus lining offers a relative haven from stomach acid, but another prize lies underneath too: stomach cells, rich in nutrients that the bacteria needs to survive.

    The way that H. pylori steals nutrients could be the key to how it ends up causing cancer. The bacterium isn’t necessarily out to hurt its human host. “H. pylori doesn’t want you to get an ulcer or to get cancer, but it needs to replicate to high enough levels in the stomach that it can be transmitted to another person,” Nina Salama, a biologist at Fred Hutchinson Cancer Center, told me. (The bacteria seem to spread through an infected person’s saliva, vomit, or feces.) But to replicate, it needs nutrients, in particular iron, which our cells probably hoard to starve pathogens.

    In response, certain strains of H. pylori have evolved genetic changes that might make its iron-mining more efficient. But this also causes more collateral damage to the host’s stomach, enough damage, perhaps, to eventually trigger cancer. First, the bacteria uses a protein called HtrA—essentially “a pair of molecular scissors,” Peek said—to cut the bonds that hold stomach cells together, so the microbes can slip between. A single mutation in this scissor protein makes it better at cutting, a group based in Germany found in a recent study, and this mutation is disproportionately found in H. pylori strains isolated from people who developed stomach cancer.

    Once H. pylori has wedged itself in between cells, it also has clever ways of accessing the nutrients inside. Certain strains carry a set of about 18 genes that collectively encode a molecular needle through which H. pylori injects bacterial proteins, triggering a cascade of changes to the cell. These hijacked cells end up giving up their iron more easily, but they also become worse at essential functions such as fixing damaged DNA. This set of approximately 18 genes, collectively called the “cag pathogenicity island,” are in fact disproportionately found in strains from cancer patients. Stomach cancer thus might be a secondary consequence of the microbe’s aggressive search for nutrients. For the H. pylori, “there’s no selective pressure to cause cancer in 80 years. The selective pressure is to acquire iron now,” Karen Guillemin, a microbiologist at the University of Oregon, said.

    But not everyone infected with one of these cancer-linked strains will develop cancer. Other factors likely play a role too: diet, environment, and genetics of the individual patient  Stomach-cancer rates vary quite widely around the world, with the highest prevalence in East Asia. In Japan, doctors routinely test for H. pylori in people with no symptoms, and prescribe antibiotics if the tests come back positive. But some scientists have argued against aggressive treatment, pointing at hints that humans derive some benefits from living with H. pylori too. Those infected, for example, tend to have lower rates of asthma and allergy. Genetic signatures associated with more pathogenic H. pylori strains, Peek told me, would help identify those at highest risk, who could most benefit from antibiotics.

    Marshall, the Australian doctor who infected himself with H. pylori, ultimately recovered just fine. His self-experiment, in addition to other studies with his collaborator Robin Warren, proved that the bacterium does indeed infect the stomach and does indeed cause stomach ulcers, which later spurred the work linking H. pylori to cancer. Understanding exactly how and why H. pylori becomes pathogenic is still key to finding the way to treat it, but in the past 40 years the significance of H. pylori to human health has become indisputable—so much so that in 2005, Marshall and Warren won the Nobel Prize in Medicine.

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    Sarah Zhang

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