Publisher Health

Understanding what drives food choices can help high-volume food service operations like universities reduce waste, according to a new study.
Researchers have concluded that food waste in places like university cafeterias is driven by how much people put on their plates, how familiar they are with what’s on the menu and how much they like — or don’t like — what they’re served.
Food waste has been studied often in households, but not so often in institutional settings like university dining commons. What drives food choices in these “all-you-care-to-eat” facilities is different because diners don’t perceive personal financial penalty if they leave food on their plates.
Published in the journal Foods, “Food Choice and Waste in University Dining Commons — A Menus of Change University Research Collaborative Study” was conducted by a team of experts from Rice University; the University of California, Davis; Stanford University; Lebanon Valley College; the University of California, Santa Barbara; and the University of California, Berkeley.
Co-author Eleanor Putnam-Farr, assistant marketing professor at Rice’s Jones Graduate School of Business, is available to discuss the findings and potential impact with news media.
The researchers conducted student surveys during the 2019 spring and fall semesters to study foods types, diner confidence and diner satisfaction. They used photos taken by diners themselves before and after eating to measure how much food was taken and how much of it went to waste. “Diners were intercepted at their dining halls and asked if they wanted to participate in a study about food choices and satisfaction, but the objective of investigating food waste behavior was not disclosed,” the authors wrote.
The study found the amount of food wasted didn’t significantly differ among types of food. Instead, researchers discovered waste was related to the amount of food diners put on their plates, how satisfied they were with their meals and how often they went to the dining commons. If students were satisfied with their food, they tended waste less of it. And diners who visited the commons most often — making them more familiar with the menus and more confident in their choices — tended to waste less.
Mixed dishes, like sandwiches or stir-fry, took up a greater percentage of the surface area on surveyed plates than animal proteins or grains and starches. Those three types of food took up a greater area of the plates than fruits, vegetables or plant proteins. The amount of food wasted, however, did not significantly differ among the various food categories.
The mixed dishes and animal proteins that took up greater portions of the plate tended to be pre-plated by the commons staff or have a suggested serving size. The study’s results showed that greater amounts of food taken by diners correlated with the item being pre-plated or served by others.
The authors recommend future research on the topic uses their multicampus approach — which enabled them to study food choice among a large and diverse group — to better understand what causes food waste and find out if it can be reduced by interventions such as posting signs that encourage healthier choices.
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James McKerrow, MD, PhD, dean of the Skaggs School of Pharmacy and Pharmaceutical Sciences at University of California San Diego, has long studied neglected tropical diseases — chronic and disabling parasitic infections that primarily affect poor and underserved communities in developing nations. They’re called “neglected” because there is little financial incentive for pharmaceutical companies to develop therapies for them.
One of these neglected diseases is Chagas disease, the leading cause of heart failure in Latin America, which is spread by “kissing bugs” carrying the parasite Trypanosoma cruzi. These parasites produce an enzyme called cruzain that helps them replicate and evade the human immune system. McKerrow’s research team looks for inhibitors of cruzain — small molecules that might form the basis for new anti-parasitic medicines. One particularly effective cruzain inhibitor is called K777.
Then, in the spring of 2020, the COVID-19 pandemic began to sweep through the United States. Researchers quickly reported that SARS-CoV-2, the coronavirus that causes COVID-19, can’t dock on and infect human cells unless a human enzyme called cathepsin L cleaves the virus’ spike protein.
And it just so happens that cathepsin L looks and acts a lot like cruzain.
In a study published March 31, 2021 by ACS Chemical Biology, McKerrow and team show that low concentrations of K777 inhibit cathepsin L can reduce SARS-CoV-2’s ability to infect four host cell lines, without harming the cells.
“Since K777 inhibits a human enzyme, not the virus itself, it’s our hope that it’s less likely the virus will evolve resistance against it,” said McKerrow, co-senior author of the study with Thomas Meek, PhD, of Texas A&M University.

The most common questions about vaccination side effects, answered.Every day nearly three million people in the United States are getting the Covid-19 vaccine. And every new jab prompts new questions about what to expect after vaccination.Last week I asked readers to send me their questions about vaccinations. Here are some answers.Q: I’ve heard the Covid vaccine side effects, especially after the second dose, can be really bad. Should I be worried?Short-lived side effects like fatigue, headache, muscle aches and fever are more common after the second dose of both the Pfizer-BioNTech and the Moderna vaccines, which each require two shots. (The Johnson & Johnson vaccine requires only a single shot.) Patients who experience unpleasant side effects after the second dose often describe feeling as if they have a bad flu and use phrases like “it flattened me” or “I was useless for two days.” During vaccine studies, patients were advised to schedule a few days off work after the second dose just in case they needed to spend a day or two in bed.Data collected from v-safe, the app everyone is encouraged to use to track side effects after vaccination, also show an increase in reported side effects after the second dose. For instance, about 29 percent of people reported fatigue after the first Pfizer-BioNTech shot, but that jumped to 50 percent after the second dose. Muscle pain rose from 17 percent after the first shot to 42 percent after the second. While only about 7 percent of people got chills and fever after the first dose, that increased to about 26 percent after the second dose.The New York Times interviewed several dozen of the newly vaccinated in the days afterward. They recounted a wide spectrum of responses, from no reaction at all to symptoms like uncontrolled shivering and “brain fog.” While these experiences aren’t pleasant, they are a sign that your own immune system is mounting a potent response to the vaccine.Q: Is it true that women are more likely to get worse side effects from the vaccine than men?An analysis of safety data from the first 13.7 million Covid-19 vaccine doses given to Americans found that side effects were more common in women. And while severe reactions to the Covid vaccine are rare, nearly all the cases of anaphylaxis, or life-threatening allergic reactions, occurred in women.The finding that women are more likely to report and experience unpleasant side effects to the Covid vaccine is consistent with other vaccines as well. Women and girls can produce up to twice as many antibodies after receiving flu shots and vaccines for measles, mumps and rubella (M.M.R.) and hepatitis A and B. One study found that over nearly three decades, women accounted for 80 percent of all adult anaphylactic reactions to vaccines.While it’s true that women may be more likely to report side effects than men, the higher rate of side effects in women also has a biological explanation. Estrogen can stimulate an immune response, whereas testosterone can blunt it. In addition, many immune-related genes are on the X chromosome, of which women have two copies and men have only one. These robust immune responses help to explain why 80 percent of autoimmune diseases afflict women. You can read more about women and vaccine side effects here.Q: I didn’t have any side effects. Does that mean my immune system didn’t respond and the vaccine isn’t working?Side effects get all the attention, but if you look at the data from vaccine clinical trials and the real world, you’ll see that many people don’t experience any side effects beyond a sore arm. In the Pfizer vaccine trials, about one out of four patients reported no side effects. In the Moderna trials, 57 percent of patients (64 or younger) reported side effects after the first dose — that jumped to 82 percent after the second dose, which means almost one in five patients reported no reaction after the second shot.A lack of side effects does not mean the vaccine isn’t working, said Dr. Paul Offit, a professor at the University of Pennsylvania and a member of the Food and Drug Administration’s vaccine advisory panel. Dr. Offit noted that during the vaccine trials, a significant number of people didn’t report side effects, and yet the trials showed that about 95 percent of people were protected. “That proves you don’t have to have side effects in order to be protected,” he said.Nobody really knows why some people have a lot of side effects and others have none. We do know that younger people mount stronger immune responses to vaccines than older people, whose immune systems get weaker with age. Women typically have stronger immune responses than men. But again, these differences don’t mean that you aren’t protected if you don’t feel much after getting the shot.Scientists still aren’t sure how effective the vaccines are in people whose immune systems may be weakened from certain medical conditions, such as cancer treatments or H.I.V. infection or because they are taking immune suppressing drugs. But most experts believe the vaccines still offer these patients some protection against Covid-19.The bottom line is that even though individual immune responses can vary, the data collected so far show that all three vaccines approved in the United States — Pfizer-BioNTech, Moderna and Johnson & Johnson — are effective against severe illness and death from Covid-19.Q: I took Tylenol before I had my Covid vaccine shots and had very little reaction to the shots. Did I make a big mistake?You shouldn’t try to stave off discomfort by taking a pain reliever before getting the shot. The concern is that premedicating with a pain reliever like acetaminophen (Tylenol) or ibuprofen (Advil, Motrin), which can prevent side effects like arm soreness as well as fever or headache, might also blunt your body’s immune response.While it’s possible that taking a pain reliever before your shots might have dampened your body’s immune response, vaccine experts say you shouldn’t worry, and you shouldn’t try to get another shot. Studies of other vaccines suggest that while premedicating can dull the body’s immune response to a vaccine, your immune system can still mount a strong enough defense to fight infection. A review of studies of more than 5,000 children compared antibody levels in children who took pain relievers before and after vaccinations and those who did not. They found that pain relievers did not have a meaningful impact on immune response, and that children in both groups generated adequate levels of antibodies after their shots.The high efficacy of all the Covid vaccines suggests that even if taking Tylenol before the shot did blunt your body’s immune response, there’s some wiggle room, and you are likely still well protected against Covid-19. “You should feel reassured that you’ll have enough of an immune response that you’ll will be protected, especially for vaccines that are this good,” said Dr. Offit.Q: What about taking a pain reliever after the shot?“It’s OK to treat” side effects with a pain reliever, said Dr. Offit, but if you don’t really need one, “don’t take it.”While most experts agree it’s safe to take a pain reliever to relieve discomfort after you get vaccinated, they advise against taking it after the shot as a preventive or if your symptoms are manageable without it. The concern with taking an unnecessary pain reliever is that it could blunt some of the effects of the vaccine. (In terms of the vaccine, there’s no meaningful difference if you choose acetaminophen or ibuprofen.)During the Moderna trial, about 26 percent of people took acetaminophen to relieve side effects, and the overall efficacy of the vaccine still was 94 percent.Q: Are the side effects worse if you’ve already had Covid-19?Research and anecdotal reports suggest that people with a previously diagnosed Covid-19 infection may have a stronger reaction and more side effects after their first dose of vaccine compared to those who were never infected with the virus. A strong reaction to your first dose of vaccine also might be a sign that you were previously infected, even if you weren’t aware of it.If you previously tested positive for Covid-19 or had a positive antibody blood test, be prepared for a stronger reaction to your first dose, and consider scheduling a few days off work just in case. Not only will it be more comfortable to stay home and recover in bed, the vaccine side effects can resemble the symptoms Covid-19, and your co-workers won’t want to be near you anyway.Q: I had Covid-19 already. Does that mean I can just get one dose?Studies suggest that one dose might be adequate for people who have a previously confirmed case of Covid-19, but so far the medical guidelines haven’t changed. If you’ve received the Pfizer-BioNTech or Moderna vaccines, you should plan to get your second dose even if you’ve had Covid-19. Skipping your second dose could create problems if your employer or an airline ask to see proof of vaccination in the future. If you live in an area where the single-dose Johnson & Johnson vaccine is available, then you can be fully vaccinated after just one dose. You can read more here about the vaccine response in people who’ve had Covid-19.Q: Will the vaccines work against the new variants that have emerged around the world?The vaccines appear to be effective against a new variant that originated in Britain and is quickly becoming dominant in the United States. But some variants of the coronavirus, particularly one first identified in South Africa and one in Brazil, appear to be more adept at dodging antibodies in vaccinated people.While that sounds worrisome, there’s reason to be hopeful. Vaccinated people exposed to a more resistant variant still appear to be protected against serious illness. And scientists have a clear enough understanding of the variants that they already are working on developing booster shots that will target the variants. The variants identified in South Africa and Brazil are not yet widespread in the United States.People who are vaccinated should still wear masks in public and comply with public health guidelines, but you shouldn’t live in fear of variants, said Dr. Peter J. Hotez, dean of the National School of Tropical Medicine at Baylor College of Medicine in Houston. “If you’re vaccinated, you should feel pretty confident about how protected you are,” said Dr. Hotez. “It’s unlikely you’ll ever go to a hospital or an I.C.U. with Covid-19. In time you’re going to see a recommendation for a booster.”I hope these answers will reassure you about your own vaccine experience. You can find a more complete list of questions and answers in our special vaccine tool “Answers to All Your Questions About Getting Vaccinated Against Covid-19.”

Eczema, or atopic dermatitis (AD), is sometimes called “the itch that rashes.” Often, the itch begins before the rash appears, and, in many cases, the itchiness of the skin condition never really goes away. Approximately 9.6 million children and 16.5 million adults in the U.S. have AD, which can have a serious effect on quality of life for patients. Although much has been learned about the uncomfortable sensation that triggers the desire to scratch, many mysteries remain about chronic itch, making it a challenge to treat. A paper by authors from Brigham and Women’s Hospital and Harvard Medical School published in The Proceedings of the National Academy of Sciences, offers new clues about the underlying mechanisms of itch. Findings suggest a key molecular player known as cysteine leukotriene receptor 2 (CysLT2R) that may be a new target for intractable chronic itch.
“In atopic dermatitis, the itching can be horrific and it can aggravate disease,” said co-corresponding author K. Frank Austen, MD, a senior physician in the Division of Allergy and Clinical Immunology at the Brigham. Austen is also the AstraZeneca Professor of Respiratory and Inflammatory Diseases, Emeritus, at Harvard Medical School. “We began collaborating for two reasons: one is an interest in science — I wandered into the study of what is now the cysteine leukotriene pathway decades ago, and I’ve been pursuing it ever since. The second reason is itch — understanding its cause and connections to neurons.”
Austen and his lab, which focuses on the molecular components that contribute to allergic inflammation, collaborated with Isaac Chiu, PhD, an assistant professor of Immunology at Harvard Medical School. The team also included researchers at the Center for Immunology & Inflammatory Diseases at Massachusetts General Hospital and at the University of Texas at Dallas.
“As a neuro-immunologist, I’m interested in how the nervous system and immune system cross-talk,” said Chiu, co-corresponding author of the study. “Itch arises from a subset of neurons, and acute itch may be a protective response to help us remove something that’s irritating the skin. However, chronic itch is not protective and can be pathological. The underlying mechanism that activates neurons and causes chronic itch is not well understood and new treatment is needed.”
Chiu, Austen and colleagues set out to elucidate the molecular mechanisms that may trigger chronic itch. To do so, they looked for gene activity in dorsal root ganglia (DRG) neurons linked to itch in mice. They found a striking level of CysLT2R, which was uniquely and highly expressed in these specific neurons. They also found expression of this receptor in human DRG neurons. This led the researchers to focus their analysis on the receptor’s role in itch signaling. Additional studies showed that activating this receptor induced itching in a mouse model of AD, but not in other mouse models. Mice that lacked CysLT2R showed decrease itching. Collectively, their findings pointed to the receptor’s key role in causing itch and potentially contributing to AD.
Lead author Tiphaine Voisin, PhD, carried out many of the preclinical experiments in mouse models of AD during her time in the Chiu lab at HMS.
“The last ten years or so of research in the field of chronic itch have shown the importance and the complexity of the interactions between the immune system and the nervous system,” said Voisin. “It was very exciting to explore the contribution of cysteine leukotrienes in these neuro-immune cross-talks leading to itch, including in a mouse model of AD.”
Leukotrienes are a class of lipid molecules that originate from white blood cells, such as mast cells, which are involved in allergy and inflammation. Today, the leukotriene inhibitor montelukast, which targets CysLT1R, is used to treat asthma but does not provide relief from itch. No clinically approved inhibitors of CysLT2R currently exist and, while the researchers have seen evidence of the receptors in humans, until an inhibitor is developed and trialed in humans, it will remain an open question as to whether the new target can lead to a therapy for patients.
While Chiu and Austen are eager to see their findings prompt treatment improvements, Austen, who has been pursuing leukotrienes since the 1970s, also notes the importance of making new discoveries and unexpected connections through research.
“I do believe that science is bottom up, not top down,” said Austen. “The joy of research is doing it for the pleasure of finding out something you didn’t know. The immune system is far more complex than we give it credit for. Understanding the involvement of nerves is an immense step forward — it’s been a missing piece in the study of inflammation. In my view, this is immensely important to connect neuroscience with those of us committed to studying inflammation.”

Telehealth has become a critical way for doctors to still provide health care while minimizing in-person contact during COVID-19. But with phone or Zoom appointments, it’s harder for doctors to get important vital signs from a patient, such as their pulse or respiration rate, in real time.
A University of Washington-led team has developed a method that uses the camera on a person’s smartphone or computer to take their pulse and respiration signal from a real-time video of their face. The researchers presented this state-of-the-art system in December at the Neural Information Processing Systems conference.
Now the team is proposing a better system to measure these physiological signals. This system is less likely to be tripped up by different cameras, lighting conditions or facial features, such as skin color. The researchers will present these findings April 8 at the ACM Conference on Health, Interference, and Learning.
“Machine learning is pretty good at classifying images. If you give it a series of photos of cats and then tell it to find cats in other images, it can do it. But for machine learning to be helpful in remote health sensing, we need a system that can identify the region of interest in a video that holds the strongest source of physiological information — pulse, for example — and then measure that over time,” said lead author Xin Liu, a UW doctoral student in the Paul G. Allen School of Computer Science & Engineering.
“Every person is different,” Liu said. “So this system needs to be able to quickly adapt to each person’s unique physiological signature, and separate this from other variations, such as what they look like and what environment they are in.”
The team’s system is privacy preserving — it runs on the device instead of in the cloud — and uses machine learning to capture subtle changes in how light reflects off a person’s face, which is correlated with changing blood flow. Then it converts these changes into both pulse and respiration rate.

In the first study to use whole genome sequencing (WGS) to discover rare genomic variants associated with Alzheimer’s disease (AD), researchers have identified 13 such variants (or mutations). In another novel finding, this study establishes new genetic links between AD and the function of synapses, which are the junctions that transmit information between neurons, and neuroplasticity, or the ability of neurons to reorganize the brain’s neural network. These discoveries could help guide development of new therapies for this devastating neurological condition. Researchers at Massachusetts General Hospital (MGH), the Harvard T. H. Chan School of Public Health, and Beth Israel Deaconess Medical Center report these findings in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.
Over the last four decades, MGH has pioneered research on the genetic origins of AD, led by Rudolph Tanzi, PhD, vice chair of Neurology and director of the hospital’s Genetics and Aging Research Unit. Notably, Tanzi and colleagues co-discovered genes that cause early onset (prior to age 60) familial AD (that is, a form that runs in families), including the amyloid protein (A4) precursor (APP), and the presenilin genes (PSEN1 and PSEN2). Mutations in these genes lead to accumulation of amyloid plaques in the brain, a hallmark of AD.
The next 30 AD gene variants that were discovered are primarily linked to chronic inflammation in the brain (or neuroinflammation), which also increases the risk for this cognitive disease. However, loss of synapses is the neurological change that is most closely correlated with the severity of dementia in Alzheimer’s disease, yet no clear genetic links between the disease and these vital connections had previously been identified. “It was always kind of surprising that whole-genome screens had not identified Alzheimer’s genes that are directly involved with synapses and neuroplasticity,” says Tanzi.
Prior to this paper, the genome-wide association study (GWAS) was the primary tool used for identifying AD genes. In a GWAS, the genomes of many individuals are scanned in search of common gene variants that occur more frequently in people who have a given disease, such as AD. But to date, common Alzheimer’s-associated gene variants have accounted for less than half of the heritability of AD. A standard GWAS misses the rare gene variants (those occurring in less than 1% of the population), a problem solved by the WGS, which scans every bit of DNA in a genome.
“This paper brings us to the next stage of disease-gene discovery by allowing us to look at the entire sequence of the human genome and assess the rare genomic variants, which we couldn’t do before,” says Dmitry Prokopenko, PhD, of MGH’s McCance Center for Brain Health, who is lead author of the study.
Identifying less-common gene mutations that increase the risk for AD is important because they may hold critical information about the biology of the disease, says Tanzi. “Rare gene variants are the dark matter of the human genome,” he says, and there are lots of them: Of the three billion pairs of nucleotide bases that form a complete set of DNA, each person has 50 to 60 million gene variants — and 77% are rare.
In their quest to find rare AD gene variants, Tanzi, Prokopenko and their colleagues performed WGS analyses on the genomes of 2,247 individuals from 605 families that include multiple members who have been diagnosed with AD. They also analyzed WGS datasets on 1,669 unrelated individuals. The study identified 13 previously unknown rare gene variants associated with AD. Strikingly, these gene variants were associated with functioning of synapses, development of neurons, and neuroplasticity.
“With this study, we believe we have created a new template for going beyond standard GWAS and association of disease with common genome variants, in which you miss much of the genetic landscape of the disease,” says Tanzi, who sees potential for their methods to be used to study the genetics of many other conditions. Moreover, he plans to use “Alzheimer’s in a dish” — three-dimensional cell culture models and brain organoids he and his colleagues have developed over the past decade — to explore what happens when the rare mutations this paper identified are inserted in neurons. “That could help guide us in novel drug discovery,” says Tanzi.
This study was supported by the Cure Alzheimer’s Fund and grants from the National Institutes of Health.
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Kidney development is a balancing act between the self-renewal of stem and progenitor cells to maintain and expand their numbers, and the differentiation of these cells into more specialized cell types. In a new study in the journal eLife from Andy McMahon’s laboratory in the Department of Stem Cell Biology and Regenerative Medicine at the Keck School of Medicine of USC, former graduate student Alex Quiyu Guo and a team of scientists demonstrate the importance of a molecule called β-catenin in striking this balance.
β-catenin is a key driver at the end of a complex signaling cascade known as the Wnt pathway. Wnt signaling plays critical roles in the embryonic development of multiple organs including the kidneys. By partnering with other Wnt pathway molecules, β-catenin controls the activity of hundreds to thousands of genes within the cell.
The new study builds on the McMahon Lab’s previous discovery that Wnt/β-catenin can initiate progenitor cells to execute a lengthy and highly orchestrated program of forming structures in the kidney called nephrons. A healthy human kidney contains a million nephrons that balance body fluids and remove soluble waste products. Too few nephrons results in kidney disease.
Previous studies from the UT Southwestern Medical Center laboratory of Thomas Carroll, a former postdoctoral trainee in the McMahon Lab, suggested that Wnt/β-catenin signaling plays opposing roles in ensuring the proper number of nephrons: promoting progenitor maintenance and self-renewal, and stimulating progenitor cell differentiation.
“It sounded like Wnt/β-catenin is doing two things — both maintenance and differentiation — that seem to be opposite operations,” said Guo. “Therefore, the hypothesis was that different levels of Wnt/β-catenin can dictate different fates of the nephron progenitors: when it’s low, it works on maintenance; when it’s high, it directs differentiation.”
In 2015, it became more possible to test this hypothesis when Leif Oxburgh, a scientist at the Rogosin Institute in New York and a co-author of the eLife study, developed a system for growing large numbers of nephron progenitor cells, or NPCs, in a Petri dish.

Researchers pushed back after the C.D.C. director asserted that vaccinated people “do not carry the virus.”The Centers for Disease Control and Prevention on Thursday walked back controversial comments made by its director, Dr. Rochelle P. Walensky, suggesting that people who are vaccinated against the coronavirus never become infected or transmit the virus to others.The assertion called into question the precautions that the agency had urged vaccinated people to take just last month, like wearing masks and gathering only under limited circumstances with unvaccinated people.“Dr. Walensky spoke broadly during this interview,” an agency spokesman told The Times. “It’s possible that some people who are fully vaccinated could get Covid-19. The evidence isn’t clear whether they can spread the virus to others. We are continuing to evaluate the evidence.”The agency was responding in part to criticism from scientists who noted that current research was far from sufficient to claim that vaccinated people cannot spread the virus.The data suggest that “it’s much harder for vaccinated people to get infected, but don’t think for one second that they cannot get infected,” said Paul Duprex, director of the Center for Vaccine Research at the University of Pittsburgh.In a television interview with MSNBC’s Rachel Maddow, Dr. Walensky referred to data published by the C.D.C. showing that one dose of the Moderna or Pfizer-BioNTech vaccine was 80 percent effective at preventing infection, and two doses were 90 percent effective.That certainly suggested that transmission from vaccinated people might be unlikely, but Dr. Walensky’s comments hinted that protection was complete. “Our data from the C.D.C. today suggests that vaccinated people do not carry the virus, don’t get sick,” she said. “And that it’s not just in the clinical trials, it’s also in real-world data.”Dr. Walensky went on to emphasize the importance of continuing to wear masks and maintain precautions, even for vaccinated people. Still, the brief comment was widely interpreted as saying that the vaccines offered complete protection against infection or transmission.In a pandemic that regularly spawns scientific misunderstanding, experts said they were sympathetic to Dr. Walensky and her obvious desire for Americans to continue to take precautions. It was only Monday that she said rising caseloads had left her with a sense of “impending doom.”“If Dr. Walensky had said most vaccinated people do not carry virus, we would not be having this discussion,” said John Moore, a virologist at Weill Cornell Medicine in New York.“What we know is the vaccines are very substantially effective against infection — there’s more and more data on that — but nothing is 100 percent,” he added. “It is an important public health message that needs to be gotten right.”Misinterpretation could disrupt the agency’s urgent pleas for immunization, some experts said. As of Wednesday, 30 percent of Americans had received at least one dose of a vaccine and 17 percent were fully immunized.“There cannot be any daylight between what the research shows — really impressive but incomplete protection — and how it is described,” said Dr. Peter Bach, director of the Center for Health Policy and Outcomes at Memorial Sloan Kettering Cancer Center in New York.“This opens the door to the skeptics who think the government is sugarcoating the science,” Dr. Bach said, “and completely undermines any remaining argument why people should keep wearing masks after being vaccinated.”All of the coronavirus vaccines are spectacularly successful at preventing serious disease and death from Covid-19, but how well they prevent infection has been less clear.Clinical trials of the vaccines were designed only to assess whether the vaccines prevent serious illness and death. The research from the C.D.C. on Monday brought the welcome conclusion that the vaccines are also extremely effective at preventing infection.The study enrolled 3,950 health care workers, emergency responders and others at high risk of infection. The participants swabbed their noses each week and sent the samples in for testing, which allowed federal researchers to track all infections, symptomatic or not. Two weeks after vaccination, the vast majority of vaccinated people remained virus-free, the study found.Follow-up data from clinical trials support that finding. In results released by Pfizer and BioNTech on Wednesday, for example, 77 people who received the vaccine had a coronavirus infection, compared with 850 people who got a placebo.“Clearly, some vaccinated people do get infected,” Dr. Duprex said. “We’re stopping symptoms, we’re keeping people out of hospitals. But we’re not making them completely resistant to an infection.”The number of vaccinated people who become infected is likely to be higher among those receiving vaccines made by Johnson & Johnson and AstraZeneca, which have a lower efficacy, experts said. (Still, those vaccines are worth taking, because they uniformly prevent serious illness and death.)Infection rates may also be higher among people exposed to a virus variant that can sidestep the immune system.Cases across the country are once again on the upswing, threatening a new surge. Dr. Walensky’s comment came just a day after she made an emotional appeal to the American public to continue taking precautions.“I am asking you to just hold on a little longer, to get vaccinated when you can, so that all of those people that we all love will still be here when this pandemic ends,” she said.Given the rising numbers, it’s especially important that immunized people continue to protect those who have not yet been immunized against the virus, experts said.“Vaccinated people should not be throwing away their masks at this point,” Dr. Moore said. “This pandemic is not over.”

A multistate group of anesthesiologists filed cases in Texas and Colorado, accusing the insurance giant of squeezing them like a “boa constrictor.”UnitedHealthcare, one of the nation’s largest health insurers, is being sued in two states by a large group of anesthesiologists who are accusing the company of stifling competition by forcing the doctors out of its network and by using its enormous clout to pressure hospitals and surgeons to stop referring patients to them.The lawsuits, filed Wednesday in Colorado and Texas, were brought by U.S. Anesthesia Partners, a sizable physician-owned practice backed by private-equity investors. The practice claims in the Texas lawsuit that United engaged in “unlawful tactics and pressure campaigns,” including “bribing” surgeons with contracts that paid them much more if they steered patients away from the group’s anesthesiologists.The doctors make similar claims in the lawsuit they filed in Colorado, where they say United orchestrated a “group boycott.” They describe United as “like a boa constrictor,” squeezing the group “from all angles.”In an emailed statement, United said the lawsuits were “just the latest example of the group’s efforts to pressure us into agreeing to its rate demands and to distract from the real reason that it no longer participates in our network.” The company said it had not yet been served with either complaint.United added that many of the private-equity-backed physician groups “expect to be paid double or even triple the median rate we pay other physicians providing the same services,” driving up the cost of care. The company says these groups have been using their increasing presence in a given regional market to demand higher rates. It says that its goal has been to keep the groups in network but that it is rethinking its approach.While insurers and the hospitals and doctors have long had ugly standoffs during contract negotiations, the parties typically come to a last-minute agreement. But United has become increasingly aggressive in its stance toward large physician groups like U.S. Anesthesia, dropping a number of them from its network, according to analysts.“United has a lot of market power and they want to use it to their advantage,” said Dean Ungar, who follows the insurance behemoth for Moody’s Investors Service, which evaluates the company’s debt. “They are willing to play hardball with some of these companies.”U.S. Anesthesia, which operates in nine states, said it had a long relationship with United and was part of the carrier’s networks in Texas and Colorado until last year.But the doctors also raise questions about the insurer’s potential conflicts of interest as its parent company, UnitedHealth Group, also offers medical services. UnitedHealth, which had $257 billion in sales last year, has become a sprawling conglomerate that includes more than 50,000 physicians, a chain of surgery centers, a pharmacy benefit manager and other assorted health care businesses in addition to its traditional insurance business.UnitedHealth directly competes with U.S. Anesthesia, according to the Texas lawsuit, through an ownership interest in Sound Physicians, a large medical practice that provides emergency and anesthesiology services. Sound Physicians is looking to expand in markets like Fort Worth and Houston, and U.S. Anesthesia claims in the lawsuit that its doctors were contacted by Sound Physicians “to induce them to leave” and challenge the noncompete provisions in their contracts to work with the United group.The major insurer throws its weight around in other ways, the lawsuit claims. While the company’s Optum unit, which operates the surgery centers and clinics, is technically separate from the health insurer, the doctors accuse United of forcing its OptumCare facilities to sever their relationships with the anesthesiology group and pushing in-network surgeons to move their operations to hospitals or facilities that do not have contracts with U.S. Anesthesia.“United and its affiliates have extended their tentacles into virtually every aspect of health care, allowing United to squeeze, choke and crush any market participant that stands in the way of United’s increased profits,” the doctors claim in their lawsuit.It is standard practice, United said, for an insurer to encourage the use of hospitals and doctors within its network.In contrast to many smaller physician groups that are struggling because of the pandemic, United has maintained a strong financial position, shoring up profits while elective surgeries and other procedures were shut down, resulting in fewer medical claims. So it has continued to expand, hiring more doctors and buying up additional practices. The company says it plans to add more than 10,000 employed or affiliated doctors this year.The relationship between insurers and providers has become more complicated as more insurance carriers own doctors’ groups or clinics. “They want to be the referee and play on the other team,” said Michael Turpin, a former United executive who is now an executive vice president at USI, an insurance brokerage.Employers that rely on UnitedHealthcare to cover their workers have a difficult time judging who benefits when insurers fail to reach an agreement to keep a provider in network. “This is just as much about profit as it is about principle,” Mr. Turpin said.United has defended its actions in the past by pointing to the role many of these doctors’ groups, financed by private equity, played in creating surprise medical bills that overwhelmed and burdened Americans around the country. Because the groups’ doctors specialize in areas like emergency care or anesthesia, patients are often shocked to find out that they are not in network even if the hospital where they received care is.Some of the doctors’ groups, like Envision Healthcare, whose doctors provide emergency-room care, pursued a strategy of keeping their doctors out of network to make more money. Patients were caught in the middle as insurers and doctors fought over out-of-network bills, and many people ended up owing large sums not covered by their health plans.When criticism of these tactics pressured Congress to consider remedies, the private-equity firms backing groups like Envision and TeamHealth spent large sums trying to block federal legislation. Lawmakers finally took action at the end of last year to protect patients from surprise bills by requiring parties to reach a fair price.But doctors say United is increasingly unwilling to come to an agreement they can accept. Envision, which eventually agreed to lower its payments and be included in the health plan’s network, said United dropped it this year because it would not agree to “drastic cuts to clinician pay.”“United turned down multiple proposals that would reduce the total cost of care for patients,” Envision said in an emailed statement. “We are left to wonder why it appears United does not want our 25,000 clinicians in their network.”The insurer has also dropped other groups. Last year, Mednax, which employed specialists in neonatology and anesthesiology, announced it had been dropped by United in four states. The company has since sold both its radiology and anesthesiology practices.

A multistate group of anesthesiologists filed cases in Texas and Colorado, accusing the insurance giant of squeezing them like a “boa constrictor.”UnitedHealthcare, one of the nation’s largest health insurers, is being sued in two states by a large group of anesthesiologists who are accusing the company of stifling competition by forcing the doctors out of its network and by using its enormous clout to pressure hospitals and surgeons to stop referring patients to them.The lawsuits, filed Wednesday in Colorado and Texas, were brought by U.S. Anesthesia Partners, a sizable physician-owned practice backed by private-equity investors. The practice claims in the Texas lawsuit that United engaged in “unlawful tactics and pressure campaigns,” including “bribing” surgeons with contracts that paid them much more if they steered patients away from the group’s anesthesiologists.The doctors make similar claims in the lawsuit they filed in Colorado, where they say United orchestrated a “group boycott.” They describe United as “like a boa constrictor,” squeezing the group “from all angles.”In an emailed statement, United said the lawsuits were “just the latest example of the group’s efforts to pressure us into agreeing to its rate demands and to distract from the real reason that it no longer participates in our network.” The company said it had not yet been served with either complaint.United added that many of the private-equity-backed physician groups “expect to be paid double or even triple the median rate we pay other physicians providing the same services,” driving up the cost of care. The company says these groups have been using their increasing presence in a given regional market to demand higher rates. It says that its goal has been to keep the groups in network but that it is rethinking its approach.While insurers and the hospitals and doctors have long had ugly standoffs during contract negotiations, the parties typically come to a last-minute agreement. But United has become increasingly aggressive in its stance toward large physician groups like U.S. Anesthesia, dropping a number of them from its network, according to analysts.“United has a lot of market power and they want to use it to their advantage,” said Dean Ungar, who follows the insurance behemoth for Moody’s Investors Service, which evaluates the company’s debt. “They are willing to play hardball with some of these companies.”U.S. Anesthesia, which operates in nine states, said it had a long relationship with United and was part of the carrier’s networks in Texas and Colorado until last year.But the doctors also raise questions about the insurer’s potential conflicts of interest as its parent company, UnitedHealth Group, also offers medical services. UnitedHealth, which had $257 billion in sales last year, has become a sprawling conglomerate that includes more than 50,000 physicians, a chain of surgery centers, a pharmacy benefit manager and other assorted health care businesses in addition to its traditional insurance business.UnitedHealth directly competes with U.S. Anesthesia, according to the Texas lawsuit, through an ownership interest in Sound Physicians, a large medical practice that provides emergency and anesthesiology services. Sound Physicians is looking to expand in markets like Fort Worth and Houston, and U.S. Anesthesia claims in the lawsuit that its doctors were contacted by Sound Physicians “to induce them to leave” and challenge the noncompete provisions in their contracts to work with the United group.The major insurer throws its weight around in other ways, the lawsuit claims. While the company’s Optum unit, which operates the surgery centers and clinics, is technically separate from the health insurer, the doctors accuse United of forcing its OptumCare facilities to sever their relationships with the anesthesiology group and pushing in-network surgeons to move their operations to hospitals or facilities that do not have contracts with U.S. Anesthesia.“United and its affiliates have extended their tentacles into virtually every aspect of health care, allowing United to squeeze, choke and crush any market participant that stands in the way of United’s increased profits,” the doctors claim in their lawsuit.It is standard practice, United said, for an insurer to encourage the use of hospitals and doctors within its network.In contrast to many smaller physician groups that are struggling because of the pandemic, United has maintained a strong financial position, shoring up profits while elective surgeries and other procedures were shut down, resulting in fewer medical claims. So it has continued to expand, hiring more doctors and buying up additional practices. The company says it plans to add more than 10,000 employed or affiliated doctors this year.The relationship between insurers and providers has become more complicated as more insurance carriers own doctors’ groups or clinics. “They want to be the referee and play on the other team,” said Michael Turpin, a former United executive who is now an executive vice president at USI, an insurance brokerage.Employers that rely on UnitedHealthcare to cover their workers have a difficult time judging who benefits when insurers fail to reach an agreement to keep a provider in network. “This is just as much about profit as it is about principle,” Mr. Turpin said.United has defended its actions in the past by pointing to the role many of these doctors’ groups, financed by private equity, played in creating surprise medical bills that overwhelmed and burdened Americans around the country. Because the groups’ doctors specialize in areas like emergency care or anesthesia, patients are often shocked to find out that they are not in network even if the hospital where they received care is.Some of the doctors’ groups, like Envision Healthcare, whose doctors provide emergency-room care, pursued a strategy of keeping their doctors out of network to make more money. Patients were caught in the middle as insurers and doctors fought over out-of-network bills, and many people ended up owing large sums not covered by their health plans.When criticism of these tactics pressured Congress to consider remedies, the private-equity firms backing groups like Envision and TeamHealth spent large sums trying to block federal legislation. Lawmakers finally took action at the end of last year to protect patients from surprise bills by requiring parties to reach a fair price.But doctors say United is increasingly unwilling to come to an agreement they can accept. Envision, which eventually agreed to lower its payments and be included in the health plan’s network, said United dropped it this year because it would not agree to “drastic cuts to clinician pay.”“United turned down multiple proposals that would reduce the total cost of care for patients,” Envision said in an emailed statement. “We are left to wonder why it appears United does not want our 25,000 clinicians in their network.”The insurer has also dropped other groups. Last year, Mednax, which employed specialists in neonatology and anesthesiology, announced it had been dropped by United in four states. The company has since sold both its radiology and anesthesiology practices.