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As life propagated across Earth in the form of the widest variety of single-celled organisms, sometime between 3.5 and a billion years ago one such organism managed an evolutionary coup: Instead of devouring and digesting bacteria, it encapsulated its prey and used it as a source of energy. As a host cell, it offered protection and nutrition in return. This is referred to as the endosymbiotic theory, according to which that single-celled organism was the primordial mother of all higher cells, out of which all animals, fungi and plants developed. Over the course of billions of years, the encapsulated bacterium became the cell’s powerhouse, the mitochondrion, which supplies it with the cellular energy currency ATP. It lost a large part of its genetic material — its DNA — and exchanged smaller DNA segments with the mother cell. However, now as in the past, mitochondria divide independently of the cell and possess some genes of their own.
How closely the cell and the mitochondrion work together in human cells today is what a team of researchers led by Dr. Christian Münch of Goethe University Frankfurt is investigating. They have now discovered how the mitochondrion calls for help from the cell when it is under stress. Triggers for such stress can be infections, inflammatory diseases or genetic disorders, for example, but also nutrient deficiencies or cell toxins.
A certain type of mitochondrial stress is caused by misfolded proteins that are not quickly degraded and accumulate in the mitochondrion. The consequences for both the mitochondrion and the cell are dramatic: Misfolded proteins can, for example, disrupt energy production or lead to the formation of larger amounts of reactive oxygen compounds, which attack the mitochondrial DNA and generate further misfolded proteins. In addition, misfolded proteins can destabilize the mitochondrial membranes, releasing signal substances from the mitochondrion that activate apoptosis, the cell’s self-destruction program.
The mitochondrion responds to the stress by producing more chaperones (folding assistants) to fold the proteins in order to reduce the misfolding, as well as protein shredding units that degrade the misfolded proteins. Until now, how cells trigger this protective mechanism was unknown.
The researchers from Goethe University Frankfurt artificially triggered misfolding stress in the mitochondria of cultured human cells and analyzed the result. “What makes it difficult to unravel such signaling processes,” explains Münch, himself a biochemist, “is that an incredibly large number take place simultaneously and at high speed in the cell.” The research team therefore availed itself of methods (transcriptome analyses) that can be used to measure over time to what extent genes are transcribed. In addition, the researchers observed, among other things, which proteins bind to each other at which point in time, at which intervals the concentrations of intracellular substances change, and what effects there are when individual proteins are systematically deactivated.
The result is that the mitochondria send two chemical signals to the cell when protein misfolding stress occurs: They release reactive oxygen compounds and block the import of protein precursors, which are produced in the cell and are only folded into their functional shape inside the mitochondrion, causing these precursors to accumulate in the cell. Among other things, the reactive oxygen compounds lead to chemical changes in a protein called DNAJA1. Normally, DNAJA1 supports a specific chaperone (folding assistant) in the cell, which molds the cell’s newly formed proteins into the correct shape.
As a consequence of the chemical change, DNAJA1 now increasingly forces itself on the folding assistant HSP70 as its helper. HSP70 then takes special care of the misfolded protein precursors that accumulate around the mitochondrion because of the blocked protein import. By doing so, HSP70 reduces its interaction with its regular partner HSF1. HSF1 is now released and can migrate into the cell nucleus, where it can trigger the anti-stress mechanism for the mitochondrion.
As biochemist Münch explains, “It was very exciting to discover how the two mitochondrial stress signals are combined into one signal in the cell, which then triggers the cell’s response to mitochondrial stress. Moreover, in this complex process, which is essentially driven by tiny local changes in concentration, the stress signaling pathways of the cell and the mitochondrion dovetail very elegantly with each other — like the cogs in a clockwork.”

New Alzheimer’s research from UVA Health suggests that enhanced light sensitivity may contribute to “sundowning” — the worsening of symptoms late in the day — and spur sleep disruptions thought to contribute to the disease’s progression.
The new insights into the disruptions of the biological clock seen in Alzheimer’s could have important potential both for the development of treatments and for symptom management, the researchers say. For example, caregivers often struggle with the erratic sleep patterns caused by Alzheimer’s patients’ altered “circadian rhythms,” as the body’s natural daily cycle is known. Light therapy, the new research suggests, might be an effective tool to help manage that.
Further, better understanding Alzheimer’s effects on the biological clock could have implications for preventing the disease. Poor sleep quality in adulthood is a risk factor for Alzheimer’s, as our brains, at rest, naturally cleanse themselves of amyloid beta proteins that are thought to form harmful tangles in Alzheimer’s.
“Circadian disruptions have been recognized in Alzheimer’s disease for a long time, but we’ve never had a very good understanding of what causes them,” said researcher Thaddeus Weigel, a graduate student working with Heather Ferris, MD, PhD, of the University of Virginia School of Medicine’s Division of Endocrinology and Metabolism. “This research points to changes in light sensitivity as a new, interesting possible explanation for some of those circadian symptoms.”
Alzheimer’s is the most common form of dementia, affecting 50 million people around the world. Its hallmark is progressive memory loss, to the point that patients can forget their own loved ones, but there can be many other symptoms, such as restlessness, aggression, poor judgment and endless searching. These symptoms often worsen in the evening and at night.
Ferris and her collaborators used a mouse model of Alzheimer’s to better understand what happens to the biological clock in Alzheimer’s disease. They essentially gave the mice “jet lag” by altering their exposure to light, then examined how it affected their behavior. The Alzheimer’s mice reacted very differently than did regular mice.
The Alzheimer’s mice, the scientists found, adapted to a six-hour time change significantly more quickly than the control mice. This, the scientists suspect, is the result of a heightened sensitivity to changes in light. While our biological clocks normally take cues from light, this adjustment happens gradually — thus, jet lag when we travel great distances. Our bodies need time to adapt. But for the Alzheimer’s mice, this change happened abnormally fast.

A medical therapy that inhibits the growth of cancer cells may one day be effective at treating Lyme disease, according to new research by a University of Massachusetts Amherst team at the New England Regional Center of Vector-borne Diseases (NEWVEC). “It’s a long way from something you’re going to pick up at CVS, but these early findings are very encouraging,” says vector-borne disease expert Stephen Rich, professor of microbiology, executive director of NEWVEC and senior author of the study published in the journal Pathogens. Lyme disease is the most common vector-borne disease in the U.S., spread by infected deer ticks. The potentially debilitating illness, which is diagnosed in about 476,000 people each year in the U.S., doesn’t always respond to antibiotics. “There are people who have cases of Lyme disease that go on and on,” Rich says. “So there’s always interest in finding new therapies or new ways to inhibit the growth of the bacterium. And based on what we’re seeing in the lab, this may be one of those ways.”
The discovery began with an “aha” moment by then-Ph.D. candidate Patrick Pearson, who was working in Rich’s lab, along with graduate student Adam Lynch. Pearson, co-author of the paper, is now a NEWVEC post-doctoral researcher at UMass Amherst. Lynch, lead author, is now a research fellow in the Department of Veterinary and Animal Sciences.
Tumor cells and Borrelia burgdorferi, the corkscrew-shaped bacterium that causes Lyme disease, share an unusual feature about the way they grow, Pearson noted and pondered. “It turns out that cancer cells and Borrelia both rely solely on glycolysis for their metabolism,” Rich explains.
Glycolysis, in turn, is dependent on one molecule called lactate dehydrogenase, or LDH. Pearson wondered whether LDH inhibitors, which are used as drug therapies to target certain cancers, might also be an effective strategy against Lyme disease.
“It was a very clever idea,” Rich says. “In principle, we thought these LDH inhibitors should work well to inhibit the growth of Lyme disease bacteria.”
And in fact, in in vitro experiments, they did. “…a range of commercially available LDH inhibitors with various mechanisms of action and origins were tested on Borrelia in Culture,” the paper states. “Of these inhibitors, gossypol, AT-101, and oxamate substantially impacted B. burgdorferigrowth in vitro and represent promising candidates against Borrelia infections in vivo.”
Rich says the research will continue at NEWVEC, which was funded by the Centers for Disease Control and Prevention last year with a $10 million award to prevent and reduce tick- and mosquito-borne diseases in New England. NEWVEC aims to bring together academic communities, public health practitioners, residents and visitors across the Northeast, where Lyme infections are concentrated.
“These experiments were done outside of hosts. Now we need to carry this out in mouse models and, eventually, in people,” Rich says.
The researchers note that this drug therapy may also be effective against another tick-borne disease, babesiosis, a malaria-like infection. “This has the potential to kill two birds with one stone,” Rich says. “And that makes this discovery even more tantalizing.”

A metabolic by-product that is more prevalent during fasting may supercharge immune cells as they fight infection and disease, reports an early stage study by Van Andel Institute scientists and collaborators.
The findings, published today in Immunity, may pave the way for future personalized dietary recommendations to augment treatments for infection, cancer and other diseases.
“This study helps us better understand how nutrition affects the immune system,” said VAI Professor Russell Jones, Ph.D., the study’s corresponding author. “This is an exciting first step and we look forward to one day translating this knowledge into dietary recommendations to boost immune function.”
The findings center on ketone bodies, which are regularly produced by the liver but become more numerous when glucose, a sugar that acts as the main power source for cells, is in short supply. This can occur during exertion such as exercise, when cells are rapidly burning through fuel, or during fasting, when there is little food available to be broken down into glucose.
To compensate, the liver steps up production of ketone bodies to feed the brain and other organs. The study shows that ketone bodies also power immune cells, a surprise finding that illuminates new connections between diet and immunity.
Like other cells in the body, T cells — the soldiers of the immune system — absorb nutrients like glucose from our diets to generate the energy required to do their jobs. Jones and colleagues demonstrated that T cells prefer ketone bodies over glucose as a fuel source. They also found that ketone bodies improve T cell function by reprogramming them to better neutralize threats. Conversely, loss of the ability to process ketone bodies causes defects in T cell function and hampers their ability to combat infection.
The authors hypothesize that ketone bodies may be an evolutionary failsafe that boosts the immune system when nutrient resources are limited, such as when one’s appetite is suppressed during illness.
“This work underscores how different nutrient fuels source distinct cellular functions,” said Peter Crawford, M.D., Ph.D., Vice Dean for Research and Professor of Medicine at University of Minnesota Medical School and study co-author. “It also fosters future interest in considering the diversity of nutrient fuel utilization patterns among different immune cell types in varying infectious disease or cancer contexts.”
Although the study suggests increasing ketone bodies through fasting or intermittent fasting regimens may enhance T cell function in certain circumstances, other studies suggest that fasting may suppress immune function. Rather than being at odds with one another, these studies illuminate the intricate interactions between diet and the immune system and underscore the need for further research into this complex relationship.
Going forward, Jones and colleagues will explore how fasting and ketone body supplementation impacts immune function, with a focus on T cells’ ability to fight cancer.

Published3 hours agoShareclose panelShare pageCopy linkAbout sharingImage source, Getty ImagesBy Smitha MundasadHealth reporter People struggle to estimate portion sizes for food such as chocolate, crisps and cheese, a survey of 1,265 Which? subscribers suggests.They may need more help to assess how healthy products are, the consumer group says.A third guessed a 185g (6.5oz) tube of Pringles contained two to four portions. But the packaging says it has six to seven – some 13 crisps each.On a 220g box of Quality Street, the label suggests a portion is two sweets.Unrealistic recommended serving sizes can mislead people into thinking they are consuming fewer calories, and less fat, sugar or salt, than they actually are, Which? says.This video can not be playedTo play this video you need to enable JavaScript in your browser.Labelling was really valuable but needed to be based on “meaningful and consistent” portion sizes, Which? nutritionist Shefalee Loth said.”People can be confused by inconsistent and unrealistic serving sizes and the way that manufacturers provide these can sometimes make it difficult to assess just how healthy a product is,” she said.Most of those surveyed said:supermarket “meal deals” were the ideal portion size for one person – but the drink and accompanying snack are often designed for two, a 300ml (half a pint) carton of orange juice, for example, or a 60g packet of mixed nutsa 225g supermarket pack of halloumi cheese was the right amount for two to four people – but the packaging suggests it would be enough to feed sevenThe Which? report found some well-known brands of crisps and chocolate were available in a range of pack sizes, with inconsistent portion sizes across these different packs. Image source, Getty ImagesWhich? asked 229 people to pour themselves a glass of wine or juice at home and then measure how much they had served. About half of white-wine drinkers poured more than the official small serving of 125mlSome 54% of orange-juice drinkers poured more than the recommended daily limit of 150mlA Food and Drink Federation representative said a range of portion sizes were available “to help consumers achieve a healthy balanced diet and to meet the varying requirements of families”.”Food and drink manufacturers are committed to providing clear and accurate information and voluntarily include traffic-light labelling on the front of packs, so people can make an informed decision on the food they buy,” the representative added.Most nutrition information on packaging is listed per 100g, in line with government guidance. More on this storySupermarket health claims ‘confusing’Published24 February 2019’Measure food with your fist’ Video, 00:02:25’Measure food with your fist’Published14 January 20192:25Ministers delay crackdown on buy-one-get-one-freePublished17 JuneAround the BBCWhat is a good portion size – BBC Food.website

Published4 hours agoShareclose panelShare pageCopy linkAbout sharingImage source, Getty ImagesBy Max MatzaBBC NewsThe rate of Americans developing a rare meat allergy from tick bites is rising, researchers say, and may have already impacted as many as 450,000 people. New data released by the Centers for Disease Control and Prevention (CDC) on Thursday shows a steep increase in cases of alpha-gal syndrome. The allergy triggers a possibly life-threatening reaction to several types of meat or animal products. US scientists have traced alpha-gal to saliva from the lone star tick. The tick is identified by the white spot on its back and is mostly found in southern and eastern parts of the US. But experts warn that their range is expanding due to climate change. Blood-sucking bites from the lone star, formally called the Amblyomma americanum, can make a person sick when they consume certain meat and animal products made from mammals. The list of dangerous foods for people suffering from alpha-gal syndrome include pork, beef, rabbit, lamb, venison, gelatine, milk, some dairy products and certain pharmaceuticals. Symptoms from the little-understood syndrome include stomach cramps, diarrhoea, hives and shortness of breath that could trigger fatal anaphylaxis. Because of how slowly the body digests meat, it can be very difficult to spot symptoms. More than 110,000 cases have been detected since 2010, the CDC says. From 2017 to 2021 the number of cases increased by around 15,000 per year. Because of how difficult it can be to diagnose, the CDC says that up to 450,000 Americans in total may have developed meat allergies due to alpha-gal. A survey of 1,500 doctors and health workers from last year found that 42% of them had never heard of alpha-gal. In the survey, which was also released by the CDC on Thursday, about one-third of the group said they were “not too confident” in their ability to identify the disease. Only 5% said they were “very confident” in their ability. A tick bite that makes you allergic to red meatCould we engineer greener humans?Lyme disease: The lives ruined by a bite from a tickThe syndrome was not discovered until 2008 by accident after US researchers found unexpected results while testing a drug used to treat cancer. The Ixodes holocyclus – aka the paralysis tick – has also caused similar meat allergies in the Sydney region of Australia. Image source, Getty ImagesExperts warn people to cover up outdoors and to regularly check their bodies for tick bites. Tick bites can cause several dangerous illnesses – such as Lyme disease – and are most common during warmer months. The CDC advises people outdoors to use insect repellent, such as those containing DEET, or to pre-treat clothing with a chemical called permethrin. More on this storyGlobal traveller now housebound after tick bitePublished14 May

Researchers at NYU College of Dentistry’s Pain Research Center have developed a gene therapy that treats chronic pain by indirectly regulating a specific sodium ion channel, according to a new study published in the Proceedings of the National Academy of Sciences (PNAS).
The innovative therapy, tested in cells and animals, is made possible by the discovery of the precise region where a regulatory protein binds to the NaV1.7 sodium ion channel to control its activity.
“Our study represents a major step forward in understanding the underlying biology of the NaV1.7 sodium ion channel, which can be harnessed to provide relief from chronic pain,” said Rajesh Khanna, director of the NYU Pain Research Center and professor of molecular pathobiology at NYU Dentistry.
Chronic pain is a significant public health issue that affects roughly a third of the U.S. population. Scientists are eager to develop pain medications that are more effective and safer alternatives to opioids.
Sodium ion channels play a key role in the generation and transmission of pain, as they are critical for nerve cells, or neurons, communicating with each other. One particular sodium ion channel called NaV1.7 emerged as a promising target for treating pain following the discovery of its importance in people with rare, genetic pain disorders. In some families, a mutation in the gene that encodes for NaV1.7 allows large amounts of sodium to enter cells, causing intense chronic pain. In other families, mutations that block NaV1.7 result in a complete lack of pain.
Scientists have been trying for years to develop pain treatments to selectively block NaV1.7 — with little success. Khanna has taken a different approach: rather than blocking NaV1.7, his goal is to indirectly regulate it using a protein called CRMP2.
“CRMP2 ‘talks’ to the sodium ion channel and modulates its activity, allowing more or less sodium into the channel. If you block the conversation between Nav1.7 and CRMP2 by inhibiting the interaction between the two, we can dial down how much sodium comes in. This quiets down the neuron and pain is mitigated,” said Khanna, the PNAS study’s senior author.

Published8 hours agoShareclose panelShare pageCopy linkAbout sharingImage source, Getty ImagesBy Michelle RobertsDigital health editorDangerous allergic reactions are rising in England and now cause some 25,000 NHS hospital stays a year, data shows. Health officials say the rate has more than doubled over 20 years, prompting them to issue advice reminding people how to recognise allergies and respond.For severe food-related allergic reactions, the rise in admissions is even greater. Provisional figures show admissions rose from under 2,000 twenty years ago to more than 5,000 in 2022/23. The data, gathered by the NHS and analysed by the Medicines and Healthcare Products Regulatory Agency, does not include people who visited outpatient or Accident and Emergency departments with allergies and were discharged without requiring a hospital stay.The figures suggest anaphylaxis is on the increase, though some of the rise could be attributed to the growth in population.Anaphylaxis can be fatal and develop suddenly at any age. People who know they are at risk should always carry two adrenaline pens which they, or someone else, can administer in an emergency.In addition, people at risk of an anaphylactic reaction should regularly check the contents of their adrenaline pens have not expired. They should see a pharmacist to get a new one if a pen is close to expiring.How to treat an allergic reactionKnowing what to do could mean the difference between life and death. Signs of a severe allergic reaction, also known as anaphylaxis, include:swelling in the throat or tonguewheezingbreathing difficultiesdizziness tirednessconfusionIf in doubt, use the adrenaline pen – sometimes called an Epipen or an adrenaline auto-injector – without delay. injecting into the outer thigh.Call 999 for help – say it is for anaphylaxis, pronounced “ana-fill-axis”.Lie the person down flat and raise their legs. Use the second adrenaline pen if there is no improvement after five minutes and help has not yet arrived.Laura Squire, MHRA Chief Officer for Healthcare Quality and Access, said: “These figures highlight just how serious the consequences of allergies can be, and the rising numbers of hospitalisations highlights the need to know how to act in an emergency.”Knowing how to use an adrenaline auto-injector and what to do afterwards is crucial when responding in an emergency, whether you’re having the reaction yourself, or helping someone else.”Anaphylaxis is scary for everyone involved, and when it strikes, it’s not easy to remember what the right steps are. That’s why we want to encourage everyone to download our guidance now so they can be confident they’re doing the right thing if they’re ever in that situation.”MHRA guidance on how to use an adrenaline penWhat to do for an allergy emergencyWhy food allergies are on the riseThe habits that help prevent allergiesWhat is an allergy and how might the body react?An allergy is the response of the body’s immune system to normally harmless substances such as pollen, certain foods or dust mites. Whilst in most people these substances pose no problem, in allergic individuals their immune system identifies the substances as a “threat” and produces an inappropriate response. The response can be relatively minor, such as localised itching. However, in more severe cases it can cause anaphylaxis – a condition which can lead to upper respiratory obstruction (airways becoming blocked) causing a person to collapse. In such circumstances, anaphylaxis can be fatal.Allergies are very common. They are thought to affect more than one in four people in the UK at some point in their lives, according to Allergy UK. They are particularly common in children. Some allergies go away as a child gets older, although many are lifelong.The most common causes of dangerous allergic reactions include:certain foods, such as peanuts, tree nuts or shellfishinsect stingscertain drugs and contrast agents used in some x-ray testsMore on this storyMums renew plea for allergy tsar after deathsPublished15 MayParents of Pret death teen launch allergy studyPublished18 May 2022Give babies peanut butter to cut allergy – studyPublished17 MarchAround the BBCThe habits that help prevent allergiesRelated Internet LinksMHRA allergy emergency adviceAllergy UKThe BBC is not responsible for the content of external sites.

She was one of hundreds of people, all of them Ashkenazi Jews, whose good health and cognitive ability at extreme old age were the subject of genetic research.Louise Levy, who along with hundreds of others 95 and older was part of study to understand how their genetic makeup led to their good physical and cognitive health during extremely long lives, died on July 17 in Greenwich, Conn. She was 112.Her daughter, Lynn Neidorf, confirmed the death, at a hospital. She said Mrs. Levy had broken a hip two months ago but, after surgery and rehabilitation that had her moving with a walker, had developed an infection that weakened her.At her death she was one of the world’s six living supercentenarians, people who have lived into a 12th decade, according to the Los Angeles-based Gerontology Research Group.“She was a light of positivity,” Ms. Neidorf, who is in her 70s, said by phone. “She had that quality babies have: People were drawn to her. They wanted to be around her.”Mrs. Levy lived independently in a senior living community in Rye, N.Y, until two years ago, during the pandemic, when she moved into its assisted living facility.When she celebrated her birthday last year, she told The Rye Record, “I’m glad I can still speak and have my sense of humor, but I would caution you not to try and live to be 112!”She had been the oldest known living person in New York State, according to LongeviQuest, which maintains a database of supercentenarians.Mrs. Levy was one of more than 700 people, all 95 or older, recruited since 1998 to participate in a study by the Institute for Aging Research at the Albert Einstein School of Medicine in the Bronx to learn the genetic reasons for their unusually long, healthy lives.“It’s not luck,” Dr. Nir Barzilai, an endocrinologist who directs the institute, said by phone. “They exceeded luck. The biggest answer is genetics.”Using the blood and plasma of the test group, all Ashkenazi Jews — a comparatively homogeneous population whose genetic variations are easier to spot — the institute’s Longevity Genes Project has discovered gene mutations that are believed to be responsible for slowing the impact of aging on people like Mrs. Levy and protecting them against high cholesterol, heart disease, diabetes and Alzheimer’s disease.“The most striking thing about them is they had a contraction of morbidity,” Dr. Barzilai said. “They are sick, as a group, for very little time at the end of their lives.”He added, “Did they do what we know we should do — exercise, diet and sleep and have social connectivity? The answer is mostly no. Sixty percent were smoking. Less than 50 percent did much household activity or biking. Fifty percent were overweight or obese. Less than three percent were vegetarians. So they weren’t special in that sense.”The goal of the research is the development of drugs that would imitate what the centenarians’ genes do to protect their health.Louise Morris Wilk was born on Nov. 1, 1910, in Cleveland. Her father, Louis, was a photographer and a movie theater manager. Her mother, Mollie (Morris) Wilk, was a homemaker. The three later moved to New York City, where Louis illustrated film posters.Louise in 1918, not long before the end of World War I.via Levy FamilyLouise attended but did not graduate from Hunter College. In 1939, she married Seymour Levy, who sold housewares for a company founded by his father. He later took over the company, and Mrs. Levy became his office manager when he moved the business into their house in Larchmont, N.Y.She continued to work into her 90s for the man who acquired the company after her husband died in 1991.“Not full time, you know — two, three days a week for an hour or two until my car conked out,” she told WCBS Radio in 2019.Mrs. Levy did not have heart disease, diabetes or Alzheimer’s disease but was treated for breast cancer and smoked cigarettes for decades, until 1965, when the U.S. Surgeon General put health warnings on cigarette packs.Even as her hearing, eyesight and mobility diminished, she stayed active with stretching classes, playing bridge and knitting sweaters for hospitalized babies. She began losing her short-term memory only in the last six months.Mrs. Levy believed that her low-cholesterol diet, positive attitude and daily glass of red wine contributed to her extended good health. “Everybody says ‘good genes,’” she told the Canadian newspaper The National Post in 2012, “but I don’t think it’s good genes.”She may have been onto something.“There is more than one way to get to 100,” Dr. Barzilai said, “but some of them are genes that are related to cholesterol.”In addition to her daughter, Mrs. Levy is survived by her son, Ralph, who is also in his 70s, four grandchildren and six great-grandchildren.Ms. Neidorf, who believes her own good health may be tied to the same genetic makeup as her mother’s, recalled that the two were nonetheless different types of people.“I was much more fresh and disobedient than she was,” Ms. Neidorf recalled. “She was sugar and spice and everything nice. I held her in great admiration because she never tried to make me be like her. She accepted who I was and believed in me.”

Many doctors said that they were unfamiliar with the condition, known as alpha-gal syndrome, the agency found.As many as 450,000 Americans may be living with alpha-gal syndrome, a meat allergy that has been linked to tick bites, with many of those people going undiagnosed, according to two new studies from the Centers for Disease Control and Prevention.In one of the new studies, both of which were published on Thursday, scientists reviewed the laboratory results of people who had been tested for the telltale antibodies, identifying 110,000 suspected cases since 2010.But that figure is probably a significant underestimate. In the second study, researchers found that 78 percent of health care providers who were surveyed had little or no knowledge of the condition, and many clinicians who had heard of the syndrome were not sure how to diagnose it.“Our 110,000 suspected cases of alpha-gal syndrome represent those that found the health care provider that did properly send off for the antibody test,” said Dr. Johanna Salzer, a disease ecologist and veterinarian at the C.D.C. and an author of both studies.When the researchers factored in this knowledge gap, they estimated that the true toll of the syndrome might be closer to a half-million, although Dr. Salzer acknowledged that the figure was “a crude estimate.”Still, it is clear that the condition is significantly underdiagnosed, said Dr. Maya Jerath, an allergist and immunologist at Washington University in St. Louis, who has treated hundreds of patients with alpha-gal syndrome. “This is a story that every patient of mine tells me, that ‘I had to go to five physicians before they could tell me what it was,’” said Dr. Jerath, who was not involved in the new studies. “It’s nice to have numbers behind it, and it’s definitely a call to action.”Alpha-gal syndrome, which was not formally identified until the 2000s, takes its name from galactose-alpha-1,3-galactose, a sugar present in beef, pork, lamb and the meat of most other mammals. (It is not present in humans or other apes.) Lone star ticks, which scientists believe are the primary culprits of the disease in the United States, can transmit the sugar to people through a bite. Some people’s immune systems may then label this foreign sugar a threat and overreact to its presence the next time they eat meat.The symptoms, which often take hours to appear, are wide-ranging, and may include hives, nausea, diarrhea or anaphylactic shock. Even patients who have the syndrome may not feel sick every time they eat meat. “It’s consistently inconsistent,” Dr. Salzer said. “So this makes it a real challenge for health care providers.”To diagnose the syndrome, clinicians can order a blood test to determine whether a patient has antibodies to alpha-gal. Until August 2021, a single commercial lab did nearly all of this antibody testing in the United States. In one of the new studies, researchers reviewed the results of the antibody tests performed at this lab from 2017 to 2022.In total, more than 90,000 people received positive tests over that time period, and the number of people with positive tests increased annually, from about 13,000 in 2017 to nearly 19,000 in 2021. Roughly 20,000 cases had been identified in an earlier study, yielding a total of 110,000 suspected cases from 2010 to 2022.The rising number of cases identified annually could stem from increasing awareness, an increase in the true prevalence of the syndrome or a combination of both. Lone star ticks are expanding their range, likely as a result of climate change, and other diseases they carry, such as ehrlichiosis, have also become more common in recent years.Alpha-gal syndrome was most common across a large swath of Southern, Mid-Atlantic and Midwestern states, where the lone star tick is known to live, the researchers found.But there were also clusters in northern Minnesota and Wisconsin, which are not known to be homes for the ticks. Although some of the people who tested positive may have acquired the disease elsewhere, the results also highlight how much remains unknown about alpha-gal syndrome. “I don’t think that the lone star tick is the full story,” Dr. Jerath said.In a second study, researchers surveyed 1,500 clinicians, including doctors, nurse practitioners and physician assistants, using an online survey. They found that 42 percent of participants had not heard of alpha-gal syndrome. An additional 35 percent said they were “not too confident” that they could diagnose the illness or manage patients who had it. Of the clinicians who did know about the syndrome, 48 percent said they did not know what test they should order to diagnose it.Dr. Salzer stressed the importance of tick bite prevention, noting that unlike some other tick-borne diseases, alpha-gal syndrome has no treatment or cure. “Alpha-gal syndrome can be a lifelong condition,” Dr. Salzer said. “It definitely needs to be a part of the conversation of why tick prevention is so important for public health.”