Category: Health

Reviewed by Jennifer Martin, PhD

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Maybe you’ve seen the headlines about how oversleeping has been linked to a greater risk of disease and death. If you’re the kind of person who regularly clocks more than eight hours of slumber, these news stories have probably made you wonder, “Why do I sleep so much? And is it bad for me?”

In this story, sleep experts help you understand the latest science. You’ll find out what really happens when you oversleep, along with how it affects your health.

(Spoiler: Chances are, you have nothing to worry about.)

How much is too much sleep?

On average, most people need somewhere between seven and nine hours of sleep each night. But that’s an average, not a good-health edict.

“As you start to move out in either direction, there are people who require slightly more and slightly less sleep,” says Chris Winter, MD, sleep specialist, author of The Sleep Solution and The Rested Child, and co-author of Precision Nutrition’s Sleep, Stress Management, and Recovery Coaching Certification.

Above (and below) average sleepers fall into three main categories.

1. People who need fewer than 7 hours of sleep

Referred to as Natural Short Sleepers, these genetically-gifted folks don’t need as much sleep as the average person.

Increased levels of a hormone called orexin allows them to feel spunky and clear-headed with just five to six hours of shuteye.

Here’s an important caveat, though. Plenty of people who get less than seven hours aren’t Natural Short Sleepers. Rather, they skimp on sleep for other reasons, ranging from revenge-bedtime procrastination to parenthood to an “always on” work ethic.

If you’re not genetically a Natural Short Sleeper, skimping on sleep likely means you’ll either…

▶ feel like garbage the next day

▶ won’t feel like garbage the next day—but only because you’re so used to the effects of sleep deprivation that you’ve no longer remember what it feels like to be well rested

In addition to the above, over time, your risk for heart disease, cancer, and type 2 diabetes can go up as well.

(More about sleep and health further down in the story.)

2. People who need more than 9 hours of sleep

Due to their genetic makeup, Natural Long Sleepers usually need 10, 11, or 12 hours in order to feel refreshed. Their genetics also cause them to feel tired more quickly than other people.

Also in this longer-sleeping category: children, teenagers, and many young adults, all of whom need more sleep so their bodies can continue to develop, says Jennifer Martin, PhD, Professor of Medicine at the University of California, Los Angeles and also a co-author Precision Nutrition’s Sleep, Stress Management, and Recovery Coaching Certification.

Certain prescription medications can also increase sleep time, says Dr. Martin.

“Usually this effect is reversed when the person stops the medication, and in some cases, the sleepiness is reduced once the person gets used to the medication,” she says.

3. People who need 13+ hours of sleep

Some people sleep 14, 17, 24 or more hours with very little interruption, and they still wake feeling tired.

“If you find you are one of these people, it might be an indication that there is something wrong with your sleep quality, not necessarily the quantity,” Dr. Winter says. For example, sleep disorders like sleep apnea and insomnia can disrupt sleep, causing people to wake feeling unrefreshed.

A variety of health conditions—including epilepsy, Parkinson’s disease, and depression—can also lead to hypersomnia, which is the inability to stay awake. Narcolepsy, another hypersomnia condition, causes people to feel tired all the time, leading them to fall asleep at inappropriate and dangerous times, such as while on a date or driving a vehicle. These disorders require medical treatment.

If you suspect any of the above is true for you, it’s a great thing to mention to your doctor.

What happens when you sleep too much?

“For the average person, if they are sleeping, they probably need to be sleeping,” says Dr. Winter.

That’s because our bodies all have a sleep set point—referred to as “homeostasis.” Get too little sleep one night and your body will respond by craving more sleep the next. Alternatively, you may have noticed: If you collect more sleep than usual by sleeping in on a weekend, you’ll likely find yourself wide awake later that evening.

There are, however, some exceptions. More about those below.

(Find out: Would YOU make a great sleep coach?)

Does oversleeping harm your health?

Despite all of the scary headlines, it’s likely that long sleep itself poses little to no health problems. That’s because, in people who sleep more than most, it’s often the result of a chronic health problem, not the cause, finds research. [1,2]

Occasionally, the problem is bi-directional, meaning the health problem disturbs sleep, which worsens the health problem, which leads to worsened sleep, and the cycle continues.

These health problems include:

▶ Sleep disorders like sleep apnea (where breathing repeatedly stops during sleep) and narcolepsy (which is characterized by severe daytime sleepiness and sleep attacks)

▶ Diabetes

▶ Hypothyroidism

▶ Depression

▶ Chronic fatigue syndrome

▶ Heart disease

For the above conditions, it’s important to note that oversleeping doesn’t cause them. Rather, it’s a symptom of them.

For example, sleep apnea repeatedly wakes people, often for brief moments, during the night, which can lead to hypersomnia (excessive sleepiness during the day) as well as a strong desire to stay in bed longer than eight hours or to take a nap during the afternoon.

“When medical problems disturb sleep, it takes a person a longer period of time to be sufficiently recovered,” says Dr. Martin.

If you regularly get more than 10 hours, and you feel energetic and clear headed during the day, that’s great! Enjoy your slumber without fear. You most likely have nothing to worry about.

On the other hand, if you spend your days craving a nap—tired, brain fogged, irritated, and decision fatigued—there may be an underlying issue worth exploring with your doctor.

(Learn more: Why people with insomnia swear by CBT-I.)

Can sleeping too much make you tired?

Ever noticed that you feel more tired when you sleep in (say, on the weekends) than you do when you get up early?

There are two likely reasons for this phenomenon.

1. Oversleeping is often a response to undersleeping

Some people sleep 10+ hours on the weekends because they’re sleeping six or fewer hours during the week.

“One reason people feel tired after sleeping a lot is that they still haven’t paid back their sleep debts from prior nights,” says Dr. Martin. “If you are very sleep deprived, it takes several days to get back on track and ‘catch up.’”

2. Sleeping in can disrupt sleep-wake signaling.

If you usually wake at 6 am, sleeping in on the weekends will disrupt your brain’s ability to release the neurochemicals needed for that refreshed, ready-to-slay-the-world feeling.

“It’s really more about sleep timing than sleep amount,” explains Dr. Winter. “The brain’s timing cues are being disrupted.”

Among those timing cues:

✅ Overhead and outdoor light that sets your brain’s circadian clock

✅ The blaring noise of your alarm clock that triggers the release of cortisol and other alertness chemicals

✅ Conversations with housemates that nudge you to “wake up! think!”

✅ Caffeine

✅ Breakfast

✅ That feeling of being rushed as you race out the door

When you occasionally oversleep, you deprive your brain of some or all of those cues. Some of the wakeup signals might not take place at all. Others, like overhead lighting and caffeine, take place hours later than your brain is used to getting them.

End result: you feel tired.

How can you tell if you’re sleeping too much?  

Dr. Winter suggests you consider this question:

During the day, if you sit down to read a book or watch a show, do you feel a strong urge to nod off?

If the answer is yes, it’s an indication that you’re not getting enough restorative sleep at night, which may be a sign of a sleep disorder or sleep quality issue, he says.

On the other hand, if you’re clocking a lot of bedtime hours and feel energized during the day, 10+ hours could just be your natural sleep pattern.

“If you are a long sleeper and feel good, don’t worry about it,” says Dr. Martin. “Do your best to spend the amount of time in bed you need.”

References

Click here to view the information sources referenced in this article.

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Treating psoriatic arthritis (PsA) isn’t like treating strep throat. You don’t just take one medicine for a few days and feel better. PsA is a complex, chronic disease that stays with you and affects many parts of your body — skin, joints, nails, heart, and lungs.

Many medications slow PsA and relieve symptoms, but the first treatment you try won’t always be the right one for you.

“There is no one-size-fits-all, and there is no one medication for psoriatic arthritis,” says Saakshi Khattri, MD, assistant professor of dermatology and rheumatology at the Icahn School of Medicine at Mount Sinai in New York. “So often there are patients who do not respond to their medication.”

There are a couple of reasons you might need to switch to a new treatment, says Ethan Craig, MD, assistant professor of clinical medicine at the University of Pennsylvania and rheumatologist at the Corporal Michael J. Crescenz VA Medical Center in Philadelphia.

“One is intolerance — the patient has a side effect of some sort. The second is ineffectiveness. Either the medication doesn’t work in the first place, or it works for a period of time and then it stops working,” he says.

When your medicine doesn’t tame your symptoms, it’s time to regroup with your rheumatologist or dermatologist and talk about other treatment options.

Signs That It’s Time to Change

The clearest signs that you need a medication switch is a new flare-up of symptoms.

Worsening joint pain and stiffness, increased fatigue, and sudden trouble doing activities that were easy for you are some of the most obvious symptoms. More subtle signs like difficulty sleeping and mood changes also suggest the medication you’re on isn’t controlling your PsA well enough.

If you’ve just started on a treatment, you do need to give it time. 

Sometimes you can have a partial response — maybe the swelling comes down in some of your joints but not in others. Then your doctor might suggest that you wait it out for 4 to 6 months to give the drug more time to work. During that time, steroids or nonsteroidal anti-inflammatory drugs (NSAIDs) can help bridge the gap until your medication kicks in.

Once you’ve been on a treatment for several months with no improvement, or if you’re no longer getting relief from a drug you’ve been taking for a while, “that’s often an indication that we need to think about switching things up,” Craig says.

Advice for Switching Meds

PsA treatment comes in many forms. Often anti-inflammatories and conventional disease modifying drugs are used (DMARDS). Biologic DMARDS are also often used; they target different pathways in the immune system. There are other options for treatment as well, including targeted synthetic DMARDS and newer oral agents.

Your doctor will take a few factors into consideration when recommending your next step, including:

Your symptoms. PsA causes a variety of symptoms. Your choice of medication may hinge on the type of symptoms you have, how much they bother you, and which drug targets them best.

For example, one of Craig’s patients worked at a ticket window. “Because he had to hand out tickets, he was very self-conscious about the appearance of his nails,” Craig says. “He was willing to be on a drug that helped his nails, even if it didn’t help his arthritis.”

The drug’s side effects. Each type of medication comes with a set of side effects, which you need to balance against its benefits. For example, methotrexate can irritate your stomach, while biologics increase the risk for infections. It’s important to think about which side effects you can tolerate and which ones you definitely don’t want.

How you take the drug. Many PsA meds come as an infusion or an injection. If you’re not a fan of needles, you might prefer a pill.

What other conditions you have. Methotrexate can damage your liver. NSAIDs are linked to heart problems. So if you already have liver or heart disease, these medications may not be safe for you.

Your insurance coverage. Ultimately, your insurance company could decide which treatment you get next. “The sad fact of the matter is that our choice of medication is often substantially constrained by insurance approval,” Craig says.

Some insurance companies will expect you to try a certain drug first and prove it doesn’t work before they’ll let you switch to the medication that you and your doctor want to use.

How to Ask Your Doctor for a New Treatment

You might already see your doctor every 3 to 4 months if you take medication. During those visits, the doctor can examine your joints, do imaging tests, and check your lab test results to see whether your PsA is under good control.

But tests don’t always tell the whole story. Your point of view is important, too. Let the doctor know if you’re having any problems with your medications, including side effects or breakthrough symptoms.

If you’re not due for a visit yet, call the office or send your doctor an email about your concerns through the patient portal.

Don’t be afraid to speak up. “A lot of patients are hesitant. They don’t want to take up the doctor’s time,” Craig says. “It’s helpful for us if they come in. I hate to see someone suffer for months. And it’s often easier to intervene earlier in the course of the disease, when things are less active.”

If your doctor isn’t on board with you switching medications, don’t be afraid to push back to get on the right treatment. “Sometimes it’s a matter of miscommunication,” he adds. “We need to be on the same page as to what the expectations are, what we’re treating, and what effect we expect.”

Updated at 3:25 p.m. ET on October 14, 2022

On one level, the world’s response to the coronavirus pandemic over the past two and half years was a major triumph for modern medicine. We developed COVID vaccines faster than we’d developed any vaccine in history, and began administering them just a year after the virus first infected humans. The vaccines turned out to work better than top public-health officials had dared hope. In tandem with antiviral treatments, they’ve drastically reduced the virus’s toll of severe illness and death, and helped hundreds of millions of Americans resume something approximating pre-pandemic life.

And yet on another level, the pandemic has demonstrated the inadequacy of such pharmaceutical interventions. In the time it took vaccines to arrive, more than 300,000 people died of COVID in America alone. Even since, waning immunity and the semi-regular emergence of new variants have made for an uneasy détente. Another 700,000 Americans have died over that period, vaccines and antivirals notwithstanding.

For some pandemic-prevention experts, the takeaway here is that pharmaceutical interventions alone simply won’t cut it. Though shots and drugs may be essential to softening a virus’s blow once it arrives, they are by nature reactive rather than preventive. To guard against future pandemics, what we should focus on, some experts say, is attacking viruses where they’re most vulnerable, before pharmaceutical interventions are even necessary. Specifically, they argue, we should be focusing on the air we breathe. “We’ve dealt with a lot of variants, we’ve dealt with a lot of strains, we’ve dealt with other respiratory pathogens in the past,” Abraar Karan, an infectious-disease physician and global-health expert at Stanford, told me. “The one thing that’s stayed consistent is the route of transmission.” The most fearsome pandemics are airborne.

Read: The plan to stop every respiratory virus at once

Numerous overlapping efforts are under way to stave off future outbreaks by improving air quality. Many scientists have long advocated for overhauling the way we ventilate indoor spaces, which has the potential to transform our air in much the same way that the advent of sewer systems transformed our water. Some researchers are similarly enthusiastic about the promise of germicidal lighting. Retrofitting a nation’s worth of buildings with superior ventilation systems or germicidal lighting is likely a long-term mission, though, requiring large-scale institutional buy-in and probably a considerable amount of government funding. Meanwhile, a more niche subgroup has zeroed in on what is, at least in theory, a somewhat simpler undertaking: designing the perfect mask.

Two and a half years into this pandemic, it’s hard to believe that the masks widely available to us today are pretty much the same masks that were available to us in January 2020. N95s, the gold standard as far as the average person is concerned, are quite good: They filter out at least 95 percent of .3-micron particles—hence N95—and are generally the masks of preference in hospitals. And yet, anyone who has worn one over the past two and a half years will know that, lucky as we are to have them, they are not the most comfortable. At a certain point, they start to hurt your ears or your nose or your whole face. When you finally unmask after a lengthy flight, you’re liable to look like a raccoon. Most existing N95s are not reusable, and although each individual mask is pretty cheap, the costs can add up over time. They impede communication, preventing people from seeing the wearer’s facial expressions or reading their lips. And because they require fit-testing, the efficacy for the average wearer probably falls well short of the advertised 95 percent. In 2009, the federal government published a report with 28 recommendations to improve masks for health-care workers. Few seem to have been taken.

These shortcomings are part of what has made efforts to get people to wear masks an uphill battle. NIOSH, the federal agency tasked with certifying and regulating masks, appears to be overworked and underfunded. To make matters more complicated, Joe and Kim Rosenberg, who in the early stages of the pandemic launched a mask company that applied unsuccessfully for NIOSH approval, told me the certification process is somewhat circular: A successful application requires huge amounts of capital, which in turn require huge amounts of investment, but investors generally like to see data showing that the masks work as advertised in, say, a hospital, and masks cannot be tested in a hospital without prior NIOSH approval. NIOSH did not return a request for comment before this story was published, but afterward, a spokesperson told me that the agency has received far more applications during the pandemic than it did before, and that it is “working closely with both current approval holders and new applicants to process applications as expeditiously as possible.”

New products aside, there do already exist masks that outperform standard N95s in one way or another. Elastomeric respirators are reusable masks that you outfit with replaceable filters. Depending on the filter you use, the mask can be as effective as an N95 or even more so. When equipped with HEPA-quality filters, elastomerics filter out 99.97 percent of particles. And they come in both half-facepiece versions (which cover the nose and mouth) and full-facepiece versions (which also cover the eyes). Another option are PAPRs, or powered air-purifying respirators—hooded, battery-powered masks that cover the wearer’s entire head and constantly blow HEPA-filtered air for the wearer to breathe.

Given the challenges of persuading many Americans to wear even flimsy surgical masks during the past couple of years, though, the issues with these superior masks—the current models, at least—are probably disqualifying as far as widespread adoption would go in future outbreaks. Elastomerics generally are bulky, expensive, limit range of motion, obscure the mouth, and require fit testing to ensure efficacy. PAPRs have a transparent facepiece and in many cases don’t require fit testing, but they’re also bulky; currently cost more than $1,000 each; and, because they’re battery-powered, can be quite noisy. Neither, let me assure you, is the sort of thing you’d want to wear to the movie theater.

Read: Is it time to start masking again?

The people who seem most fixated on improving masks are a hodgepodge of biologists, biosecurity experts, and others whose chief concern is not another COVID-like pandemic but something even more terrifying: a deliberate act of bioterrorism. In the apocalyptic scenarios that most worry them—which, to be clear, are speculative—bioterrorists release at least one highly transmissible pathogen with a lethality in the range of, say, 40 to 70 percent. (COVID’s is about 1 percent.) Because this would be a novel virus, we wouldn’t yet have vaccines or antivirals. The only way to avoid complete societal collapse would be to supply essential workers with PPE that they can be confident will provide infallible protection against infection—so-called perfect PPE. In such a scenario, N95s would be insufficient, Kevin Esvelt, an evolutionary biologist at MIT, told me: “70-percent-lethality virus, 95 percent protection—wouldn’t exactly fill me with confidence.”

Existing masks that use HEPA filters may well be sufficiently protective in this worst-case scenario, but not even that is a given, Esvelt told me. Vaishnav Sunil, who runs the PPE project at Esvelt’s lab, thinks that PAPRs show the most promise, because they do not require fit testing. At the moment, the MIT team is surveying existing products to determine how to proceed. Their goal, ultimately, is to ensure that the country can distribute completely protective masks to every essential worker, which is firstly a problem of design and secondly a problem of logistics. The mask Esvelt’s team is looking for might already be out there, just selling for too high a price, in which case they’ll concentrate on bringing that price down. Or they might need to design something from scratch, in which case, at least initially, their work will mainly consist of new research. More likely, Sunil told me, they’ll identify the best available product and make modest adjustments to improve comfort, breathability, useability, and efficacy.

Esvelt’s team is far from the only group exploring masking’s future. Last year, the federal government began soliciting submissions for a mask-design competition intended to spur technological development. The results were nothing if not creative: Among the 10 winning prototypes selected in the competition’s first phase were a semi-transparent mask, an origami mask, and a mask for babies with a pacifier on the inside.

In the end, the questions of how much we should invest in improving masks and how we should actually improve them boil down to a deeper question about which possible future pandemic concerns you most. If your answer is a bioengineered attack, then naturally you’ll commit significant resources to perfecting efficacy and improving masks more generally, given that, in such a pandemic, masks may well be the only thing that can save us. If your answer is SARS-CoV-3, then you might worry less about efficacy and spend proportionally more on vaccines and antivirals. This is not a cheery choice to make. But it is an important one as we inch our way out of our current pandemic and toward whatever waits for us down the road.

Read: The pandemic’s legacy is already clear

For the elderly and immunocompromised, super-effective masks could be useful even outside a worst-case scenario. But more traditional public-health experts, who don’t put as much stock in the possibility of a highly lethal, deliberate pandemic, are less concerned about perfecting efficacy for the general public. The greater gains, they say, will come not from marginally improving the efficacy of existing highly effective masks but from getting more people to wear highly effective masks in the first place. “It’s important to make masks easier for people to use, more comfortable and more effective,” Linsey Marr, an environmental engineer at Virginia Tech, told me. It wouldn’t hurt to make them a little more fashionable either, she said. Also important is reusability, Jassi Pannu, a fellow at the Johns Hopkins Center for Health Security, told me, because in a pandemic, stockpiles of single-use products will almost always run out.

Stanford’s Karan envisions a world in which everyone in the country has their own elastomeric respirator—not, in most cases, for everyday use, but available when necessary. Rather than constantly replenishing your stock of reusable masks, you would simply swap out the filters in your elastomeric (or perhaps it will be a PAPR) every so often. The mask would be transparent, so that a friend could see your smile, and relatively comfortable, so that you could wear it all day without it cutting into your nose or pulling on your ears. When you came home at night, you would spend a few minutes disinfecting it.

Karan’s vision might be a distant one. America’s tensions over masking throughout the pandemic give little reason to hope for any unified or universal uptake in future catastrophes. And even if that happened, everyone I spoke with agrees that masks alone are not a solution. They’re almost certainly the smallest part of the effort to ensure that the air we breathe is clean, to change the physical world to stop viral transmission before it happens. Even so, making and distributing millions of masks is almost certainly easier than installing superior ventilation systems or germicidal lighting in buildings across the country. Masks, if nothing else, are the low-hanging fruit. “We can deal with dirty water, and we can deal with cleaning surfaces,” Karan told me. “But when it comes to cleaning the air, we’re very, very far behind.”

This article was originally published in Undark Magazine.

Ten years ago, 12-year-old Rory Staunton dove for a ball in gym class and scraped his arm. He woke up the next day with a 104-degree Fahrenheit fever, so his parents took him to the pediatrician and eventually the emergency room. It was just the stomach flu, they were told. Three days later, Rory died of sepsis after bacteria from the scrape infiltrated his blood and triggered organ failure.

“How does that happen in a modern society?” his father, Ciaran Staunton, asked me.

Each year in the United States, sepsis kills more than a quarter million people—more than stroke, diabetes, or lung cancer. One reason for all this carnage is that if sepsis is not detected in time, it’s essentially a death sentence. Consequently, much research has focused on catching sepsis early, but the condition’s complexity has plagued existing clinical support systems—electronic tools that use pop-up alerts to improve patient care—with low accuracy and high rates of false alarm.

That may soon change. Back in July, Johns Hopkins researchers published a trio of studies in Nature Medicine and npj Digital Medicine showcasing an early-warning system that uses artificial intelligence. The system caught 82 percent of sepsis cases and significantly reduced mortality. While AI—in this case, machine learning—has long promised to improve health care, most studies demonstrating its benefits have been conducted using historical data sets. Sources told me that, to the best of their knowledge, when used on patients in real time, no AI algorithm has shown success at scale. Suchi Saria, the director of the Machine Learning and Healthcare Lab at Johns Hopkins University and the senior author of the studies, said in an interview that the novelty of this research is how “AI is implemented at the bedside, used by thousands of providers, and where we’re seeing lives saved.”

The Targeted Real-Time Early Warning System scans through hospitals’ electronic health records—digital versions of patients’ medical histories—to identify clinical signs that predict sepsis, alert providers about at-risk patients, and facilitate early treatment. Leveraging vast amounts of data, TREWS provides real-time patient insights and a unique level of transparency in its reasoning, according to the Johns Hopkins internal-medicine physician Albert Wu, a co-author of the study.

Wu says that this system also offers a glimpse into a new age of medical electronization. Since their introduction in the 1960s, electronic health records have reshaped how physicians document clinical information; nowadays, however, these systems primarily serve as “an electronic notepad,” he added. With a series of machine-learning projects on the horizon, both from Johns Hopkins and other groups, Saria says that using electronic records in new ways could transform health-care delivery, providing physicians with an extra set of eyes and ears—and helping them make better decisions.

It’s an enticing vision, but one in which Saria, the CEO of the company developing TREWS, has a financial stake. This vision also discounts the difficulties of implementing any new medical technology: Providers might be reluctant to trust machine-learning tools, and these systems might not work as well outside controlled research settings. Electronic health records also come with many existing problems, from burying providers under administrative work to risking patient safety because of software glitches.

Saria is nevertheless optimistic. “The technology exists; the data is there,” she says. “We really need high-quality care-augmentation tools that will allow providers to do more with less.”

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Currently, there’s no single test for sepsis, so health-care providers have to piece together their diagnoses by reviewing a patient’s medical history, conducting a physical exam, running tests, and relying on their own clinical impressions. Given such complexity, over the past decade, doctors have increasingly leaned on electronic health records to help diagnose sepsis, mostly by employing a rules-based criteria—if this, then that.

One such example, known as the SIRS criteria, says a patient is at risk of sepsis if two of four clinical signs—body temperature, heart rate, breathing rate, white-blood-cell count—are abnormal. This broadness, although helpful for catching the various ways sepsis might present itself, triggers countless false positives. Take a patient with a broken arm: “A computerized system might say, ‘Hey, look, fast heart rate, breathing fast.’ It might throw an alert,” says Cyrus Shariat, an ICU physician at Washington Hospital in California. The patient almost certainly doesn’t have sepsis but would nonetheless trip the alarm.

These alerts also appear on providers’ computer screens as a pop-up, which forces them to stop whatever they’re doing to respond. So, despite these rules-based systems occasionally reducing mortality, there’s a risk of alert fatigue, where health-care workers start ignoring the flood of irritating reminders. According to M. Michael Shabot, a surgeon and the former chief clinical officer of Memorial Hermann Health System, “It’s like a fire alarm going off all the time. You tend to be desensitized. You don’t pay attention to it.”

Read: The burnout crisis in American medicine

Already, electronic records aren’t particularly popular among doctors. In a 2018 survey, 71 percent of physicians said that the records greatly contribute to burnout, and 69 percent said that they take valuable time away from patients. Another 2016 study found that, for every hour spent on patient care, physicians have to devote two extra hours to electronic health records and desk work. James Adams, the chair of the Department of Emergency Medicine at Northwestern University, calls electronic health records a “congested morass of information.”

But Adams also says that the health-care industry is at an inflection point to transform the files. An electronic record doesn’t have to simply involve a doctor or nurse putting data in, he says; instead, it “needs to transform to be a clinical-care-delivery tool.” With their universal deployment and real-time patient data, electronic records could warn providers about sepsis and various other conditions—but that will require more than a rules-based approach.

What doctors need, according to Shabot, is an algorithm that can integrate various streams of clinical information to offer a clearer, more accurate picture when something’s wrong.

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Machine-learning algorithms work by looking for patterns in data to predict a particular outcome, like a patient’s risk of sepsis. Researchers train the algorithms on existing data sets, which helps the algorithms create a model for how that world works and then make predictions on new data sets. The algorithms can also actively adapt and improve over time, without the interference of humans.

TREWS follows this general mold. The researchers first trained the algorithm on historical electronic-records data so that it could recognize early signs of sepsis. After this testing showed that TREWS could have identified patients with sepsis hours before they actually got treatment, the algorithm was deployed inside hospitals to influence patient care in real time.

Saria and Wu published three studies on TREWS. The first tried to determine how accurate the system was, whether providers would actually use it, and if use led to earlier sepsis treatment. The second went a step further to see if using TREWS actually reduced patient mortality. And the third interviewed 20 providers who tested the tool on what they thought about machine learning, including what factors facilitate versus hinder trust.

In these studies, TREWS monitored patients in the emergency department and inpatient wards, scanning through their data—vital signs, lab results, medications, clinical histories, and provider notes—for early signals of sepsis. (Providers could do this themselves, Saria says, but it might take them about 20 to 40 minutes.) If the system suspected organ dysfunction based on its analysis of millions of other data points, it flagged the patient and prompted providers to confirm sepsis, dismiss the alert, or temporarily pause the alert.

“This is a colleague telling you, based upon data and having reviewed all this person’s chart, why they believe there’s reason for concern,” Saria says. “We very much want our frontline providers to disagree, because they have ultimately their eyes on the patient.” And TREWS continuously learns from these providers’ feedback. Such real-time improvements, as well as the diversity of data TREWS considers, are what distinguish it from other electronic-records tools for sepsis.

In addition to these functional differences, TREWS doesn’t alert providers with incessant pop-up boxes. Instead, the system uses a more passive approach, with alerts arriving as icons on the patient list that providers can click on later. Initially, Saria was worried this might be too passive: “Providers aren’t going to listen. They’re not going to agree. You’re mostly going to get ignored.” However, clinicians responded to 89 percent of the system’s alerts. One physician interviewed for the third study described TREWS as less “irritating” than the previous rules-based system.

Saria says that TREWS’s high adoption rate shows that providers will trust AI tools. But Fei Wang, an associate professor of health informatics at Weill Cornell Medicine, is more skeptical about how these findings will hold up if TREWS is deployed more broadly. Although he calls these studies first-of-a-kind and thinks their results are encouraging, he notes that providers can be conservative and resistant to change: “It’s just not easy to convince physicians to use another tool they are not familiar with,” Wang says. Any new system is a burden until proven otherwise. Trust takes time.

TREWS is further limited because it only knows what’s been inputted into the electronic health record—the system is not actually at the patient’s bedside. As one emergency-department physician put it, in an interview for the third study, the system “can’t help you with what it can’t see.” And even what it can see is filled with missing, faulty, and out-of-date data, according to Wang.

But Saria says that TREWS’s strengths and limitations complement those of health-care providers. Although the algorithm can analyze massive amounts of clinical data in real time, it will always be limited by the quality and comprehensiveness of the electronic health record. The goal, Saria adds, is not to replace physicians, but to partner with them and augment their capabilities.

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The most impressive aspect of TREWS, according to Zachary Lipton, an assistant professor of machine learning and operations research at Carnegie Mellon University, is not the model’s novelty, but the effort it must have taken to deploy it on 590,736 patients across five hospitals over the course of the study. “In this area, there is a tremendous amount of offline research,” Lipton says, but relatively few studies “actually make it to the level of being deployed widely in a major health system.” It’s so difficult to perform research like this “in the wild,” he adds, because it requires collaborations across various disciplines, from product designers to systems engineers to administrators.

As such, by demonstrating how well the algorithm worked in a large clinical study, TREWS has joined an exclusive club. But this uniqueness may be fleeting. Duke University’s Sepsis Watch algorithm, for one, is currently being tested across three hospitals following a successful pilot phase, with more data forthcoming. In contrast with TREWS, Sepsis Watch uses a type of machine learning called deep learning. Although this can provide more powerful insights, how the deep-learning algorithm comes to its conclusions is unexplainable—a situation that computer scientists call the black-box problem. The inputs and outputs are visible, but the process in between is impenetrable.

On the one hand, there’s the question of whether this is really a problem: Doctors don’t always know how drugs work, Adams says, “but at some point, we have to trust what the medicine is doing.” Lithium, for example, is a widely used, effective treatment for bipolar disorder, but nobody really understands exactly how it works. If an AI system is similarly useful, maybe interpretability doesn’t matter.

Wang suggests that that’s a dangerous conclusion. “How can you confidently say your algorithm is accurate?” he asks. After all, it’s difficult to know anything for sure when a model’s mechanics are a black box. That’s why TREWS, a simpler algorithm that can explain itself, might be a more promising approach. “If you have this set of rules,” Wang says, “people can easily validate that everywhere.”

Indeed, providers trusted TREWS largely because they could see descriptions of the system’s process. Of the clinicians interviewed, none fully understood machine learning, but that level of comprehension wasn’t necessary.

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In machine learning, although the specific algorithmic design is important, the results have to speak for themselves. By catching 82 percent of sepsis cases and reducing time to antibiotics by 1.85 hours, TREWS ultimately reduced patient deaths. “This tool is, No. 1, very good; No. 2, received well by clinicians; and No. 3, impacts mortality,” Adams says. “That combination makes it very special.”

However, Shariat, the ICU physician at Washington Hospital in California, was more cautious about these findings. For one, these studies only compared patients with sepsis who had the TREWS alert confirmed within three hours to those who didn’t. “They’re just telling us that this alert system that we’re studying is more effective if someone responds to it,” Shariat says. A more robust approach would have been to conduct a randomized controlled trial—the gold standard of medical research—where half of patients got TREWS in their electronic record while the other half didn’t. Saria says that randomization would have been difficult to do given patient-safety concerns, and Shariat agrees. Even so, he says that the absence “makes the data less rigorous.”

Shariat also worries that the sheer volume of alerts, with about two out of three being false positives, might contribute to alert fatigue—and potentially overtreatment with fluids and antibiotics, which can lead to serious medical complications such as pulmonary edema and antibiotic resistance. Saria acknowledges that TREWS’s false-positive rate, although lower than that of existing electronic-health-record systems, could certainly improve, but says it will always be crucial for clinicians to continue to use their own judgment.

Read: Will probiotics ever live up to the hype?

The studies also have a conflict of interest: Saria is entitled to revenue distribution from TREWS, as is Johns Hopkins. “If this goes prime time, and they sell it to every hospital, there’s so much money,” Shariat says. “It’s billions and billions of dollars.”

Saria maintains that these studies went through rigorous internal and external review processes to manage conflicts of interest, and that the vast majority of study authors don’t have a financial stake in this research. Regardless, Shariat says it will be crucial to have independent validation to confirm these findings and ensure the system is truly generalizable.

The Epic Sepsis Model, a widely used algorithm that scans through electronic records but doesn’t use machine learning, is a cautionary example here, according to David Bates, the chief of general internal medicine at Brigham and Women’s Hospital. He explains that the model was developed at a few health systems with promising results before being deployed at hundreds of others. The model then deteriorated, missing two-thirds of patients with sepsis and having a concerningly high false-positive rate. “You can’t really predict how much the performance is going to degrade,” Bates says, “without actually going and looking.”

Despite the potential drawbacks, Orlaith Staunton, Rory’s mother, told me that TREWS could have saved her son’s life. “There was complete breakdown in my son’s situation,” she said; none of his clinicians considered sepsis until it was too late. An early-warning system that alerted them about the condition, she added, “would make the world of difference.”

After Rory’s death, the Stauntons started the organization End Sepsis to ensure that no other family would have to go through their pain. In part because of their efforts, New York State mandated that hospitals develop sepsis protocols, and the CDC launched a sepsis-education campaign. But none of this will ever bring back Rory, Ciaran Staunton said: “We will never be happy again.”

This research is personal for Saria as well. Almost a decade ago, her nephew died of sepsis. By the time it was discovered, there was nothing his doctors could do. “It all happened too quickly, and we lost him,” she says. That’s precisely why early detection is so important—life and death can be mere minutes away. “Last year, we flew helicopters on Mars,” Saria says, “but we’re still freaking killing patients every day.”

Just a few months ago, it looked like the U.S. had lost its chance to eliminate the spread of monkeypox – that is, stamp out the outbreak and get cases down to zero, except for new infections that come from abroad.

Experts worried it was just a matter of time before the virus started spreading more widely in the U.S., especially in settings like daycare centers and college dorms.

Now it’s clear those concerns did not materialize. Some infectious disease experts are even raising the idea that the U.S. could eliminate the virus.

Monkeypox cases have declined since a peak in early August – from 440 cases a day, down to 60 – and they’re the lowest they’ve been since June. The virus has continued to circulate almost entirely within gay and queer sexual networks. And vaccine supply is plentiful, even outstripping the current demand.

“Where we are now is the best case scenario, in terms of what can happen when you actually commit the tools you have to fight an outbreak,” says Dr. Boghuma Titanji, an infectious disease specialist at Emory University.

So what changed the trajectory?

Health experts attribute the success to changes in behavior among those at high risk for monkeypox and quick uptake of vaccines. But a growing body of evidence suggests another factor is also helping slow down the outbreak: the virus can spread only under very particular circumstances.

Monkeypox not likely to spread through saliva and surfaces

Initially, there was a lot of concern that monkeypox could spread widely at daycares or in schools, but, overall, there has been very little spread among children.

Only about 0.2% of U.S. cases have been in kids under 16. And, so far, there’s no evidence that a sick child or teacher has spread the virus to another person at a school or daycare center. (College campuses are a separate issue. Several campuses have reported cases among students, but none have reported large outbreaks, at this point).

With children, the concern stemmed from the understanding that the virus can spread through saliva – meaning it can spread when you’re up close in somebody’s face while talking or coughing. Monkeypox can also spread when a person touches objects and surfaces that were contaminated by someone with an infection. But in reality, it’s quite rare to catch monkeypox in either of these ways.

Several studies have found that often there isn’t very much virus in the upper respiratory tract. Instead, the highest levels of virus occur on sores found on the skin and inside the anus.

In one of those studies, researchers at Israel Institute of Biological Research measured the levels of virus in 44 monkeypox patients. They took samples from lesions on the patients’ skin and swabs of their throats. They found that the skin lesions contained 17-times the infectious virus particles, on average, than the swabs from the throat.

Another study, published last month, obtained similar results, but these researchers went even further: they also analyzed levels of viral DNA in patients’ blood, urine, semen, and swabs from the anus, in addition to samples taken from the skin and throat. Although high levels of monkeypox DNA occurred in a few people’s throats and semen, those samples, on average, contained much less virus than the samples from the anus or lesions on the skin. Urine and blood contained the lowest level of virus.

Together with a few previous studies, these newer findings explain why monkeypox is spreading almost exclusively through contact during sex, especially anal and oral sex, during the current outbreak.

Even with sex, monkeypox only causes outbreaks in particular circumstances

But this research still doesn’t explain why the disease hasn’t spread widely in women who, after all, are having sex, too.

Since the beginning of the U.S. outbreak, the CDC data show that the vast majority of cases have remained in men. The rates of infection are also very high among transgender men and women. Meanwhile, only about 2% of cases have occurred in women.

Turns out, it takes more than just having sex to keep a monkeypox outbreak going.

In a study, published last month in the journal Science, researchers found that monkeypox spreads at very different rates in different groups of people – and that rate depends greatly on people’s sexual activity. Researchers from Nagasaki University and London School of Hygiene & Tropical Medicine built a mathematical model of the global outbreak. Then they looked to see how the number of sexual partners alters the transmission of monkeypox in their network. Overall, monkeypox outbreaks were highly likely in only one particular type of sexual network: where a small number of people have a high number of sexual partners.

Outside of that, outbreaks of monkeypox are very rare. The study found chains of transmission nearly always stop on their own because the chance of a person spreading the virus to another person is low.

In the U.S. outbreak, monkeypox “has really been contained in a core group of sexually active men who have sex with men, with multiple partners,” says Dr. Jeffrey Klausner, a professor of medicine and public health at the University of Southern California who was not involved with the study. And within this group, some are at higher risk: “It’s not in those long-term monogamous relationships, or men who have an additional occasional partner every couple of months …This is really [concentrated among] men who have multiple new partners every week.”

And as people within these active sexual networks acquire immunity to monkeypox – either by recovering from infections or getting vaccinated – the number of people who are suspectible to infection is falling.

Can monkeypox be eliminated in the U.S.?

Some say it may be possible to stop monkeypox transmission chains in the U.S. and bring cases down to nearly zero (at least, not counting the cases that will come from other parts of the world where the virus is still spreading).

“I think we can expect to see regional elimination, potentially national elimination, where we would not see a sustained number of cases,” says Klausner, who points out that in some large cities, including San Francisco, Chicago and New York, only a few cases are being detected each day.

Still, new infections have not declined evenly across all cities, and the proportion of cases among men of color is rising.

In fact, CDC data show that monkeypox cases are down dramatically in white men, but nearly 70% of cases are now being detected in Black or Latino men. Health officials have acknowledged that these populations are getting vaccinated at lower rates than white men.

And not all experts are as optimistic about eliminating the virus domestically.

There are still key unknowns that could affect the trajectory of the outbreak, such as whether people without symptoms (or only mild symptoms) are spreading monkeypox unknowingly, and how well the vaccines work – both at preventing monkeypox infections and transmission. “Do they offer 100%, 75% or 50% protection?” Titanji says. “And is that protection for the rest of your life? Or will you need subsequent vaccination to maintain a level of protection?”

These are open questions.

Then there’s the virus itself and how it could change. Could it gain a foothold among animal populations in the U.S. or Europe and establish a permanent virus reservoir? Or could it mutate in ways that may increase its infectiousness to humans?

“These are factors that will potentially impact whether we are able to eliminate this virus and go back to where we were before,” Titanji says, “So the jury’s still out.”

Still, monkeypox may not need to be completely eliminated in the U.S. for it to no longer be a national public health emergency. As cases decline in major cities, outbreaks may be more limited and localized.

If that happens, the challenge will be making sure it doesn’t “become another neglected, sexually transmissible infection, joining the ranks of gonorhea, chlamydia and syphilis,” Titanji says. These are all preventable diseases, but they still cause long-term health problems for many people, particularly in historically marginalized communities.

So far, COVID-19 has come with one small silver lining for health: cases of influenza have dropped dramatically. During the first flu season during the pandemic, lockdowns kept people indoors and away from one another, limiting the virus’ ability to spread. And once people began mingling more during the next flu seasons, widespread use of masks blocked influenza’s chances of infecting large numbers of people.

But that could change this flu season, as mask mandates have disappeared and more people are interacting in close quarters in school, workplaces, sports events, public transport, and more. Health experts are warning that flu cases could rise again this winter, and that the combination of influenza and COVID-19 together could pose a real public-health threat that sends more people to the hospital and in need of intensive care. Already, the flu season in the southern hemisphere—which runs from April to October and serves as a harbinger of what’s to come for the U.S.—has been severe, with cases in Australia three times higher than average compared to the past five years. That could mean influenza will sweep through North America and Europe with equally aggressive force this winter, alongside rising cases of COVID-19.

That opens the possibility that people could get the two infections at the same time—which experts believe could be both unpleasant and dangerous. “Are two viruses that cause huge inflammatory responses together going to make that response worse? Theoretically, yes,” says Dr. Khalilah Gates, a pulmonary critical care physician at Northwestern University.

Gates and others stress that there aren’t extensive data yet to be sure exactly what will happen when people are infected with both influenza and SARS-CoV-2. But the limited early data—some from people, but mostly from animals—are not encouraging. Already, doctors know that people who get both the flu and a cold at the same time tend to be sicker than those who are only infected with one virus. The same could be true when flu and COVID-19 combine; classic symptoms, including fever, chills, fatigue, and coughing, could become more intense for some people. In one 2021 study on COVID-19 co-infections, including 17 people who tested positive for both influenza and COVID-19 at King Fahad Hospital in Medina, Saudi Arabia, their rates of hospitalization and death were higher than those for people infected with COVID-19 a type of bacteria that can cause respiratory tract infections.

In the largest study so far looking at co-infection of the two viruses, published in April, researchers at the University of Edinburgh reported similar trends. Dr. J. Kenneth Baillie, professor of experimental medicine at the university, and his colleagues analyzed the health records of more than 212,000 people admitted to hospitals in the U.K. for COVID-19, who were also tested for other infections. People infected with influenza and SARS-CoV-2 were four times as likely to need mechanical ventilation, and twice as likely to die, compared to people who just had COVID-19.

Read More: Scientists Are Worried About New COVID-19 Variants—But Most Americans Aren’t

“We can, with some confidence, say that being infected with flu and SARS-CoV-2 at the same time increases the risk of both needing to go on a ventilator and needing intensive care, and of death,” says Baillie.

Animal studies also show that those who are co-infected with SARS-CoV-2 and influenza tend to do worse than those infected with either virus alone. In March, researchers in South Korea found that co-infected mice were sicker for a longer time than those with just one viral infection, and they also had higher levels of inflammation that contributed to pneumonia. The co-infected animals also showed lower levels of virus-fighting antibodies and immune T cells against each virus, compared to mice infected with either influenza or SARS-CoV-2 alone.

In another study involving mice, published in 2020, researchers from Wuhan University reported even more concerning data on how influenza and SARS-CoV-2 might interact. They found that influenza can make it easier for SARS-CoV-2 to infect cells in the respiratory tract, including the lungs, of mice. This priming was unique to influenza, because it activates the same receptor, also found in people, that SARS-CoV-2 uses to enter and infect cells. Getting sick with the flu can therefore potentially make animals more vulnerable to getting infected with SARS-CoV-2.

“You definitely don’t want either infection, and you don’t want them together,” says Dr. Adam Ratner, director of pediatric infectious diseases at Hassenfeld Children’s Hospital at NYU Langone Health. “Together, they have the potential to be really serious and really deadly, including in people who are not elderly and without underlying health conditions.”

Another issue that concerns doctors is the fact that both influenza and COVID-19 can put people at higher risk of other infections, most notably pneumonia. Getting infected with both either at the same time, or in quick succession, could make people more vulnerable to additional infections as well.

While treatments exist for both influenza and COVID-19, there aren’t strong data assuring doctors and patients that combining them will be safe or effective. The antiviral drugs Tamiflu for influenza and Paxlovid (nirmatrelvir-ritonavir) or Lagevrio (molnupiravir) for SARS-CoV-2 can minimize the severity of symptoms of either disease, but must be taken soon after infection begins. That could be challenging for patients and doctors to determine, and missing the optimal treatment window may prevent the medications from controlling the virus well.

Read More: To Avoid Paxlovid Rebound, Some Experts Call for Longer Courses of Treatment

Baillie says that while his study showed that the risks of needing intensive care or dying are higher if people are infected with both influenza and SARS-CoV-2, it’s not clear if the people who are getting hospitalized are already at higher risk of more severe outcomes. Because both flu and COVID-19 can cause mild symptoms in some people, it may be the case that there is more co-infection occurring in the population that isn’t severe and doesn’t require medical care. Studies so far have estimated that anywhere from about 1% to 4.5% of people might be infected with both viruses—although this may be an underestimate, since most of those studies included people who were tested at hospitals and therefore might have been sick enough to need additional care.

Still, the potential that the two viruses could put some people at higher risk of needing ventilators or additional health care is making doctors wary. “As an intensive-care doctor, I’m bracing myself for a difficult winter,” says Baillie. “Whatever happens, hospitals are already busy worldwide with COVID-19 still circulating, and are fully expecting with flu that more patients will require intensive care, so I think it will be a difficult winter for hospitals and ICUs.”

Fortunately, there are things people can do to protect themselves from the likelihood of getting infected with either virus. Getting vaccinated against both the flu and COVID-19, including getting the latest COVID-19 booster shot—which targets the variant that’s causing most infections now—can lower both the chances of getting infected and of developing severe disease. Wearing masks, especially in crowded indoor settings where there is poor ventilation, could also help. “I don’t want flu and COVID-19 together,” says Gates. “I don’t want to know what that feels like, so I’m going to keep my mask on if I’m inside or around people that I’m not familiar with their vaccine status.”

Gates says she is closely monitoring cases in her community for her daughter as well. Because she didn’t want her to feel different from other students, most of whom aren’t wearing masks in class, she and her husband decided to allow her daughter to go to school without a mask. But if cases of either flu or COVID-19 increase at the school or in their community, she will ask her daughter to start wearing a mask.

Taking steps like these will be important for not only lowering individual people’s risk of getting infected with either or both viruses, but for keeping rates of disease down in the country overall.

Contact us at [email protected].

Analysis by Dr. Joseph Mercola
Fact Checked

• October 17, 2022Download PDF

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Analysis by Dr. Joseph Mercola
Fact Checked

• October 17, 2022Download PDF

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Fall and winter have always been peak seasons for respiratory viruses. As the weather cools in many parts of the U.S., people are forced into indoor environments where viruses can spread more easily. Holiday gatherings and travel can also become breeding grounds for disease.

That’s one reason why experts are worried that COVID-19 case counts may rise in the U.S. in the coming weeks. But there’s also another. To help forecast COVID-19 rates for the U.S., experts often look to Europe—and the data there aren’t promising. More than 1.5 million COVID-19 diagnoses were reported across Europe during the week ending Oct. 2, about 8% more than the prior week, according to the World Health Organization’s (WHO) latest global situation report, published Oct. 5. More than 400,000 of those diagnoses came from Germany, and almost 265,000 came from France.

“We’re concerned,” said Maria Van Kerkhove, the WHO’s technical lead on COVID-19, at an Oct. 5 press briefing. “In the Northern Hemisphere, we’re entering autumn and the winter months, so we will see co-circulation of other viruses like influenza….We need health systems to be prepared.”

The U.S. doesn’t always follow in Europe’s footsteps. The Alpha variant, for example, caused a larger spike in Europe than in the U.S. But European outbreaks related to Delta and Omicron predated similar surges in the U.S.

COVID-19 in the U.S. has been at a “high-plains plateau” for months, says Michael Osterholm, director of the Center for Infectious Disease Research and Policy at the University of Minnesota. Since the spring, roughly 300 to 500 people have died from COVID-19 each day—a rate that is still tragically high but relatively stable.

Read More: What Happens If I Get COVID-19 and the Flu at the Same Time?

The situation in Europe “may be a harbinger of things to come,” Osterholm says. He fears a “perfect storm” may be brewing, threatening to turn that U.S. plateau into another surge. Waning immunity, low booster uptake, ever-evolving subvariants that are increasingly good at evading the immune system, and people behaving as if the pandemic is over all suggest “we are headed to the end of the high-plains plateau,” Osterholm says. “I just don’t know what [the next phase] looks like.”

Federal case counts aren’t showing an uptick in the U.S. yet; in fact, daily diagnoses and hospitalization rates have fallen steadily since July. But case counts have become increasingly unreliable as more people rely on at-home tests and states pull back on reporting. Osterholm says he pays closer attention to death and hospitalization rates, but both lag behind actual spread of the virus, since it can take time for infections to become serious enough to result in hospitalization or death.

Meanwhile, the CDC’s wastewater surveillance dashboard, which tracks the level of virus detected in wastewater samples across the country, suggests circulation is increasing in multiple parts of the country, including portions of the Northeast and Midwest.

Taken together, the signs suggest a surge is coming, says Arrianna Marie Planey, an assistant professor of health policy and management at the University of North Carolina’s Gillings School of Global Public Health.

“I don’t like to use the word ‘inevitable’ because all of this is preventable,” Planey says. “It’s just that prevention is harder and harder at this stage of the pandemic,” when mitigation measures like mask mandates have fallen away and many people either don’t know about or don’t want to get the new Omicron-specific boosters.

Planey has been encouraging people she knows to get boosted and making sure they know about tools like Evusheld (a vaccine alternative for people who are immunocompromised or unable to get their shots) and the antiviral drug Paxlovid. She says she’d like to see more urgency from the government, including stronger communication about the need to get boosted and a continued push for those who haven’t been vaccinated at all to get their primary shots.

The problem, Osterholm says, is getting people to actually heed those warnings. Many polls show that Americans are ready to leave the pandemic behind, even if the virus continues to spread and mutate in the future.

That leaves public-health experts with the frustrating job of repeating the same advice they’ve given for the last several years, to an increasingly detached audience. “There’s no joy in saying, ‘I told you so,’” Planey says, “because people are sick and dying.”

Write to Jamie Ducharme at [email protected].

The U.S. on Wednesday authorized updated COVID-19 boosters for children as young as 5, seeking to expand protection ahead of an expected winter wave.

Tweaked boosters rolled out for Americans 12 and older last month, doses modified to target today’s most common and contagious Omicron relative. While there wasn’t a big rush, federal health officials are urging that people seek the extra protection ahead of holiday gatherings.

Now the Food and Drug Administration has given a green light for elementary school-age kids to get the updated booster doses, too—one made by Pfizer for 5- to 11-year-olds, and a version from rival Moderna for those as young as 6.

There’s one more step before parents can bring their kids in for the new shot: The Centers for Disease Control and Prevention, which recommends how vaccines are used, must sign off.

Americans may be tired of repeated calls to get boosted against COVID-19, but experts say the updated shots have an advantage: They contain half the recipe that targeted the original coronavirus strain and half protection against the dominant BA.4 and BA.5 Omicron versions.

Read More: What Happens If I Get COVID-19 and the Flu at the Same Time?

These combination or “bivalent” boosters are designed to broaden immune defenses so that people are better protected against serious illness whether they encounter an Omicron relative in the coming months—or a different mutant that’s more like the original virus.

“We want to have the best of both worlds,” Pfizer’s Dr. Bill Gruber, a pediatrician, told The Associated Press. He hopes the updated shots will “re-energize interest in protecting children for the winter.”

The updated boosters are “extremely important” for keeping kids healthy and in school, said Dr. Jason Newland, a pediatric infectious disease specialist at Washington University in St. Louis.

Parents should know “there is no concern from the safety perspective with the bivalent vaccines, whether Moderna or Pfizer,” Newland added.

Only people who’ve gotten their initial vaccinations—with any of the original-formula versions—qualify for an updated booster. That means about three-fourths of Americans 12 and older are eligible. As of last weekend, only at least 13 million had gotten an updated booster, White House COVID-19 coordinator Dr. Ashish Jha estimated Tuesday.

To pediatricians’ chagrin, getting children their first vaccinations has been tougher. Less than a third of 5- to 11-year-olds have had their two primary doses and thus would qualify for the new booster.

This age group will get kid-size doses of the updated booster—and they can receive it at least two months after their last dose, whether that was a primary vaccination or an earlier booster, the FDA said.

Pfizer said it could ship up to 6 million kid-sized doses within a week of authorization, in addition to ongoing adult-dose shipments.

Until now, Moderna’s updated booster was cleared only for adults. Wednesday’s FDA action authorized the booster for teens as well as children as young as age 6.

As for even younger tots, first vaccinations didn’t open for the under-5 age group until mid-June—and it will be several more months before regulators decide if they’ll also need a booster using the updated recipe.

Exactly how much protection does an updated COVID-19 booster shot offer? That’s hard to know. Pfizer and Moderna are starting studies in young children.

But the FDA cleared the COVID-19 booster tweaks without requiring human test results—just like it approves yearly changes to flu vaccines. That’s partly because both companies already had studied experimental shots tweaked to target prior COVID-19 variants, including an earlier Omicron version, and found they safely revved up virus-fighting antibodies.

“It’s clearly a better vaccine, an important upgrade from what we had before,” Jha said earlier this week.

Jha urged adults to get their updated shot in October—like they get flu vaccinations—or at least well before holiday gatherings with high-risk family and friends. People who’ve recently had COVID-19 still need the booster but can wait about three months, he added.

Contact us at [email protected].