The study challenges the concept of Mendelian diseases, or diseases and disorders attributed to a single genetic mutation. The idea is that Mendelian diseases — such as the neurological disease Huntington's and the bleeding disorder hemophilia — are passed down in predictable ways in families, and if a given person carries a disease-causing mutation, they will have it.

These diseases stand in contrast to those caused by multiple genes and environmental factors, which makes their occurence harder to predict in family lines.

"What we suggest is that there is overlap there," Dr. Eric Pierce, an ophthalmologist at Harvard Medical School and the senior author of the new study, told Live Science. In other words, many diseases thought to have simple, Mendelian causes might be a lot more complex than previously thought.

And this doesn't only apply to inherited blindness. Similar results have been found for other genes once thought to be strongly linked to health conditions. A 2023 study on ovarian insufficiency, a condition that causes infertility and early menopause, found that 99.9% of supposedly disease-causing variants were actually present in healthy women. And certain kinds of inherited diabetes also have more complex genetics than previously believed, according to 2022 research.

"We're in an era of discovering a lot more about the complexity of our genomes," said Anna Murray, a geneticist at the University of Exeter who led the ovarian insufficiency research.

Simple or complex?

Pierce and his colleagues focused on inherited retinal disorders (IRDs), a group of diseases that cause significant vision loss, sometimes as early as age 10 but certainly by age 40, said study co-author Dr. Elizabeth Rossin, also a Harvard ophthalmologist. Researchers have teased out the genetic roots of these diseases by doing genetic testing on affected patients and their families.

But that method can lead to a problem called ascertainment bias, Pierce said. True, you'll learn that some genetic variants are associated with the disease. But because you're studying only people with the disease and their relatives, you don't get a clear notion of how many people have the same gene variants and don't go blind.

To widen their view, the researchers used data from two large biobanks that contain genetic sequencing data from people, as well as their medical diagnoses and demographic information. One, the All of Us biobank, is a program run by the National Institutes of Health and included nearly 318,000 individuals with both genetic and electronic health record data at the time of the study. The other, the UK Biobank, is comparatively less diverse but contains data from 500,000 individuals, including about 100,000 with images of their retinas submitted to the database.

The researchers picked the 167 genetic variants thought to have the strongest causal link to IRDs and searched for them in the All of Us database. They then used the health record data to see if the people with the variants had vision loss. To their surprise, depending on which diagnostic codes they used, only 9.4% to 28.1% of people with the variants had any indication of a retinal disorder or vision problems.

"You would expect, given what we know about these diseases, that nearly 100% of the people would have blindness," Rossin told Live Science. "But it was far fewer than that."

To validate their findings, the researchers turned to the UK Biobank, this time using the included retinal imagery to seek out evidence of IRDs themselves. They found that only between 16.1% and 27.9% carriers of the gene variants had indications of possible retinal disease.

People who were older who carried these retinal disease genes weren't any likelier to have gone blind. And there was no other evidence that their results were because they were catching people who might later lose their vision. Instead, Pierce says, it seems that the complexity of these presumed Mendelian diseases has been underestimated.

"The mutation we used to think caused disease 100% of the time doesn't exist in isolation," he said. Instead, people carry tens or hundreds of thousands of other genes, some of which may protect against retinal disease, he added.

New avenues for treatment

In theory, those protective gene variants could lead to ways to treat these retinal disorders.

"It's going to take a lot of data in order to find these types of low-effect variants," Pierce said. "There are likely many of them, each contributing a little bit to the protection against disease."

There are good reasons to study the genes of patients with particular disorders, Murray said. For instance, finding genes associated with a condition — even if they don't always cause it — can help researchers pinpoint the biology underlying the disease. In ovarian insufficiency, these kinds of patient-centered studies have shown that genes associated with DNA repair are important for the disorder. But such studies should still be taken with a grain of salt.

"It is only now that we have the ability to look at the granular detail of the genetic sequence in hundreds of thousands of people," she said. To learn more, these databases need to become more diverse, she added. And at the same time, she added, biomedical researchers need better lab models of diseases in which to test certain gene mutations and their effects.

"There are likely some [diseases] where it really is a one-to-one correspondence," Pierce said. "But my prediction would be [that] the majority of these disorders are going to share this new complexity."

The new findings appeared Jan. 8 in the American Journal of Human Genetics.

The symptoms: The man was on a ski trip in November 2008 when an avalanche knocked him unconscious and left him buried under snow for 15 minutes. His body tissues were starved of oxygen while he was trapped, leading him to develop a condition called hypoxia. His friend rescued him and immediately began CPR upon releasing him from the snow, Berend Feddersen, a neurologist at the University of Munich in Germany, and the lead author of a report on the case, previously told Live Science. He was then taken to a hospital.

The hypoxia left the man with a movement disorder that caused uncontrollable twitching in the muscles of his legs and mouth when he walked and talked, respectively. He didn't experience these muscle jerks in his arms.

What happened next: After a stint in the hospital, the man was moved to a rehabilitation facility. While at this center, he started a sudoku puzzle — a regular pastime of his prior to the injury.

As he solved the sudoku, the muscles in his left arm repeatedly jerked. But these movements immediately ceased when he stopped work on the puzzle.

The diagnosis: The man appeared to be having clonic seizures — repeated jerking movements — in his arm while solving sudoku, so the medical team ran brain scans to better understand what was happening.

An electroencephalogram, which measures activity on the brain's surface, revealed the patient was experiencing a right centroparietal seizure pattern — meaning the seizures stemmed from the central and parietal regions in the right hemisphere of his brain. MRI did not show any evidence of disease or abnormality that might be driving this seizure activity.

The medical team then performed a functional MRI (fMRI) on the patient while he solved a sudoku; this type of scan tracks activity throughout the brain via blood flow. The scan revealed "widespread activation," although activity in the centroparietal cortex was particularly high, the doctors wrote in a report of the case. A closer inspection using a form of MRI called diffusion tensor imaging, which creates maps of the brain's white-matter fibers, showed fewer inhibitory fibers in this brain region.

The loss of those inhibitory fibers — which help keep the activity of brain cells in check — resulted in a three-fold increase in activity of the nerve running down the patient's left arm. The doctors wrote that the hypoxia the man experienced during the avalanche is the "most likely" cause of this damage.

In turn, the over-activation of the right centroparietal cortex resulted in focal epileptic seizures, which are seizures focused in one discrete region of the brain. Specifically, the patient had developed reflex epilepsy, in which seizures are triggered by certain stimuli, like particular lights or music.

In this case, the three-dimensional image the patient imagined while solving sudoku triggered the seizures, Feddersen said. The patient did not experience clonic seizures when reading, writing or calculating. But the doctors could prompt a seizure by giving the man other visual-spatial tasks, such as placing a random string of numbers in order from smallest to largest.

The treatment: The patient was prescribed anti-epileptic medication, which stopped his seizures; he was more than five years seizure-free as of 2015, the report says. He also received physical therapy, which helped ease the twitches he experienced when walking and talking.

He also gave up solving sudoku puzzles.

What makes the case unique: About 3.8% of people will develop epilepsy in their life, with around 4% to 7% of those patients experiencing reflex seizures. Although this was the first known case of a sudoku puzzle triggering seizures, a common type of reflex epilepsy is called "praxis induction," in which visual-motor tasks — like playing chess or cards — set off muscle jerks.

For instance, in 2015, doctors reported the cases of five men with epilepsy in China who had seizures induced by playing the ancient Chinese game of Zipai. These men, ages 19 to 44 years old, stopped having seizures when they avoided playing Zipai. Similarly, in January 2025, doctors in Taiwan reported on 30 patients who had reflex seizures triggered by playing Mah-Jong.

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

This article is for informational purposes only and is not meant to offer medical advice.

The previously recommended daily intake of protein was around 0.8 grams for each kilogram of body weight. That recommendation aimed at meeting the nutritional needs of an average, sedentary adult. Now, the new dietary guidelines suggest people should consume between 1.2 and 1.6 grams of protein per kg of body weight per day.

So, to meet the new recommendations, a person weighing 154 pounds (70 kg) would need to consume around 84 to 112 grams (3 to 4 ounces) of protein per day, as opposed to 56 grams (2 ounces) under the old recommendation.

"It is unclear why the [Dietary Guidelines for Americans] increased the recommendation by 50% to 100%," Alice Lichtenstein, an American Heart Association fellow and nutrition science professor at Tufts University, told Live Science in an email.

Notably, scientists previously estimated that the average U.S. adult's protein consumption generally exceeded the old guideline. A 2013 study estimated it at 1.2 to 1.4 grams per kg of body weight per day, while a 2021 dietary data brief noted men and women were consuming 97 grams and 69 grams on a given day, respectively.

Nonetheless, the shift in guidance raises some questions: Are there benefits to upping your protein intake? And is there an upper limit you shouldn't cross?

Experts told Live Science that there's no single, agreed-upon maximum amount of protein you can eat in a day. That said, if you're not particularly active, pushing your protein intake beyond what the old recommendation suggested is unlikely to be very beneficial, they said. Additionally, it would be harmful to boost your protein intake at the expense of eating other macronutrients, like fat and carbs.

Why is protein important?

Proteins are the body's building blocks, forming everything from muscles and hormones to digestive enzymes and the hemoglobin that carries oxygen in the blood.

Protein-rich foods include meat, fish and eggs, as well as tofu, beans and nuts. The proteins in these foods get broken down by our bodies into their component parts — amino acids — which cells can use to produce the proteins we need. While the body can produce some amino acids on its own, there are nine, called essential amino acids, that we can get only through our diet.

A given person's protein requirements vary depending on a number of factors, with one of the more crucial ones being how much they exercise. So generally, increases in protein intake should be accompanied by increases in activity levels, Lichtenstein told Live Science.

"Most of the studies that I am aware of have not demonstrated that increasing protein intake above current recommendations increases lean muscle mass," she said. "If it does, it needs to be coupled with certain types of physical activity, not a strong point for most people." Those types of activity might include strength and endurance training, for instance.

Historically, it's been recommended that people who regularly exercise get about 1.1 to 1.5 grams per kg per day, while people training for athletic events might eat up to 1.7 grams per kg per day.

Notably, active people still need to take in adequate energy from carbs and fats. If they don't, the body may resort to using amino acids as fuel, effectively increasing the amount of protein they need to make up for the loss of protein building blocks in the body.

Another factor that influences our protein requirements is age. As you get older, the body's ability to build new muscle proteins gets disrupted, leading to muscle loss and frailty. Studies suggest that eating more protein — about 1 to 1.2 grams per kg of body weight a day — could help mitigate these effects seen in middle-aged and older people.

Effects of high-protein diets

Research has tied high-protein diets, typically considered around 1.2 to 2 grams per kg of body weight per day, to both positive and negative health outcomes.

In one review of studies on the topic, researchers compared high- and low-protein diets and found that the former was tied to greater weight loss and thus lower BMI. However, another review tied high-protein consumption to a higher risk of bone-density loss and kidney stones.

An overconsumption of protein may increase levels of the amino acid leucine, which can then interfere with how immune cells clear plaque from blood vessels, one study of humans and lab mice found. This could boost the risk of heart attack or stroke. Based on this finding, the study authors suggested that getting more than 22% of your daily calories from protein — around 1.6 grams per kg of body weight — could do more harm than good.

Leucine is found in a variety of animal- and plant-based protein sources. Additionally, protein sources that are high in purine — such as red meat, organs like kidney, and certain types of seafood — can lead to gout and kidney stones if consumed in excess.

"It's important to note that there is no single, official upper limit," Bridget Cassady, a registered dietitian nutritionist (RDN) at Abbott, told Live Science in an email. "An amount that is considered 'excessive' will be different based on your needs varying with age, body weight, activity level, health status."

Broadly speaking, though, Cassady said that healthy individuals can safely consume "moderately high" amounts of protein — around 2 grams per kg per day — as long as it's part of a balanced diet. Protein consumption should not come at the expense of other nutrients; if it starts crowding out fiber-rich plants, healthy fats, or whole-food carbohydrates, that's when protein intake could start becoming a concern, she said.

At the extreme, a super high-protein diet could put strain on the kidneys, which can filter only so much urea — a protein waste product — from the blood at a given time. That's why people with existing kidney problems are advised to avoid high-protein diets, according to Cleveland Clinic. If your urine turns bubbly or foamy, that can mean there's a high level of protein in the urine, which could signal kidney damage.

This article is for informational purposes only and is not meant to offer medical or dietary advice.

According to the study, published in December in the journal Science Advances, this viral DNA switches on genes that give cells in early-stage mouse embryos the potential to become almost any cell type in the body. The viral DNA — known as MERVL — itself gets activated by a protein called the "Dux transcription factor," which binds to the sequence and essentially kick-starts the embryo's development.

Although it's important in the womb, if Dux stays activated too long, it kills cells. The human version of Dux, called DUX4, causes a progressive muscle-wasting disorder when quirks in its genetic code cause it to be active for too long in muscle cells. That inherited disease, called facioscapulohumeral muscular dystrophy (FSHD), currently has no cure.

The new study not only unravels the roles of MERVL and Dux in the womb but also teases apart these harmful effects that can appear later in life. It's an "important piece of work," said Sherif Khodeer, a postdoctoral research fellow who focuses on stem cell and developmental biology at the university KU Leuven but was not involved in the study.

A powerful gene-editing tool

Researchers at the Medical Research Council Laboratory of Medical Sciences in England used a gene-editing tool called CRISPR activation (CRISPRa) to untangle the close relationship between Dux and MERVL. Unlike traditional CRISPR, which cuts DNA to change its code, CRISPRa boosts the activity of specific genes without changing the underlying DNA sequence.

The team used CRISPRa to switch on either Dux or MERVL in mouse embryonic stem cells. This enabled the researchers to examine how each factor influenced early embryonic development.

When the researchers switched on only MERVL, the stem cells showed "totipotency," or the ability to become any cell type — an important feature of the very earliest embryos. But the cells were missing key traits, the researchers found. This suggests that, while MERVL plays an important role in early mouse embryo development, Dux is also required.

Turning on Dux alone, on the other hand, produced cells that looked much more like natural early embryonic cells. So, the researchers think Dux activates the genes necessary for the embryo's development, independently of MERVL.

Because Dux and MERVL are so closely linked during the earliest stages of embryonic development, scientists previously suspected that MERVL might also contribute to Dux's harmful effects later in life. But the new study suggests this isn't the case.

The researchers tested how Dux causes cell damage by looking at its effects in stem cells with and without a gene called NOXA, which is known to be involved in cell death triggered by various stressors. They found that Dux turns on this NOXA gene, which produces a protein that triggers cell death. When the team removed NOXA, Dux caused much less harm. That showed that NOXA is responsible for the toxicity, not MERVL.

A potential therapeutic target

NOXA was already known to be elevated in FSHD, the human muscle-wasting disease. It's possible that developing a drug to inhibit NOXA could prevent cell death in the condition, thereby helping to improve the survival of muscle cells, the study authors think.

"Facioscapulohumeral muscular dystrophy is a complex disease," senior study author Michelle Percharde, head of the chromatin and development group at the Medical Research Council Laboratory of Medical Sciences , said in a statement.

"Even though all cells of a patient have the genetic changes that cause it, only a subset of cells activate DUX4," she explained. "Understanding what triggers DUX4 activation just in muscle cells, as well as how this compares to activation in early development, are key questions we hope to explore in future research."

It would be "valuable to compare" how mouse Dux and human DUX4 function, Khodeer said, adding that future studies should also explore precisely how MERVL controls nearby genes and when and how MERVL is switched off during mouse embryo development.

Crucially, Khodeer pointed out that MERVL is not present in the human genome. But scientists suspect that certain parts of the human genome could be equivalent to MERVL. As in mice, these stretches of DNA are leftover from ancient viral infections.

Khodeer said the new results raise several questions. For example, do early human embryos develop via the same mechanisms seen in mice? And which bits of ancient viral DNA in humans might play roles similar to MERVL at this early stage of development? "Answering these questions could clarify species-specific differences in early developmental regulation," he told Live Science in an email.

The compound is one of more than 600 produced in a study published in December in the journal Nature Communications. The researchers used a robot to synthesize the compounds, combining metal and organic molecule building blocks to generate a huge chemical library in just a week.

This streamlined approach, which also produced five other potential antibiotics, could dramatically accelerate both drug discovery and parallel areas of chemical research, study lead author Angelo Frei, an inorganic chemist at the University of York in the U.K., told Live Science.

As the prevalence of drug-resistant bacterial infections increases, there's a need for new, effective antibiotics that can kill germs that no longer respond to existing drugs. So far, the search has focused on organic — meaning carbon-based — molecules, leaving metal complexes almost completely unexplored.

These metal-containing compounds significantly differ in shape compared to their flatter organic alternatives; and their three-dimensional shapes give rise to distinct chemical and biological properties. This attribute, combined with their ease of synthesis, makes these molecules an exciting potential source of future antibiotics, the study authors say.

But as there's little existing data on the antimicrobial properties of metal complexes, Frei's team needed an efficient method to rapidly make and test as many compounds as possible. Their solution was to merge straightforward and robust chemistry with state-of-the-art automation.

The team began by creating a panel of 192 different ligands, the organic molecules that bind to the metal center and determine the overall complex's final properties. They did so by using a liquid-handling robot to perform "click chemistry." This robust reaction fuses two types of starting materials — called azides and alkynes — to construct nitrogen-containing rings known as triazoles. These nitrogen rings bond strongly to metals.

In the next step of the process, the robot combined each of the 192 ligands with five different metals to generate a total of 672 metal complexes.

"We opted to use liquid-handling robots to do the chemistry because it's just combining different reagents in the right ratios," Frei said. After making the azides, "then we added the alkynes and the catalyst to do the click reaction, and then we used those ligands on different metals. It can all be done in one pot with robots," he said.

Each product was analyzed to confirm the expected complex had formed and then immediately tested for antibacterial activity and potential toxicity to human cells. In this way, the team quickly identified the safest and most potent compounds, without wasting time on lengthy purification steps.

"It allows us to go from hundreds of compounds to maybe dozens of compounds that are interesting," Frei explained.

Complexes containing iridium and rhenium exhibited particularly high levels of antibacterial activity. Overall, 59 of the iridium compounds and 61 of the rhenium compounds inhibited the growth of Staphylococcus aureus, an important cause of hospital-associated infections that can range from mild to deadly. For both metals, the toxicity toward human cells was variable. From these initial screening results, the team selected the six compounds that most effectively balanced antibacterial activity with low toxicity for further study.

"When we have identified those really promising ones, we can then go back to the bench and remake them, isolate them, and characterize them, to confirm what we saw previously with the [unpurified] mixture," Frei said.

In this second round of tests, one of the iridium complexes was the clear standout winner. The compound was about 50 to 100 times more active against bacteria than it was toxic to human cells. This large difference is vital to ensure that the complex is simultaneously effective in treating an infection but safe to use on human tissues.

Mark Blaskovich, a molecular bioscientist at the University of Queensland in Australia who wasn't involved in the work, was impressed by the efficiency of Frei's approach and the diversity of the compounds created by the automated synthesis. However, substantial work remains to transform their antibiotic candidates into viable clinical drugs, he said.

The "most important next steps" are to show that the most promising compounds have drug-like properties, meaning they are chemically stable and don't have a lot of off-target effects on the body, he told Live Science in an email. In addition, research needs to demonstrate how these compounds work in a living body, "ideally in the 'gold standard' mouse models of infection," he said.

In order to get these potential antibiotics approved for clinical use, eventually, studies in lab animals would be followed by clinical trials that could definitively show the drugs are both safe and effective for people.

For the time being, though, Frei intends to build upon this initial library of compounds, leveraging artificial intelligence to help target specific properties.

"We can use this data to make smarter decisions," he said. "So we can do machine learning and train models to correlate which structural features lead to good activity and low toxicity and then have the model predict for us which compounds we should make next."

Save up to 69% on the New Balance Women's Fresh Foam X 1080 V14 running shoe at Amazon. Men's collection has also been discounted, with up to 39% off on selected sizes and colors.

Kate Carter, our long-standing running expert, gave them a solid 4.5-star rating in her New Balance 1080 V14 running shoes review. We also included them in our guide to the best running shoes for supination as the best option for everyday runs. Trust us when we say you will be hard-pressed to find a better offer in this price range.

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That said, the New Balance Fresh Foam X 1080 V14 may not be for everyone. These running shoes are extremely well-cushioned, meaning they were designed to prioritise comfort over responsiveness. As Kate pointed out, they may not have enough bounce and power transfer to see you through speedwork and racing competitions. When it comes to anything else, however, the New Balance Fresh Foam X 1080 V14 is a fabulous pick — and now, you can get this excellent daily trainer at its lowest-ever price.

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Check out our other guides to the best telescopes, binoculars, star projectors, cameras, fitness trackers, running shoes, rowing machines and more.

The human stomach evolved to create and withstand extremely corrosive conditions. "Its role is to break down the components of physical food into smaller pieces, with the idea being that, by the time the preparation reaches the small bowel, it's in small enough components that we can absorb it," Dr. Sally Bell, a gastroenterologist at Monash University in Australia, told Live Science.

The stomach contains specialist cells with the sole job of producing destructive chemicals to aid digestion. The main component of this gastric juice is hydrochloric acid, a potent chemical that's strong enough to dissolve metal. There are also smaller amounts of the digestive enzymes pepsin and lipase, which break down proteins and fats, respectively.

This harsh environment also has a secondary defensive role, said Dr. Benjamin Levy III, a gastroenterologist at University of Chicago Medicine. "Gastric juices also help the body kill bacterial pathogens so that we don't get sick and strategically impede the development of bacterial overgrowth," Levy told Live Science. This is especially important for destroying potential foodborne pathogens, he said.

Without protection, this combination of strong acid and protein-digesting enzymes would quickly begin to eat into the stomach wall, first forming painful ulcers before ultimately burning a hole. However, cells that line the inside of the stomach — a layer known as the epithelium — have developed a special secretion to protect the organ from attack.

"These cells are unique in that they produce this very thick, sticky layer of mucus which is alkaline and buffers the acid," Bell explained. "It's proteinaceous material that is rich in bicarbonate, essentially, so it protects the stomach lining from its own acid and its own enzymes."

In a healthy digestive system, this mucous barrier covers the walls of the stomach and is continually renewed by the epithelial cells to provide constant protection. However, problems can arise when the layer becomes damaged. Even small breaks can allow acid and pepsin to penetrate under the mucus, which can lead to chronic inflammation and ulcers, Levy said.

One cause of such damage is the overuse of nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen and naproxen. "NSAIDs damage the stomach lining by inhibiting cyclooxygenase (COX-1)," an enzyme that's responsible for the production of hormone-like compounds called prostaglandins, Levy said.

"This reduces prostaglandin production, which causes a decrease in both mucus and bicarbonate secretion," Levy explained.

Certain lifestyle choices, such as smoking or drinking, can also increase the risk of this type of digestive disorder by acting as direct toxins to the lining, Bell noted. In addition, acidic or spicy foods can overwhelm the stomach's natural protection to cause irritation or trigger reflux into the esophagus.

Despite the extremely acidic conditions, it's possible for bacterial infections to sometimes cause problems in the stomach. For example, "Helicobacter pylori have the ability to secrete proteases and lipases that degrade the gastric mucus and harm the phospholipid layer of the epithelial surface," Levy said. Once detected, H. pylori can be treated with a combination of antibiotics.

The bottom line? Stomach acid plays an integral role in digestion and defense against disease, so the organ has developed a remarkable capacity to protect itself and renew its lining.

This article is for informational purposes only and is not meant to offer medical advice.

The new food chart emphasizes meats, dairy and what it calls "healthy fats," as well as fruits and vegetables. It accompanies new nutrition guidance that upholds some well-established diet recommendations while breaking with others.

The Departments of Agriculture and Health and Human Services released the new dietary guidelines on Wednesday (Jan. 7), and in doing so, they retired MyPlate, a visual guide to healthy eating that replaced the food pyramid in 2011. The so-called New Pyramid is an inverted triangle with protein, dairy and "healthy fats" at the top, alongside vegetables and fruits. At the bottom of the flipped pyramid are whole grains.

The brief guidelines accompanying the New Pyramid place a heavy emphasis on avoiding highly processed foods, refined carbohydrates and added sugars, noting that the unrefined sugars found in foods like fruit and milk are not considered "added."

The guidelines also specify that healthy fats include those found in meats, poultry, eggs, omega-3–rich seafood, nuts, seeds, full-fat dairy, olives and avocados. Olive oil (mostly unsaturated fat) and butter and beef tallow (mostly saturated fat) are listed as good options for cooking oils. That said, the guidelines don't change the long-standing guidance about limiting one's consumption of saturated fats, stating that they should not exceed 10% of a person's total daily calories.

The guidelines significantly increase recommended protein intake, NBC reported. Established guidelines say that 0.8 grams of protein per 2.2 pounds (1 kilogram) of body weight would meet the daily nutrition requirements of the average, sedentary adult. Higher amounts are recommended for physically active adults (about 1.1 to 1.5 grams per kg) and older adults (about 1 to 1.2 grams per kg).

The new guidelines recommend a baseline daily protein intake of 1.2 to 1.6 grams per kilogram of body weight. So for a 150-pound (68 kg) person, that's a jump from 54.4 grams of protein a day to about 81.6 to 108.8 grams.

Health Secretary Robert F. Kennedy Jr. had delayed releasing new dietary guidelines for months after rejecting the work of a 20-person scientific advisory committee assembled under President Joe Biden, STAT reported. The committee was poised to recommend plant-forward diets, rather than meat-centric ones, and had concluded that the existing research on ultraprocessed foods was inadequate to develop clear recommendations.

(The definition of "ultraprocessed" can be difficult to pin down, and while many experts agree ultraprocessed foods are unhealthy to eat in excess, it's hard to know if every food under the ultraprocessed umbrella carries the same health risks.)

The new guidelines, meanwhile, put a notable emphasis on meat and dairy and say to avoid highly processed foods, without clearly defining what "highly processed" means. They do say to avoid packaged, prepared and ready-to-eat meals; foods that are salty or sweet; sugar-sweetened beverages; and foods containing artificial flavors, or preservatives, or low-calorie, non-nutritive sweeteners.

Some experts worry that the guidelines' emphasis on meat and dairy — including the notable inclusion of steak, ground beef and a carton of full-fat milk on the illustration of the inverted pyramid — may promote high intakes of red meat and dairy products. This "will not lead to optimally healthy diets or a healthy planet," Dr. Walter Willett, a professor of epidemiology and nutrition at Harvard T.H. Chan School of Public Health, told CNN in an email.

"These guidelines recommend heavily meat-based diets — protein is a euphemism for meat," Marion Nestle, a nutritionist and professor emeritus at New York University, told STAT via email.

MyPlate previously sorted foods into five categories — fruits, vegetables, grains, protein, and dairy and fortified soy alternatives — and provided general recommendations for how much food a person should eat from each category based on their age and sex. As a rule of thumb, fruit and vegetables made up half the plate, and proteins and grains comprised the other half, with a small amount of dairy featured on the side. Healthy oils were defined as vegetable oils and those found in seafood and nuts.

MyPlate also emphasized that additional factors beyond age and sex — such as height, weight, physical activity levels, and whether you are pregnant or breastfeeding — may affect daily nutrition needs. About 150 pages of guidelines detailed those nuances, and also set specific intake limits on added sugars, saturated fats, sodium and alcohol.

The new guidelines also acknowledge that a person's nutrition needs may vary depending on various factors, and they provide some brief guidance for specific populations, such as infants, pregnant and lactating women, and older adults.

They don't note a specific limit for daily alcohol intake, instead saying that people should generally "consume less" for better overall health. They also specified groups, such as pregnant women, who should avoid it altogether.

They added that those with a "family history of alcoholism [should be] be mindful of alcohol consumption and associated addictive behaviors." (While genetics do play a role in who is vulnerable to alcohol use disorder, genes are not the only factor at play, and people without a family history can also develop the addiction.)

These national dietary guidelines influence what's included in school lunches and military meals, as well as federal food assistance programs such as the Supplemental Nutrition Assistance Program (SNAP), NBC reported. A White House spokesperson said the new guidance will be phased into schools and federal food programs over the next two years.

This article is for informational purposes only and is not meant to offer medical or dietary advice.

The trace DNA, embedded in a red chalk sketch called the "Holy Child" that some claim was made by da Vinci, shows similarities with genetic material recovered from a letter penned in the 1400s by Frosino di ser Giovanni da Vinci, a cousin of Leonardo da Vinci's grandfather, Antonio da Vinci.

Specifically, the drawing and the letter contain Y chromosome sequences that match those of a haplogroup, or genetic lineage, with a common ancestor in Tuscany, where Leonardo da Vinci was born. The researchers published their findings Tuesday (Jan. 6) to the preprint database bioRxiv, so they have not yet been peer reviewed.

Because Y chromosome sequences are passed down almost unchanged from father to son, the recovery of these sequences is "a great starting point" for researchers who want to piece together Leonardo da Vinci's DNA, Charlie Lee, a geneticist who leads the Jackson Laboratory for Genomic Medicine in Connecticut who was not involved in the study, told Science.

However, some experts don't think Leonardo da Vinci drew "Holy Child" himself, believing instead that one of his students made the sketch.

As a result, "it's a flip of a coin" whether the DNA from the drawing is da Vinci's, said Lee. The genetic material could belong to a student or to any number of curators with Tuscan roots who handled the drawing over the years, Science reported.

Researchers want to reconstruct da Vinci's DNA to help authenticate some of his art. Some experts also suggest the Italian polymath's genetic material could reveal biological reasons for his exceptional artistic and other abilities, such as better-than-normal vision.

However, there are many hurdles in the way. For one, da Vinci's tomb in France was partially destroyed during the French Revolution, and his remains lost, or at least mixed with others, during a move to a new supposed burial site at the Chapel of Saint-Hubert in Ambroise.

Yet although this grave may contain bones rich in the Renaissance polymath’s DNA, researchers are not granted access to sequence genetic material from the tomb until a reliable comparison sample is found elsewhere.

This has left scientists with few options but to try to extract DNA from da Vinci's artworks. This poses challenges as some pieces are off limits and others — such as "Study of the Front Legs of a Horse" — have no traces of human DNA. "Holy Child" is the only drawing attributed to Leonardo da Vinci that has yielded human DNA to date; however, its authorship is debated.

Another problem is that da Vinci's mother, Caterina di Meo Lippi, is buried in an unknown location. Caterina was a teenage servant when she gave birth to Leonardo. If found, her remains could provide a match with the "Holy Child" drawing for mitochondrial DNA, a type of DNA that is passed on from mother to child and typically found in bigger quantities on objects than DNA from chromosomes is.

Scientists have also been denied access to da Vinci's father's tomb in Florence, where they may have been able to find Y chromosome DNA to match with "Holy Child." And da Vinci himself doesn't have any known direct descendants, because he never married or had children.

One remaining option is to find other male da Vinci relatives to compare the Y chromosome sequences from "Holy Child" with. Researchers are currently analyzing three bones recovered from a family vault in Italy where Leonardo's grandfather Antonio da Vinci is buried, and are also sampling DNA from known living descendants. The teams are also sequencing DNA from a lock of hair that was excavated in 1863 in Ambroise and that may have come from Leonardo da Vinci's beard, Science reported.

Finally, researchers are searching for letters and other documents written by male relatives that may have preserved their author's DNA. The letter from Frosino di ser Giovanni da Vinci is one such artifact. For the new study, scientists compared DNA from the letter with around 90,000 known markers that separate Y chromosome sequences into lineages called haplogroups. The Y chromosome DNA in the letter and the "Holy Child" sketch belonged to the haplogroup E1b1b, which Leonardo da Vinci and his extended family may have belonged to.

Scientists extracted DNA from the drawing by gently swabbing it. This method could help authenticate all kinds of artworks whose origins are uncertain, experts told Science.

Overall, the preprint "is a great paper" that uses "cutting-edge stuff" to draw its conclusions, S. Blair Hedges, a professor and evolutionary biologist at Temple University in Pennsylvania who was not involved in the study, told Science.

The study authors are now working on the various leads available to them. Aside from the lock of hair — if it really is Leonardo da Vinci's — and direct evidence from the polymath's tomb, the most likely source of DNA is from manuscripts and drawings that we know da Vinci penned himself, the researchers said.

The scientists hope their paper will help convince officials and archivists to let them swab more of Leonardo da Vinci's works. For example, a 72-page notebook of observations known as the "Codex Leicester" has a fingerprint that is almost certainly da Vinci's, making it a good candidate, Domenico Laurenza, an art historian at the University of Cagliari who was not involved in the study, told Science.

The research, conducted with mouse cells, live mice, and human tissues, reveals a previously unsung role of mitochondria, the powerhouses of cells. It shows that support cells within the nervous system can ship mitochondria to the nerves that respond to pressure, temperature and pain. But problems with that shipping process can deplete the nerves' energy reserves, causing them to malfunction.

Whereas nerves would normally send a signal to the brain in response to some stimulus, dysfunctional nerves "fire sometimes spontaneously, even without stimulation," said senior study author Ru-Rong Ji, director of the Duke University School of Medicine's Center for Translational Pain Medicine and a professor of anesthesiology and neurobiology.

"That will drive chronic pain and also will lead to neurodegeneration," Ji told Live Science, "because if you fire like crazy, eventually, that neuron probably will degenerate."

The new study, published Wednesday (Jan. 7) in the journal Nature, points to potential new ways of heading off that neuronal breakdown — and one strategy could involve transferring mitochondria directly into nerves.

Fresh mitochondria reduce pain

The research zoomed in on satellite glial cells, unique cells that physically wrap themselves around the "roots" of nerve cells located near the spinal cord. The bodies of these nerve cells cluster together near the spine, and from each cluster, bundles of long fibers extend to different parts of the body, from head to toe. The longest of these fiber bundles belong to the sciatic nerve, which measures just over 3 feet (1 meter) long.

The sheer length of the fibers poses a "real challenge," because for a nerve to function properly, mitochondria made in the nerve's root must travel down to the end of each fiber, and that in itself requires energy to do, Ji said. That raises a question of how nerves maintain this power-hungry supply chain.

Scientists once thought that cells had to make all of their own mitochondria, but in recent years, they have uncovered evidence that cells swap mitochondria. This can occur between cells of the same type or between cells of different types, such as between a stem cell and an immune cell, for example. To facilitate the swap, cells construct tiny structures called tunneling nanotubes for the mitochondria to travel through, like spitballs sliding from one end of a straw to another.

Ji and his team wondered whether satellite glial cells might be able to send mitochondria to the nerve cells they encircle — and it turns out that they can.

"We demonstrate that these cells actually extend these tunneling nanotubes to deliver in the mitochondria. This [finding] is unique in this study," Ji said.

In a series of experiments with mouse cells and human tissues, the researchers took snapshots of the tiny tubes that formed between glia and nerve cells, noting distinct "bulges" that appeared in the tubes as materials traveled through them. By tacking a fluorescent tag onto mitochondria, they were able to track instances in which powerhouses from glial cells made their way into the nerves.

The nanotubes were transient structures that broke down soon after a given transfer was complete. Experiments showed that a protein called MYO10 was critical to the tubes' construction, helping to extend them out from the glia. But additionally, the mitochondria could sometimes be transferred without the tubes, either inside tiny bubbles released by glia or through special channels that formed between the membranes of the donor and recipient cells.

In healthy lab mice, the researchers found that disrupting these different modes of mitochondria shipment made the mice more sensitive to pain. That's because it spurred damage in the nerves and caused them to fire abnormally.

They also looked at mice with various types of nerve damage, such as from exposure to chemotherapy drugs or from diabetes. These nerve-damaging conditions also disrupted the mitochondrial exchange from glia to some degree, and this contributed to nerve pain in the lab mice. Transferring healthy glia into the mice alleviated the pain, though, by providing them with a fresh source of healthy mitochondria.

A new view on glia

Notably, nerve damage from diabetes and chemotherapy tends to hit the smallest nerve fibers the hardest, whereas medium and large fibers show more resilience. In the team's experiments, they found that the larger nerve fibers appeared to receive a higher volume of mitochondria from glia, while small fibers got fewer by comparison. In short, it seems that glia have a "preference" toward lending their mitochondria to larger fibers, the study authors wrote.

"That is still a puzzle. We don't know why that's the case," Ji said. But nonetheless, it might begin to explain why small fibers are more vulnerable to damage in these conditions, triggering symptoms of numbness, painful tingling or burning in the feet and hands.

More studies are needed to fully understand how mitochondria are shuttled from glia to nerve cells in health and disease. This fundamental research could pave the way to future treatments for nerve pain, the team thinks. In theory, treatments could be aimed at boosting the activity of satellite glial cells, so they produce and transfer more mitochondria.

Or alternatively, mitochondria could be harvested from cells grown in the lab, purified, and then injected straight into nerves as a treatment, he added.

Historically, glia were solely thought of as the glue of the nervous system, providing structural support to neurons by binding them together. But scientists have since uncovered that glia are involved in processes once thought to be handled only by neurons, like memory. And the new study suggests glia may actually be physically plugged into neuronal networks, Ji said.

"If they can transport mitochondria, such a very large organelle, in that tube, then you can transport many other things, right?" he suggested. "That means the neurons and the glial cells, they are much more connected than we thought."

The symptoms: The man visited a urology clinic in a hospital and described discomfort in his bladder. He had no issues with urination and no history of surgery or disease in that region of his body. Nor was he experiencing the typical symptoms of a urinary tract infection, such as feeling a constant need to urinate or having a burning sensation during urination.

What happened next: When doctors conducted a physical examination of the man's abdomen, they detected a large, smooth and solid mass above his pubis — the front of the pelvis where two pubic bones are connected by cartilage.

The dense mass wasn't attached to the pelvic area or abdominal wall, and an ultrasound scan revealed that it was an egg-shaped object about 4.3 inches (11 centimeters) in diameter, according to a report of the man's case.

The diagnosis: Physicians at the hospital identified the mass as an unusually large bladder stone. Also known as calculi, these objects grow when minerals in urine accumulate into crystals; about 85% of their makeup is calcium. They can form in the bladder when it doesn't empty fully, which causes the minerals in urine to concentrate and crystalize.

Bladder stones typically form directly in the bladder, but sometimes, they can originate from small kidney stones that migrate from the kidneys into the bladder or into the muscular tube between them, called the ureter.

The tiniest bladder stones are invisible to the naked eye, but they can vary greatly in size. Small stones typically go undetected and are passed during normal urination. However, larger stones can obstruct the flow of urine and irritate the walls of the urinary tract, and they may cause pain, interrupted urination or internal bleeding.

The treatment: After checking to make sure the egg-like stone was not obstructing or constricting any part of the patient's urinary tract, doctors removed the stone surgically, in a procedure called a cystolithotomy. The mass was so large that they needed to extend the incision to the back of the bladder.

The extracted stone weighed 1.8 pounds (826 grams) and measured about 5 inches (13 cm) long, 4 inches (10 cm) wide and 3 inches (8 cm) tall.

Surgeons installed a catheter to assist the man with urination as he healed, and they removed it seven days after the surgery.

What makes the case unique: Stones in the urinary tract are relatively common, but bladder stones make up only about 5% of cases, with kidney stones being much more common. Giant stones that require surgical removal, such as the one affecting the patient, "are very rare," according to the case report.

Remarkably, this sizable stone is dwarfed by the current record-holder for bladder stones: a mass weighing 4.2 pounds (1.9 kilograms) and measuring 7 inches (17.9 cm) long. Doctors in Brazil surgically removed the stone from a male patient in 2003.

Still, the large size of the bladder stone extracted from the man Iran was highly unusual, the surgeons wrote. "Regarding the characteristics of the stone in our case, our report was the first one in Iran and in the world," they said.

This article is for informational purposes only and is not meant to offer medical advice.

For an exercise novice, however, this endless sea of workout gear and gadgets can be downright overwhelming. But if that is you, do not worry! You do not need a gym's worth of exercise equipment, a high-end Garmin watch or a professional athlete's wardrobe to begin. Starting simple is often the most effective strategy for a long-term lifestyle change — not to mention that it is much easier on the wallet.

With that in mind, we rounded up a list of essential, science-backed purchases for a beginner, prioritizing ease-of-use, safety and versatility. Plus, we sprinkled in some fitness deals to help your post-Christmas budget go that little bit further.

Here’s what to buy (and what to skip) to launch your fitness journey in strategic fashion — and save yourself some money in the process.

The essentials: Gear that gets you out the door

Before investing in a premium running watch or one of the best rowing machines, focus on the basics. Buying the right footwear and workout clothing is an essential first step on your fitness journey. This is not about fashion; it is about comfort and safety.

Footwear: Your most important investment

This is your non-negotiable purchase. Appropriate footwear helps you maintain good foot health, reduces the risk of injuries and boosts your overall well-being, according to a 2024 review published in the journal Applied Sciences. Choose shoes that are stable, comfortable to wear and suitable for your intended activities.

That said, do not get bogged down in premium brands and ultra-specialized shoes. Start with a quality pair of all-purpose trainers or cross-trainers. The best beginner-friendly options have a good balance of cushioning and stability for a mix of gym workouts, walking, jogging and low- to moderate-intensity aerobics. Good looks are just the cherry on top.

Workout clothing: It is all about comfort

Workout clothing should help you withstand the demands of intense exercise, not actively impede your attempts to get fit. Look for synthetic, moisture-wicking fabrics like polyester or spandex — they help regulate body temperature and prevent sweat from lingering on your skin, while cotton, for example, holds sweat and can cause chafing.

Then, focus on freedom of movement. A well-designed piece of activewear will allow for freedom of movement and not slip off or irritate your skin during intense workouts. Start with a few core pieces to build a rotation: a few tops and bottoms, several pairs of sports socks and, for women, a couple of good-quality sports bras.

Again, there is no need to invest in premium brands and highly specialized activewear; affordable lines from major retailers work perfectly fine. Comfort here is key — if you feel good, you are more likely to get moving.

The best retailers for finding deals on beginner-friendly workout clothing:

• Puma: Now up to 60% off on Puma Essentials and Puma Elevated Essentials
• Adidas: End of Year Sale with up to 60% off on shoes and activewear
• Reebok: End-of-Season Sale with up to 50% off selected styles
• CRZ Yoga: A budget alternative to Lululemon, now with up to 81% off on yoga pants, leggings, tops and jumpsuits
• Target's All in Motion: A highly-rated line of affordable workout clothing, running shoes and exercise equipment
• Amazon's Aurola: Soft and versatile workout tops and bottoms for under $35

The home-gym starter pack: Simple, space-savvy exercise equipment

While you may be tempted to splash out on a premium treadmill or super-smart exercise bike, hold off on the big purchases for now. You can build remarkable strength, endurance and mobility with basic, space-savvy equipment too, and at a much lower cost. A yoga mat, adjustable dumbbells and resistance bands, for example, are very beginner-friendly, offering maximum versatility with a minimal footprint.

If you are not entirely sure how to use them, look up beginner-friendly home exercise video tutorials or join an online fitness class. January fitness sales are not just about physical gear — many fitness apps and services are discounted, too, or offer free taster sessions. There is also plenty of good-quality content that is entirely free of charge.

Fitness trackers: A source of useful data and exercise advice

A well-chosen fitness tracker can provide a lot of valuable feedback and positive reinforcement in the early stages of your fitness journey. Counting your daily steps, tracking an active workout and reviewing your past activities can help you make more sense of your workouts and general progress.

Training by "feel" is hard for beginners, and continuous heart rate measurements provide objective data on your efforts. It helps you understand zones: are you in a moderate, fat-burning zone or pushing into high intensity? This ensures your easy days are genuinely promoting recovery and your hard days are truly effective.

Moreover, the goal-setting and "closing your rings" features (a visual representation of your progress towards your daily exercise goals) leverage gamification, and this in itself can be a powerful motivator. Not to mention, many fitness trackers come in handy outside of the gym or running track, too.

However, do not get swayed by the trends here. A basic Fitbit, Garmin or Apple Watch SE will track steps, heart rate, sleep, and active minutes just as well as the more advanced and expensive models. They also tend to be more beginner-friendly in terms of their user interfaces and the language they use to describe your fitness stats.

What NOT to buy (right away)

The allure of a shiny new machine is strong, but impulsive buys often become expensive clothes racks. Here are some tips on how to avoid costly mistakes as an exercise beginner.

Hold off on major equipment. Do not start by buying an expensive treadmill, elliptical, or full home-gym system. Use your foundational gear or a gym trial for one month at least. If you have consistently stuck with your routine, then research what machine would best suit the activities you have genuinely enjoyed.

Avoid over-specialization. You do not need cycling shoes until you are sure indoor cycling is your go-to sport. Similarly, you do not need Olympic weightlifting shoes for general strength training. Let your sustained interest guide niche purchases, not the other way around.

Beware of fads and "quick fix" gadgets. If a product promises insane results with minimal effort, it is likely selling a fantasy. Sustainable fitness is built on consistent effort, not electrical muscle stimulators, ab belts or dodgy supplements. Stick to the good-old healthy diet and regular workouts, and you will be primed for success in 2026.

The bottom line

The goal of your initial purchases is not to equip a pro athlete from the get-go, but to minimize barriers to exercise and help you establish healthy habits. Every item should make it easier to say "yes" to your workout and harder to make an excuse.

This New Year, invest first in the basics that support consistency. Let your proven dedication over weeks and months, not your initial January enthusiasm, guide your future investments. Your journey starts not with the fanciest gear, but with the first step taken in the right shoes.

We hope that our list will help you do just that.

This policy change effectively downgrades the recommendations for several shots, such as those against rotavirus, the flu and hepatitis A. Rather than being recommended to all children by default, those vaccines will now be recommended to only certain "high-risk" groups or will be accessible through "shared clinical decision-making" between parents and providers.

The concept of shared clinical decision-making emphasizes that, if a child's caregivers wish to give them a routine vaccine, they should first consult with a medical provider. While that idea may sound benign, it could sow confusion around which vaccines are considered effective and medically necessary, Dr. Daniel Jernigan, former director of the Centers for Disease Control and Prevention's (CDC) National Center for Emerging and Zoonotic Infectious Diseases, told STAT. And it could introduce logistical hurdles to accessing vaccines.

"By making these vaccines a shared clinical decision making, it introduces one more barrier that prevents a child from getting a life-saving vaccine," Jernigan said.

The new recommendations

The new recommendations group vaccines and immunizations into three categories:

• Those recommended for all children
• Those recommended for certain high-risk groups
• Those that can be given based on "shared clinical decision-making"

Federal guidance still recommends that all children receive shots against 11 diseases: measles, mumps, rubella, polio, pertussis, tetanus, diphtheria, Haemophilus influenzae type B (Hib), pneumococcal disease, varicella (chickenpox), and human papillomavirus (HPV). However, HHS is recommending only one dose of HPV vaccine instead of the usual two, STAT reported.

Certain "high-risk" populations are recommended to be immunized for RSV, hepatitis A, hepatitis B, dengue, and two types of meningococcal disease. (Note that immunizations against respiratory syncytial virus, or RSV, include a prenatal vaccine given to mothers and antibody drugs given to kids. There is no RSV vaccine available for children.)

Vaccines against meningococcal disease and hepatitis A and B are also listed under the "shared decision-making" category, as are shots against rotavirus, COVID-19 and the flu.

"Abandoning recommendations for vaccines that prevent influenza, hepatitis and rotavirus, and changing the recommendation for HPV without a public process to weigh the risks and benefits, will lead to more hospitalizations and preventable deaths among American children," Michael Osterholm of the University of Minnesota's Center for Infectious Disease Research and Policy, told The Associated Press.

'Dangerous and unnecessary' changes

Stakeholders had been bracing for this policy change for several weeks by the time it was announced Monday (Jan. 5).

In early December, President Donald Trump called on federal officials to compare the U.S. childhood vaccine schedule to that of "peer nations," implying that other countries have superior policies. In mid-December, Politico reported that Robert F. Kennedy Jr., the head of the Department of Health and Human Services (HHS), had intended to make the U.S. vaccine schedule more like that of Denmark — which recommends shots against only 11 diseases in its schedule.

Comparable countries often recommend vaccines and immunizations against about 12 to 15 pathogens, while Austria and the U.S. have historically sat on the high end at around 17.

Experts have emphasized that the United States' vaccine schedule has been rigorously tested and that the decision to change it was not made using new data on its safety or effectiveness. They also noted that the policies of Denmark — a small country of roughly 6 million people with universal health care and a fairly homogenous population — may not serve the U.S. population, given that it's much larger and contends with a splintered health care system and greater health inequities. (The U.S. population is roughly 340 million.)

"The truth is that while vaccine guidance is largely similar across developed countries, it may differ by country due to different disease threats, population demographics, health systems, costs, government structures, vaccine availability, and programs for vaccine delivery," the American Academy of Pediatrics (AAP) noted.

These location-specific factors weigh upon which vaccines health officials recommend to a given country's children. But despite the differences between America and Denmark, federal officials are now claiming that Denmark's approach is the superior one regardless of context.

Officials had already been shifting away from giving full-throated recommendations of routine vaccines. For example, HHS previously recommended "shared clinical-decision making" for giving COVID-19 vaccines to kids and providing hepatitis B vaccines to infants of mothers who test negative for the virus.

Various stakeholders are expected to break with the CDC's new recommendations. For instance, medical societies, city and state health departments, and regional health alliances have rejected the CDC's other vaccine policy changes, and the AAP has sued HHS for allegedly violating established rules around vaccine regulatory changes when the agency tweaked its COVID-19 vaccine guidance.

"Today's announcement by federal health officials to arbitrarily stop recommending numerous routine childhood immunizations is dangerous and unnecessary," AAP president Dr. Andrew Racine, said in a statement, according to the clinical news source Contemporary Pediatrics.

"The longstanding, evidence-based approach that has guided the U.S. immunization review and recommendation process remains the best way to keep children healthy," Racine said, "and protect against health complications and hospitalizations."

This article is for informational purposes only and is not meant to offer medical advice.

Since researchers first established the link between diet, cholesterol and heart disease in the 1950s, risk for heart disease has been partly assessed based on a patient’s cholesterol levels, which can be routinely measured via blood work at the doctor’s office.

However, accumulating evidence over the past two decades demonstrates that a biomarker called C-reactive protein – which signals the presence of low-grade inflammation – is a better predictor of risk for heart disease than cholesterol.

As a result, in September 2025, the American College of Cardiology published new recommendations for universal screening of C-reactive protein levels in all patients, alongside measuring cholesterol levels.

What is C-reactive protein?

C-reactive protein is created by the liver in response to infections, tissue damage, chronic inflammatory states from conditions like autoimmune diseases, and metabolic disturbances like obesity and diabetes. Essentially, it is a marker of inflammation – meaning immune system activation – in the body.

C-reactive protein can be easily measured with blood work at the doctor’s office. A low C-reactive protein level – under 1 milligram per deciliter – signifies minimal inflammation in the body, which is protective against heart disease. An elevated C-reactive protein level of greater than 3 milligrams per deciliter, signifies increased levels of inflammation and thus increased risk for heart disease. About 52% of Americans have an elevated level of C-reactive protein in their blood.

Research shows that C-reactive protein is a better predictive marker for heart attacks and strokes than “bad,” or LDL cholesterol, short for low-density lipoprotein, as well as another commonly measured genetically inherited biomarker called lipoprotein(a). One study found that C-reactive protein can predict heart disease just as well as blood pressure can.

Why does inflammation matter in heart disease?

Inflammation plays a crucial role at every stage in the development and buildup of fatty plaque in the arteries, which causes a condition called atherosclerosis that can lead to heart attacks and strokes.

From the moment a blood vessel is damaged, be it from high blood sugar or cigarette smoke, immune cells immediately infiltrate the area. Those immune cells subsequently engulf cholesterol particles that are typically floating around in the blood stream to form a fatty plaque that resides in the wall of the vessel.

This process continues for decades until eventually, one day, immune mediators rupture the cap that encloses the plaque. This triggers the formation of a blood clot that obstructs blood flow, starves the surrounding tissues of oxygen and ultimately causes a heart attack or stroke.

Hence, cholesterol is only part of the story; it is, in fact, the immune system that facilitates each step in the processes that drive heart disease.

Can diet influence C-reactive protein levels?

Lifestyle can significantly influence the amount of C-reactive protein produced by the liver.

Numerous foods and nutrients have been shown to lower C-reactive protein levels, including dietary fiber from foods like beans, vegetables, nuts and seeds, as well as berries, olive oil, green tea, chia seeds and flaxseeds.

Weight loss and exercise can also reduce C-reactive protein levels.

Does cholesterol still matter for heart disease risk?

Though cholesterol may not be the most important predictor of risk for heart disease, it does remain highly relevant.

However, it’s not just the amount of cholesterol – or more specifically the amount of bad, or LDL, cholesterol – that matters. Two people with the same cholesterol level don’t necessarily have the same risk for heart disease. This is because risk is determined more so by the number of particles that the bad cholesterol is packaged into, as opposed to the total mass of bad cholesterol that’s floating around. More particles means higher risk.

That is why a blood test known as apolipoprotein B, which measures the number of cholesterol particles, is a better predictor of risk for heart disease than measurements of total amounts of bad cholesterol.

Like cholesterol and C-reactive protein, apolipoprotein B is also influenced by lifestyle factors like exercise, weight loss and diet. Nutrients like fiber, nuts and omega-3 fatty acids are associated with a decreased number of cholesterol particles, while increased sugar intake is associated with a larger number of cholesterol particles.

Furthermore, lipoprotein(a), a protein that lives in the wall surrounding cholesterol particles, is another marker that can predict heart disease more accurately than cholesterol levels. This is because the presence of lipoprotein(a) makes cholesterol particles sticky, so to speak, and thus more likely to get trapped in an atherosclerotic plaque.

However, unlike other risk factors, lipoprotein(a) levels are purely genetic, thus not influenced by lifestyle, and need only be measured once in a lifetime.

What’s the best way to prevent heart disease?

Ultimately, heart disease is the product of many risk factors and their interactions over a lifetime.

Therefore, preventing heart disease is way more complicated than simply eating a cholesterol-free diet, as once thought.

Knowing your LDL cholesterol level alongside your C-reactive protein, apolipoprotein B and lipoprotein (a) levels paints a comprehensive picture of risk that can hopefully help motivate long-term commitment to the fundamentals of heart disease prevention. These include eating well, exercising consistently, getting adequate sleep, managing stress productively, maintaining healthy weight and, if applicable, quitting smoking.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

We love that this device is integrated into something you would ordinarily use in the pool. There is no need to remember an additional device, such as a watch or training band. It is also inherently swim-specific. There aren't heaps of menus, workout types, or other distractions you would find on a multi-sport device. If swimming is the only exercise you're interested in tracking, these could be a good fit.

The Smart Swim 2 comes with five interchangeable nose bridges and adjustable straps to help you achieve a secure fit. Once you have fitted the goggles to your face, the optical heart rate sensor sits snugly against it. In our hands-on FORM Smart Swim 2 review, we found the heart rate readings to be spot on, with no missed or erratic readings, unlike some swim trackers we have reviewed.

While these aren't the most comfortable swimming goggles in the world, as they require a tight fit to ensure data accuracy, they are about as comfortable as any other swimming goggles we've worn for extended periods in the water. They all need to be snug to the face to ensure a leak-free swim after all.

While testing, we found that the reduced peripheral vision takes a little while to get used to, as does switching between looking 'at' the data and looking 'through' the data, as this is likely something you haven't done before. We quickly adapted to it, and over time, it just became part and parcel of our swimming experience.

• Our experts have reviewed and rated the best fitness trackers, running shoes, rowing machines and more. Everything you need to kick-start your 2026 fitness routine.

The real strength of the FORM Smart Swim 2 is the hands-off real-time feedback in the pool. If, like us, you're prone to losing count of your laps/lengths in the pool, you can relax into your swim and not have to think about the numbers. Turn detection, automatic pause detection and lap counting work with impressive accuracy, taking the guesswork out of tracking swims. You can connect and sync your data with third-party platforms, such as Strava, if you wish.

The accompanying app provides structure through workouts and training plans, but access to the full range requires a subscription, priced at around $15 (£13) per month or $99 (£84) per year. In the grand scheme of things, though this may seem a bit annoying, it is still great value.

Key features: Customizable transparent 'in-eye' display for metrics such as heart rate tracking, number of lengths, lap split times and overall distance.

Product launched: April 2024.

Price history: The price was consistently $279 (aside from a few flash-sale drops) but has been $199 since the start of November, possibly because consumers are now favoring the updated Form Smart Swim 2 Pro.

Price comparison: Amazon: $199 | Walmart: $223.73 | Best Buy: $199

Reviews consensus: The Smart Swim 2 goggles have a rating of 4.1 out of 5 on Amazon, with many users reporting significant improvements in their swimming technique and overall experience. A frequently mentioned benefit is the 'swim straight' feature, which is particularly useful for helping open-water swimmers stay on track.

Live Science: ★★★★½ | T3: ★★★★ | Toms Guide: ★★★½

✅ Buy it if: Your primary focus is data logging or improving your swims. These are purpose-built for swimmers.

❌ Don't buy it if: You want to track multiple sports, for that, you'll be better off taking a look at one of the best fitness trackers. Our favourite overall, the Amazfit, is on sale for just $119.99 with a 40% discount right now.

Check out our other guides to the best budget fitness trackers, sleep trackers, smart rings and much more.

But is it possible for adults to have extra bones?

Some adults do indeed have more than 206 bones. These extras, known as accessory bones or supernumerary bones, may occur when bones do not fuse together the standard way during development, per a 2024 study in the journal Scientific Reports.

However, there often aren't obvious signs that someone has more than the typical number of bones.

"It is very easy to not know that someone has an accessory bone," Dr. Vandan Patel, an orthopedic surgeon at the Institute for Foot and Ankle Reconstruction at Mercy Medical Center in Baltimore, told Live Science. Most of the time, accessory bones do not cause any symptoms. "Oftentimes, we learn that someone has an accessory bone when they have an X-ray done for something unrelated and they are found incidentally," he explained.

Even when accessory bones are seen on X-rays, they are frequently overlooked or misinterpreted as fracture fragments or age-related changes, said Eren Ogut, an associate professor of anatomy at Istanbul Medeniyet University. All in all, "studies suggest that they occur in roughly 10 to 30% of the general population," but "their true prevalence is likely higher than commonly appreciated," Ogut told Live Science.

Accessory bones are common in the foot and ankle, Patel said. The most common accessory bone is known as the os trigonum, he said. "This is seen in up to 10 to 25% of people," Patel noted. "It is located in the back of the ankle joint. It can cause pain, especially when pointing the toes and the ankle down, such as in a ballet dancer in en pointe position."

Another common accessory bone is called the os tibiale externum, also known as accessory navicular. "It is seen in up to 12% of the population," Patel said. "It is located on the inside of the foot, next to the normal navicular bone. Sometimes the navicular bone appears enlarged. It can cause pain in the arch and is often seen with flat-foot deformity."

Doctors also know about a number of uncommon accessory bones, often through studies of cadavers or medical imaging, Ogut said. One example is the os acetabuli, an accessory bone of the hip that may be associated with hip pain, he noted. This accessory bone is seen in less than 5% of the general population, Ogut noted in a 2025 review article in the Bratislava Medical Journal.

Sometimes it's possible to possess accessory ribs. Up to 1% of people have one or even two extra bones in their neck at birth known as cervical ribs, according to the Cleveland Clinic. This rare bone doesn't resemble a typical rib; it can be more vertical or diagonal instead of horizontal like the ribs in the chest. Most of the time, cervical ribs cause no problems, but they can lead to pain or weakness in the arm. In such cases, physical therapy or medicine can help. A surgeon can also remove them, as they don't serve a purpose, the clinic noted.

Human skeleton quiz: What do you know about the bones in your body?

T cells help train other immune cells to fight off disease. But as the body ages, the activity of these T cells declines, and they become less responsive to threats. Additionally, the thymus gland — where T cells mature — begins to shrink with age. These impacts of aging may explain why vaccines and immune-boosting cancer therapies don't work as well in older adults as they do in younger adults, Nature News reported.

In the new study, published Dec. 17 in the journal Nature, scientists tried to counteract these age-driven changes using messenger RNA (mRNA).

Among other roles, mRNA relays instructions from DNA to cells' protein-building organelles, serving as a template from which new proteins are made. The team behind the new study studied T cells in aging mice, pinpointing three proteins that seemed to decline with age, contributing to the aging process. They then generated mRNA for those three proteins, encased them in tiny bubbles of fat, and injected them into middle-aged mice, which were around 16 months old.

These mRNA-filled bubbles traveled through the bloodstream to the liver, where they accumulated. Most T cells are in the bloodstream, and because the liver filters blood, T cells were likely cycled through the liver, where they were exposed to this waiting supply of mRNA.

Mice treated with the mRNA made more T cells than mice that were left untreated. The treated mice's T cells also responded better to vaccination and to cancer immunotherapy, the experiments suggested.

The benefits of the treatment, which was given to the mice twice a week, disappeared quickly when the scientists paused the injections. That's not necessarily surprising, given that mRNA molecules degrade very quickly in the body, whether they were originally made by cells or produced in a lab.

"The transient nature of mRNA delivery necessitates repeated administrations to sustain therapeutic effects," the study authors wrote in the paper. That said, "the long-term consequences of continuous exposure to these factors, especially in aged individuals should be analysed through extensive long-term safety studies."

In short, more research is needed to see if the same approach could work in humans. You can read more about the study in Nature News.

There, these people would likely have encountered their distant cousins: Neanderthals.

These small bands of modern-human relatives had hooded brows, large heads and squat bodies, and they had spent epochs acclimating to Europe's colder climate. At several points across millennia, these two forms of humanity would meet, mingle and mate.

Tens of thousands of years later, these ancient encounters have left traces in the genetic code of billions of humans alive today. The lingering genes affect us in ways large and small, from our appearance to our risk of disease.

"In some places in our genome, we're more Neanderthal than we are human," Joshua Akey, a professor of integrative genomics at Princeton University, told Live Science.

These were our closest human relatives, and this is their legacy.

The first encounter

By 75,000 years ago, but possibly up to 250,000 years ago, the ancestors of most modern Eurasians first ventured out of Africa and into Eurasia. Here, modern humans came face-to-face with Neanderthals, who last shared a common ancestor with modern humans hundreds of thousands of years earlier and had been living in these continents ever since. On multiple occasions over the millennia, the groups interbred.

Related: Could Neanderthals talk?

At first, modern humans inherited whole chromosomes from Neanderthals, Sriram Sankararaman, a professor of computer science, human genetics and computational medicine at UCLA, told Live Science. However, from generation to generation, via a process known as genetic recombination, these stretches of DNA were broken up and shuffled around.

Neanderthal DNA was generally "deleterious" to modern humans, meaning it was rapidly weeded out of modern humans' DNA through evolution. This resulted in "deserts of Neanderthal DNA," or large regions of the modern human genome lacking it, Sankararaman said. For instance, scientists think the Y chromosome in males doesn't contain any Neanderthal genes. It may be that genes on the Neanderthal Y were incompatible with other human genes or they may have been randomly lost via a process known as genetic drift.

In people who inherited Neanderthal DNA, the X-chromosome also contains a lot less Neanderthal ancestry than other, non-sex chromosomes carry. This is probably because any harmful or nonfunctional mutations on the X chromosome will be expressed in males, because they lack a matching, functional copy of the gene to compensate. That likely created strong evolutionary pressure to remove such harmful Neanderthal genes from the modern human X, Emilia Huerta-Sanchez, an associate professor of ecology, evolution, and organismal biology at Brown University, told Live Science.

But some Neanderthal DNA helped modern humans survive and reproduce, and thus it has lingered in our genomes. Nowadays, Neanderthal DNA occupies, on average, 2% of the genomes of people outside Africa. However, the frequency of Neanderthal DNA that codes for beneficial traits may be as high as 80% in some regions of the genome, Akey said.

Our physical appearance

For many people, the legacy of Neanderthals is apparent in a highly visible feature: skin color.

A Neanderthal gene variant on chromosome 9 that influences skin color is carried by 70% of Europeans today. Another Neanderthal gene variant, found in most East Asians, regulates keratinocytes, which protect the skin against ultraviolet radiation via a dark pigment called melanin.

Neanderthal gene variants are also associated with a greater risk of sunburn in modern humans. Likewise, around 66% of Europeans carry a Neanderthal allele linked to a heightened risk of childhood sunburn and poor tanning ability.

Neanderthals had spent millennia at higher latitudes with less direct sun exposure, which is needed for vitamin D production. Therefore, changes to hair and skin biology may have allowed modern humans to quickly capitalize on lower levels of sunlight while still producing enough vitamin D to be healthy, John Capra, an evolutionary geneticist at Vanderbilt University, told Live Science.

"One of the cool things about interbreeding is that instead of waiting for new beneficial mutations to arise, which is a really slow process, you introduce a ton of genetic variation at once," essentially fast-tracking evolution, Huerta-Sanchez said.

Related: What's the difference between Neanderthals and Homo sapiens?

In addition, our ancestors had to adapt to colder Eurasian weather. To do so, they may have acquired Neanderthal genes that affected face shape. In a 2023 study, scientists discovered that modern humans inherited tall-nose genes from Neanderthals. A taller nose may have allowed more cold air to be heated to body temperature in the nose before reaching the lungs, suggested Kaustubh Adhikari, co-senior study author and a statistical geneticist at University College London.

The clock that makes our cells tick

Neanderthal DNA also may have helped H. sapiens adjust to the bigger differences in day and night length at northern latitudes.

Lingering Neanderthal genes affect our circadian clock, which regulates internal processes such as body temperature and metabolism. For instance, some early risers can thank Neanderthals for their circadian clock genes, Capra and colleagues found.

This may have helped our ancestors adapt to shorter winter days farther from the equator, Capra said.

"It seems like it's not that being a morning person is what matters," Capra said. "It's that that's a signal of how essentially flexible your clock is and how able it is to adapt to the variation in light-dark cycles with seasons," he said.

Our internal defenses

Many of the strongly retained Neanderthal genes are tied to immune function.

By the time H. sapiens arrived in Europe, Neanderthals had already spent hundreds of thousands of years fighting infections specific to Eurasia. By mating with Neanderthals, modern humans got an instant infusion of those infection-fighting genes.

"Those pieces of Neanderthal DNA, especially the immune ones, that were already adapted against pathogens that Neanderthals had been living with for a long time started to rise in frequency under natural selection in modern human populations," David Enard, an assistant professor of ecology and evolutionary biology at the University of Arizona, told Live Science.

While many of the ancestral pathogens that sickened ancient humans are lost to time, some of the Neanderthal genes that helped fight them off still work against modern pathogens. For example, a 2018 study by Enard and a colleague revealed that modern humans inherited Neanderthal DNA that helped them combat RNA viruses, a group that today includes the flu (influenza), HIV and hepatitis C.

Related: 10 unexpected ways Neanderthal DNA affects our health

The darker side of Neanderthal DNA

Some of the Neanderthal genes that once helped our ancestors may be harmful in the modern world.

For the most part, Neanderthal genes are not strongly expressed in the brain, which hints that they were strongly selected against during evolution. Neanderthal genes have been linked to mood disorders such as depression and to brain signaling pathways that make people more likely to become addicted to nicotine.

And even the immune boost from Neanderthals may have a downside. In 2016, scientists discovered that Neanderthal genes that prime the immune system to fight pathogens may also predispose people to allergic diseases. In addition, Neanderthal genes have been tied to a higher risk of developing autoimmune diseases, such as Graves' disease, caused by an overactive thyroid; and rheumatoid arthritis, which inflames the joints and even "Viking disease," in which one or more fingers become bent or frozen.

One Neanderthal gene variant may have made us more likely to have a severe case of COVID-19. That variant, found on chromosome 3, is found in half of South Asians and one-sixth of Europeans. But even there, the picture is complicated, as other Neanderthal genes, carried by up to half of people in Eurasia and the Americas, are associated with a reduced risk of severe COVID-19.

"Unfortunately, there are no diseases we can really say, or even traits in general, we can say, 'Oh, you can blame your Neanderthal DNA for that,'" Capra said.

That's especially true for some of the biggest health ailments, such as heart disease and cancer, where dozens or hundreds of genes, along with myriad environmental factors, affect your risk of disease.

What lies ahead

So how long will the traces of these long-lost humans linger in our genomes? Over hundreds of thousands of years, some of these Neanderthal fragments will gradually be eliminated from our genomes. Others will become firmly embedded, Akey said.

In the meantime, there's still much more to learn about how Neanderthals left their mark on us.

"Being able to leverage new genomic technology like CRISPR and gene editing is going to play an important role in understanding the actual underlying biology of how Neanderthal sequences contribute to human traits and diseases," Akey said.

Deciphering what these genes actually do could aid the development of treatments for certain conditions, he said.

And the gene flow wasn't one-way; scientists are also trying to determine how modern-human DNA may have influenced Neanderthals and are applying artificial intelligence (AI) methods to ancient genomes to create a more detailed picture of what our long-lost cousins were like.

Figuring out the role of Neanderthal DNA in our genomes does more than help us understand our health. These bits of DNA can provide clues as to what makes us unique, Sankararaman said.

"Neanderthal DNA entered our genomes at an important time in our history," Sankararaman said, when our ancestors were moving into new environments.

"By looking at the fate of these bits of DNA," he said, "we can hope to understand what were the functionally important regions in our genome over this period of time."

Editor's Note: This story was originally published in March 2024.

Their breakfast was still scattered around their enclosure for them to find. Ripley, one of the male chimpanzees, quickly gathered up some fruits and vegetables, sometimes using his feet almost like hands. After he ate, he used his feet to grab the fire hoses hanging around the enclosure and even held pieces of straw and other toys in his toes.

I found myself feeling a bit envious. Why can't people use our feet like this, quickly and easily grasping things with our toes just as easily as we do with our fingers?

I'm a biological anthropologist who studies the biomechanics of the modern human foot and ankle, using mechanical principles of movement to understand how forces affect the shape of our bodies and how humans have changed over time. Your muscles, brain and how human feet evolved all play a part in why you can't wiggle individual toes one by one.

Comparing humans to a close relative

Humans are primates, which means we belong to the same group of animals that includes apes like Riley the chimp. In fact, chimpanzees are our closest genetic relatives, sharing almost 98.8% of our DNA.

Evolution is part of the answer to why chimpanzees have such dexterous toes while ours seem much more clumsy.

Our very ancient ancestors probably moved around the way chimpanzees do, using both their arms and legs. But over time our lineage started walking on two legs. Human feet needed to change to help us stay balanced and to support our bodies as we walk upright. It became less important for our toes to move individually than to keep us from toppling over as we moved through the world in this new way.

Human hands became more important for things such as using tools, one of the hallmark skills of human beings. Over time, our fingers became better at moving on their own. People use their hands to do lots of things, such as drawing, texting or playing a musical instrument. Even typing this article is possible only because my fingers can make small, careful and controlled movements.

People's feet and hands evolved for different purposes.

Muscles that move your fingers or toes

Evolution brought these differences about by physically adapting our muscles, bones and tendons to better support walking and balance. Hands and feet have similar anatomy; both have five fingers or toes that are moved by muscles and tendons. The human foot contains 29 muscles that all work to help you walk and stay balanced when you stand. In comparison, a hand has 34 muscles.

Most of the muscles of your foot let you point your toes down, like when you stand on tiptoes, or lift them up, like when you walk on your heels. These muscles also help feet roll slightly inward or outward, which lets you keep your balance on uneven ground. All these movements work together to help you walk and run safely.

The big toe on each foot is special because it helps push your body forward when you walk and has extra muscles just for its movement. The other four toes don't have their own separate muscles. A few main muscles in the bottom of your foot and in your calf move all four toes at once. Because they share muscles, those toes can wiggle, but not very independently like your fingers can. The calf muscles also have long tendons that reach into the foot; they're better at keeping you steady and helping you walk than at making tiny, precise movements.

In contrast, six main muscle groups help move each finger. The fingers share these muscles, which sit mostly in the forearm and connect to the fingers by tendons. The thumb and pinky have extra muscles that let you grip and hold objects more easily. All of these muscles are specialized to allow careful, controlled movements, such as writing.

So, yes, I have more muscles dedicated to moving my fingers, but that is not the only reason I can't wiggle my toes one by one.

Divvying up brain power

You also need to look inside your brain to understand why toes and fingers work differently. Part of your brain called the motor cortex tells your body how to move. It's made of cells called neurons that act like tiny messengers, sending signals to the rest of your body.

Your motor cortex devotes many more neurons to controlling your fingers than your toes, so it can send much more detailed instructions to your fingers. Because of the way your motor cortex is organized, it takes more "brain power," meaning more signals and more activity, to move your fingers than your toes.

Even though you can't grab things with your feet like Ripley the chimp can, you can understand why.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

The patient is one of six taking part in the first clinical trial of pig-to-human kidney transplants. The goal: to see whether gene-edited pig kidneys can safely replace failing human ones.

A decade ago, scientists were chasing a different solution. Instead of editing the genes of pigs to make their organs human-friendly, they tried to grow human organs — made entirely of human cells — inside pigs. But in 2015 the National Institutes of Health paused funding for that work to consider its ethical risks. The pause remains today.

As a bioethicist and philosopher who has spent years studying the ethics of using organs grown in animals — including serving on an NIH-funded national working group examining oversight for research on human-animal chimeras — I was perplexed by the decision. The ban assumed the danger was making pigs too human. Yet regulators now seem comfortable making humans a little more pig.

Why is it considered ethical to put pig organs in humans but not to grow human organs in pigs?

Urgent need drives xenotransplantation

It's easy to overlook the desperation driving these experiments. More than 100,000 Americans are waiting for organ transplants. Demand overwhelms supply, and thousands die each year before one becomes available.

For decades, scientists have looked across species for help — from baboon hearts in the 1960s to genetically altered pigs today. The challenge has always been the immune system. The body treats cells it does not recognize as part of itself as invaders. As a result, it destroys them.

A recent case underscores this fragility. A man in New Hampshire received a gene-edited pig kidney in January 2025. Nine months later, it had to be removed because its function was declining. While this partial success gave scientists hope, it was also a reminder that rejection remains a central problem for transplanting organs across species, also known as xenotransplantation.

Researchers are attempting to work around transplant rejection by creating an organ the human body might tolerate, inserting a few human genes and deleting some pig ones. Still, recipients of these gene-edited pig organs need powerful drugs to suppress the immune system both during and long after the transplant procedure, and even this may not prevent rejection. Even human-to-human transplants require lifelong immunosuppressants.

That's why another approach — growing organs from a patient's own cells — looked promising. This involved disabling the genes that let pig embryos form a kidney and injecting human stem cells into the embryo to fill the gap where a kidney would be. As a result, the pig embryo would grow a kidney genetically matched to a future patient, theoretically eliminating the risk of rejection.

Although simple in concept, the execution is technically complex because human and pig cells develop at different speeds. Even so, five years prior to the NIH ban, researchers had already done something similar by growing a mouse pancreas inside a rat.

Cross-species organ growth was not a fantasy — it was a working proof of concept.

Ethics of creating organs in other species

The worries motivating the NIH ban in 2015 on inserting human stem cells into animal embryos did not come from concerns about scientific failure but rather from moral confusion.

Policymakers feared that human cells might spread through the animal's body — even into its brain — and in so doing blur the line between human and animal. The NIH warned of possible "alterations of the animal's cognitive state." The Animal Legal Defense Fund, an animal advocacy organization, argued that if such chimeras gained humanlike awareness, they should be treated as human research subjects.

The worry centers on the possibility that an animal's moral status — that is, the degree to which an entity's interests matter morally and the level of protection it is owed – might change. Higher moral status requires better treatment because it comes with vulnerability to greater forms of harm.

Think of the harm caused by poking an animal that's sentient compared to the harm caused by poking an animal that's self-conscious. A sentient animal — that is, one capable of experiencing sensations such as pain or pleasure — would sense the pain and try to avoid it. In contrast, an animal that's self-conscious — that is, one capable of reflecting on having those experiences — would not only sense the pain but grasp that it is itself the subject of that pain. The latter kind of harm is deeper, involving not just sensation but awareness.

Thus, the NIH's concern is that if human cells migrate into an animal's brain, they might introduce new forms of experience and suffering, thereby elevating its moral status.

The flawed logic of the NIH ban

However, the reasoning behind the NIH's ban is faulty. If certain cognitive capacities, such as self-consciousness, conferred higher moral status, then it follows that regulators would be equally concerned about inserting dolphin or primate cells into pigs as they are about inserting human cells. They are not.

In practice, the moral circle of beings whose interests matter is drawn not around self-consciousness but around species membership. Regulators protect all humans from harmful research because they are human, not because of their specific cognitive capacities such as the ability to feel pain, use language or engage in abstract reasoning. In fact, many people lack such capacities. Moral concern flows from that relationship, not from having a particular form of awareness. No research goal can justify violating the most basic interests of human beings.

If a pig embryo infused with human cells truly became something close enough to count as a member of the human species, then current research regulations would dictate it's owed human-level regard. But the mere presence of human cells doesn't make pigs humans.

The pigs engineered for kidney transplants already carry human genes, but they aren't called half-human beings. When a person donates a kidney, the recipient doesn't become part of the donor's family. Yet current research policies treat a pig with a human kidney as if it might.

There may be good reasons to object to using animals as living organ factories, including welfare concerns. But the rationale behind the NIH ban that human cells could make pigs too human rests on a misunderstanding of what gives beings — and human beings in particular — moral standing.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

We're closer than ever to achieving functional cures for once-intracable diseases, including HIV. Stem-cell treatments are repairing blinding eye damage and stabilizing failing hearts. Emerging cancer treatments promise to extend patients' lives and decrease the likelihood that their disease will return. And cutting-edge treatments are sparing children from devastating genetic diseases.

But even as the promise of decades of medical research is being realized, the foundations of the field are coming under attack. Can these emerging treatments really save us from harm when long-standing tenets of public health and medical research are being eroded before our eyes?

That's the question circling my brain as I look ahead to 2026. While I'd love to focus solely on how far we've come, it's impossible to ignore the ground we've lost in recent months.

Exciting developments to watch

As anticipated, 2025 was a breakthrough year for gene therapy, and I expect 2026 to bring more exciting developments in the field.

KJ Muldoon, a baby born with a rare genetic disease, became the first person to receive a customized CRISPR treatment. The two CRISPR-based therapies approved to date are one-size-fits-all, and they require cells to be removed, edited in a lab, and then reintroduced into the body. KJ's treatment, by contrast, was made to tweak a specific mutation in his cells, and the editing took place inside his body.

One of KJ's doctors told me that they're now working with the Food and Drug Administration to make these bespoke treatments easier for patients to access, so hopefully, more people will benefit from such therapies in the coming months. (Notably, though, baby KJ's treatment used mRNA — a molecule that also formed the basis of the first COVID-19 vaccines. The federal government is retreating from mRNA vaccines, but other uses of the technology may be spared.)

In the meantime, scientists are trialing a gene therapy for Huntington's disease that may slow its progression — a feat never realized with any existing treatment. A CRISPR treatment for high cholesterol is making its way through trials, as is a gene therapy for congenital deafness and a new cancer therapy that involves base editing immune cells. And in preclinical research, scientists are developing new gene-editing systems that could someday enable "mutation agnostic" treatments that work for many people, as a complement to therapies that correct very specific mutations.

This year, we also saw results from a U.K.-based clinical trial of "mitochondrial donation," a technique that's been in the works for years and is finally being tested in people. The approach, done in the context of in vitro fertilization, aims to prevent mothers who carry harmful mutations in their mitochondrial DNA from passing those mutations to their kids. In the early trial, the approach appeared to be successful, and I'll be interested to see how the research proceeds.

We've also seen GLP-1s — Ozempic and other drugs in the same class — become more commonplace, and we've been learning about their potential benefits beyond weight loss and blood-sugar control. There are early signals that these drugs may help treat migraine, alcohol use disorder and heart failure, for instance. I expect these findings will spur interesting research into the underlying relationship between these conditions and metabolism.

That said, I don't think the drugs will be a silver bullet for all diseases — they just failed in a hotly anticipated Alzheimer's disease trial, for example. Nonetheless, research on GLP-1s may uncover previously unappreciated drivers of disease that could be tackled by other means in the future.

I'll also be keen to follow emerging research on senolytics — drugs that clear senescent, or biologically aged, cells from the body.

Xenotransplantation — the transplantation of animal organs into humans — continues to progress by leaps and bounds as experiments and trials with humans unfold around the world.

And as research increasingly reveals the role of viruses in dementia, I expect the next few years of studies could fundamentally rewrite our understanding of neurodegenerative disease and how to treat it.

Dissolution of public health

From a technological and research standpoint, there's a lot to be excited about. But the horizon looks darker when you cast your eyes to the realm of public health and the systems that fund and regulate research and new drugs, at least in the United States.

President Trump's second administration ushered controversial new appointments across the country's leading health agencies — as well as deep budget cuts. Vaccine and medical-establishment skeptic Robert F. Kennedy Jr., now at the helm of the Department of Health and Human Services, spearheaded dramatic changes across its divisions, such as the National Institutes of Health (NIH) and the Centers for Disease Control and Prevention (CDC).

The NIH has signaled that it's deemphasizing the practice of studying both sexes. Given that females are understudied at baseline, experts worry that such a move will widen existing knowledge gaps. The agency's leadership has also argued that collecting demographic data — on study participants' race, ethnicity or gender identity — should be avoided except in circumstances deemed "scientifically justified," a phrase with no clear definition.

In the next year, I expect these moves to derail research aimed at understanding health disparities and improving care for marginalized and understudied populations. Disrupting this research today means prolonging these disparities in the future.

Former CDC leaders have reported witnessing a profound disconnect between RFK Jr. and the agency's scientific staff, a lack of strategy surrounding policy changes, and a dismissal of established research findings. Meanwhile, a new vaccine advisory committee handpicked by RFK Jr. has cast doubt on the well-established childhood vaccine schedule.

Some recent committee decisions have been more confusing than directly consequential, such as those regarding the measles vaccine and the COVID-19 vaccines. Still, set against the backdrop of RFK Jr. broadly undermining trust in vaccines, even these changes could lower vaccination rates in a country already poised to lose its measles elimination status. And other committee decisions, such as recommendations to delay hepatitis B vaccination for newborns, have the potential to cause direct and significant harm right away.

As the CDC is dismantled and its career scientists are ignored, devalued or fired, I anticipate further holes to be poked in the nation's public-health safety net in 2026. Some decisions may primarily stoke confusion and mistrust around established medical practice. Others may bar access to care by revoking federal insurance coverage or withholding reimbursement to hospitals that provide certain types of care.

The exact impacts of forthcoming changes will likely be piecemeal, varying from state to state, similar to how we've seen abortion access splinter in the wake of Roe v. Wade's overturn. But nationwide, it's fair to expect upticks in vaccine-preventable disease.

For trustworthy health guidance, I would recommend sources such as the American Academy of Pediatrics, the American College of Obstetricians and Gynecologists and other professional medical associations; the independent health-policy resource KFF; and the University of Minnesota's Center for Infectious Disease Research and Policy, including its Vaccine Integrity Project. Local health departments and regional coalitions, such as the West Coast Health Alliance, should also help fill the information gap left by federal agencies.

But given that the average person is already bombarded with conflicting health guidance — especially online — I'm concerned that the loss of centralized sources of science-backed information will ultimately put more people at risk of preventable disease.

Beyond America, and into the future

The Trump administration also shuttered the U.S. Agency for International Development (USAID) this year, pushing a handful of the agency's prior functions under the Department of State.

USAID, previously the world's largest foreign aid agency, had programs aimed at combating infectious diseases like HIV and tuberculosis, reducing malnutrition, cleaning water systems, and bolstering maternal health care around the world. Its loss left governments and organizations scrambling to make up the funding shortfall, but they likely won't be able to fill the gap completely, stakeholders have warned. Even if they do, delays in funding still mean delays in care, which can be deadly.

Prior to USAID's closure, experts worldwide were cautiously optimistic about bringing an end to the HIV epidemic by 2030. Now, models suggest that the loss of the agency could usher millions more HIV cases and deaths in low- and middle-income countries than anticipated over the next five years. Looking beyond HIV to all of USAID's former programs, estimates suggest that the closures have already contributed to hundreds of thousands of deaths from infectious diseases and malnutrition worldwide.

The U.S. is not immune to the ripple effects of USAID's dissolution.

"One of USAID's most critical functions is to fight the spread of infectious diseases that have the capacity to spark a global pandemic," Dr. Chris Beyrer, an epidemiologist and director of the Duke Global Health Institute, wrote for Live Science in March. "While much of this work is carried out far from the U.S., infectious diseases know no borders, and we have seen countless instances of viruses that arise in one part of the world but quickly find their way to other countries."

This, to me, underscores a key point about public health: It's a group project. Improving conditions for those most vulnerable to disease benefits everyone in the long run, not only by reducing suffering and saving lives but by cutting health care costs and bolstering economies. One could say the same about the efforts to curb climate change and environmental pollution — efforts that the current administration is also repudiating.

I look forward to following the development of groundbreaking medical treatments over the upcoming year. These emerging technologies promise to alleviate the suffering of individual patients — if they can access them. But even as we celebrate those accomplishments, I worry that their benefits simply won't reach a huge portion of the populace.

Headlines about the next great gene therapy will run alongside news of rising infection rates and deadlier climate-driven disasters. Early data hint that senolytics could help stave off age-related diseases — but even as those drugs get developed, falling vaccination rates mean we could return to a time when a lot more people die in childhood than have in recent decades.

My hope for 2026 is that the scientists and stakeholders still committed to protecting public health will persevere and find ever-expanding support so that everyone can reap the benefits of medical science.

This article is for informational purposes only and is not meant to offer medical advice.

The symptoms: A man went to the dermatology department of a hospital after experiencing an array of symptoms for about three years. When he submerged his hands in water, such as during hand-washing, the skin on the back of the man's hands thickened and became overly wrinkly, with white bumps and growths appearing.

Whenever this occurred, his hands felt very itchy and like they were burning, and the symptoms were worse in the summer months, he told doctors. Symptoms did not arise during winter, and his palms were unaffected year-round.

The man had previously sought treatment at his local clinic, where he was diagnosed with chronic eczema — which causes skin to become dry, thick and itchy — and prescribed a strong retinoid ointment, which he used intermittently. However, this treatment didn't work, and his symptoms gradually worsened. His wrists and elbows had also started to develop the skin lesions over the 1.5 years prior to the hospital visit.

The patient had no family history of similar skin conditions and did not experience excessive sweating or have any allergies, and he had never injured his hands. The man attributed the worsening of his condition to him washing his hands more frequently during the COVID-19 pandemic, the doctors wrote in the report of the case.

What happened next: During a physical examination at the hospital, the man's hands were immersed in water for 10 minutes, immediately causing the tops of his hands, fingers and wrists to grow red, scaly and wrinkly with white lesions. Notably, the "excessive wrinkling" and bumps ended in a straight line on the sides of his hands, leaving his palms unaffected.

The doctors took biopsies from the white bumps on his right hand, which revealed that the sweat ducts in the top layer of skin had widened and contained more sweat glands than normal. The results also showed he had hyperkeratosis, meaning his body was producing too much of the protein keratin, causing the outer layer of skin to thicken.

The medical team wrote that "the patient's clinical process was quite interesting," because the symptoms of the skin condition appeared only after his hands were immersed in water and all symptoms disappeared around 30 minutes after his hands dried.

The diagnosis: The doctors diagnosed the patient with a condition called aquagenic syringeal acrokeratoderma (ASA) based on how his symptoms appeared in the clinic and the results of the biopsy. In almost all other cases, however, it affects the palms of the hands, not the backs of the hands or fingers.

The short-lived symptoms of this skin disease are known as the "hand in the bucket sign," because they occur after the hands are submerged in water. The symptoms normally disappear within a few hours of drying, but a subset of people with ASA have persistent skin lesions that are aggravated by water exposure, according to the Genetic and Rare Diseases Information Center (GARD).

The cause of ASA is currently unknown, but it may be linked to "an acquired sweat gland abnormality" or some trigger that causes thickening of the skin, according to research published in the Journal of the American Academy of Dermatology.

The treatment: The patient was treated with topical hydrocortisone urea ointment, which is a corticosteroid and skin moisturizer that can be applied directly to the affected area. It is typically used to treat skin irritation, swelling and redness.

The doctors also recommended that the patient avoid getting his hands wet more than what was strictly necessary. The man was still attending follow-up appointments when the doctors wrote about his case, and they noted that his symptoms had eased substantially after just one month.

What makes the case unique: ASA is thought to be a rare condition, although its exact prevalence is unknown.

Data suggests the condition is most common in female adolescents, the case report authors noted. It also occurs in about 40% to 84% of cystic fibrosis (CF) patients and carriers, meaning people who have just one copy of the CF gene mutation, according to GARD. (You need two copies to develop CF.) This pattern hints at ASA being caused in part by mutations in that gene, at least in some cases.

The patient described in this case was the first known to have ASA that didn't affect his palms, the doctors wrote in the report. It's unclear why his case manifested differently than others previously reported.

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

This article is for informational purposes only and is not meant to offer medical advice.

This is the vision for the Autonomous Closed-Loop Intervention System (ACIS), a device being developed by scientists at NTT Research, an arm of global technology company NTT. The device has been tested in animal experiments but not in human patients yet.

The researchers' eventual goal is to allow the heart to rest and minimize its oxygen use in that critical recovery window after a patient experiences a cardiac emergency. The jobs that would be handled by ACIS are usually done by medical providers — but the idea is that the device could standardize and optimize the process to deliver better outcomes while relieving strain on doctors' already-limited resources.

"We think that this system will outperform the standard of care," said Dr. Joe Alexander, director of NTT Research's Medical and Health Informatics (MEI) lab.

ACIS stemmed from a larger effort spearheaded by the MEI Lab known as the Bio Digital Twin program. Its aim is to construct advanced virtual models of organ systems that can be personalized with an individual patient's data, providing a detailed and dynamic representation of their medical status and a testable model for developing treatment plans.

Live Science spoke with Alexander about Digital Twins, ACIS and his vision for how they might transform health care.

Nicoletta Lanese: When we're talking about a Bio Digital Twin, is it fair to say it's a virtual copy of the patient?

Dr. Joe Alexander: Probably the layperson would think of a Bio Digital Twin as a copy of the person. But actually, it's just a system of equations, modeling and simulation to represent a person to the extent that is relevant for the disease. It's a very specific application, so there's no single Bio Digital Twin representing the [whole] person.

In our case, although we set out to build a family of Bio Digital Twins to represent different organ systems for different types of important diseases, we're starting with the cardiovascular system. So when I talk about a Cardiovascular Bio Digital Twin, I'm not talking about even a copy of the heart; I'm talking about a mathematical representation of all of the systems necessary for looking at the cardiovascular system in a particular patient.

In the case of ACIS, we're looking at acute heart failure and acute myocardial infarction [colloquially known as a heart attack].

NL: Could you talk about what kind of data goes into the model?

JA: This Cardiovascular Bio Digital Twin is representing pressures and flows throughout the cardiovascular system, including pressures and flows generated by all four chambers of the heart. … We are able to represent the cardiovascular system dynamics in pressures, flows and volumes.

NL: And how do you make that actionable for an individual patient?

JA: We're in the early stages of it, but we have a road map for how to do it. Basically, we first go after representing the "normal" cardiovascular system for patients. So, if we can get data around "normal," then that's very good. [Editor's note: The MEI Lab is working with partners such as the National Cerebral and Cardiovascular Center in Japan to get access to this kind of data.]

But probably what's most important is finding populations that are relevant to the particular patient — so, in this case, patients with cardiovascular disease or patients with heart failure. So we go after that population-level data; let's say for heart failure. Then, from that data, we can estimate parameters for our cardiovascular model that represent the general population of patients with heart failure.

Within that population, as you know, there's a lot of variability. So are there other characteristics specific to our patient that we can use? Maybe results from echocardiogram [EKG]; maybe age; maybe comorbidities [other medical conditions]; sex, male or female; or environment. And if there is genetic information available, then we can find a subpopulation that's even more relevant to the patient.

Now, with ACIS, we [would] actually hook up a patient to the "first guess" of our Cardiovascular Bio Digital Twin for what would match that patient based on population-level data. Since it's a feedback control system, the feedback will automatically adjust the parameter values to deliver the necessary drugs or device therapies that that particular patient needs for some prespecified cardiac output. In that way, we can further fine-tune the Digital Twin for that patient.

NL: Can you describe how ACIS and its feedback loop work?

JA: The idea is that it's a "self-driving" therapeutic, just like a self-driving car. But in this case, "self-driving" is delivering the appropriate drugs or, in severe cases, medical-device therapies that a patient may need.

We have a system where we specify — just type in the keyboard — the desired cardiac output, heart rate, left atrial pressure, arterial pressure that we want the patient to achieve. Then, syringes that are filled with the appropriate drugs to create those changes are driven by our model, or "best guess" for that particular patient. This is all after a patient has had the primary lesion [like a blood vessel blockage] treated in the cath lab.

Let's say they had a vessel that was occluded; it's already been opened up or a stent has been placed, and they go to the ICU [intensive care unit] or CCU [coronary care unit] in order to recover. Recovery means that the heart needs an opportunity to rest. That means letting the heart work as little as possible to maintain the desired cardiac output.

We have a certain regimen of drugs that are given. Catecholamines improve the ability of the heart to contract. Nitrates reduce afterload of the heart so it doesn't have to work against such a high load when it tries to inject into the arterial system. Diuretics decrease the circulating blood volume and remove blood from the lungs, which has built up due to the acute failure.

These drugs are typically given by a physician; they'll give one drug and look at the response, give another drug, the response, and manage that patient over several days. When our system achieves proper function — and we're almost there, I think — all those drugs can be given at once if we know how the system will respond. That saves us a lot of time in treating the patient.

The drugs are delivered by these autonomously controlled syringes; then the patient responds to them, and that response is fed back in this system. Those values are compared to the ones that we typed in the keyboard, and if there's a difference, then feedback systems work to reduce that difference. It also gives information to our Digital Twin for that patient, so that in the future, we have better representations of those resistors and capacitors in the model.

NL: What stage of development has ACIS reached at this point?

JA: So, in animal experiments in dogs, last year for the first time, we experimentally induced acute heart failure and we were able to let this autonomous system correct the cardiac output, arterial pressure autonomously, while minimizing myocardial [heart muscle] oxygen consumption.

Since that first successful experiment about a year ago, we've had several other successful [animal] experiments, all the while improving our feedback system to be more complex, making it so that it can operate based on intermittent data, so you don't have to be continuously sampling. You can do it episodically.

We have several more years of work in optimizing this system, we think, in animal experimentation — probably about three years more. And then we'll be ready for first-in-human studies where ACIS will be used but with a clinician in the loop [for the initial human tests]. What ACIS would do is tell the physician what doses of these various drugs to deliver, and the physician would then make a decision whether to do it or not, as a safety measure.

Now, what I've been describing so far has mostly been about drugs, but the same algorithms work for medical devices, such as left ventricular assist devices [LVAD, a type of mechanical pump] or extracorporeal membrane oxygenation devices [ECMO, which circulates the blood to let the heart and lungs rest]. This is all within the scope of what we expect to achieve in experimental animals within the next three years before going to first-in-human studies.

NL: What are the next steps toward getting ACIS approved? What might the trials look like?

JA: It would be kind of like [testing] an autonomous or self-driving vehicle — level 1 through 4 degrees, or stages, of autonomy.

In other words, allowing the system to have increasing responsibility and watching the performance until settling into acceptance of an autonomous system where then, still, probably a specialist would monitor it — like someone sitting in the seat of a self-driving car, ready to take over if things go wrong. I see that kind of progression, similar to the self-driving vehicle.

NL: And in the long run, would ACIS always have some kind of clinician supervision?

JA: I still hold to the concept of "autonomous," but I suspect that there will be a cardiologist somewhere roaming around, monitoring, perhaps, a number of patients at once.

I'm very committed to the idea that the device that we conceive of can actually outperform the cardiologist. And I know that we'll rub some cardiologists the wrong way. But we expect to demonstrate that point, or strongly suggest that that's true, by doing experiments in animals where we compare the ACIS system to clinically trained cardiologists. We expect reduced infarct size [degree of heart tissue death] from ACIS compared to the standard of care from cardiologists.

NL: Assuming this device gets approved in the future, where do you see it having the most benefit?

JA: There's the so-called Quintuple Aim of Health Care, which says to improve the patient experience, improve the physician experience, improve population health, reduce the cost of care, and improve health equity. These aims, I think, are all addressed by ACIS.

The patient would have more attention and minute-to-minute care — you wouldn't have a resident trying to juggle many patients at once. You could have a less-specialized clinical caretaker who is watching the behavior of the device, and so that would improve not only the patient experience and quality of the patient's care but also the health care provider's experience. They wouldn't have to be overworked to such an extent.

We think that this system will outperform the standard of care because [on paper] you more rapidly converge on the minimization of myocardial oxygen consumption and have better recovery during the hospital stay. So the patients have fewer readmissions and complications after being released. There's always some injury to the heart [with these cardiac events], and maybe, there may be some infarction of the heart. So we think that this level of care could reduce infarct size, so you preserve more of the heart, during treatment.

NL: And when you eventually hand off ACIS for clinical testing, what would the next project be?

JA: For us, the natural progression within the next 10 years, probably within the next five years, would be chronic heart failure. In chronic heart failure, you have to deal with more complexity, such as [tissue] remodeling, where the ventricles get thicker or get dilated. That kind of remodeling changes the mechanics.

You also have to deal with data from patients who are not in the hospital. We plan on building registries of patients [with Digital Twins] who would have been acutely ill to have access to that data for treating them outside. But then we have to also rely on things like wearable technologies, and we've been working on that as well. We have collaborations with folks at the Technical University of Munich who are developing special biosensors and biomaterials and implantable sensors and so forth that could help provide the data that would be important to doing predictive health maintenance in patients with chronic heart failure.

And in chronic heart failure, we have to deal with comorbidities and complications like kidney failure … and anemia. The combination of fluid overload and anemia all due to renal failure really makes the heart suffer from a lack of oxygen and causes slow deterioration.

I'm sure that complexity alone will keep me busy for the rest of my life. We have a lot of work to do with chronic heart failure; that would be next for sure.

Editor's note: This interview has been lightly edited for length and clarity.

The initial trials will focus on assessing the safety of the vaccine, which was initially developed with funding from the U.S. Department of Defense. The shot was previously tested in rats and showed promising results. Now, it's been licensed by startup ARMR Sciences, which will begin enrolling patients for Phase I clinical trials in the Netherlands in 2026, starting in either January or February.

"Our goal as a company is to eliminate the lethality of the drug supply," said Colin Gage, co-founder and CEO of ARMR. "We want to go about doing that by attacking the root cause of not only addiction, but also, obviously, overdose."

How does the vaccine work?

The vaccine works by keeping fentanyl out of the brain, which it does by making the molecule a target of the immune system.

Fentanyl is a synthetic opioid with effects 50 times stronger than heroin. Opioids, also called narcotics, broadly work by binding to opioid receptors in the brain and spinal cord, triggering changes in nerve cell signaling that prevent pain and can create a euphoric high.

But these opioid receptors are also found in the part of the brain that controls breathing, so fentanyl can also reduce respiration to a deadly degree if used in excess. A 2-milligram dose of fentanyl — similar in volume to about a dozen grains of salt — can be fatal, according to the Drug Enforcement Agency (DEA).

If a person overdosing on fentanyl is treated with naloxone (better known by the brand name Narcan), quickly enough, these effects can be reversed. This antidote also binds to opioid receptors, thus blocking the effects of fentanyl.

ARMR's vaccine takes a different approach: It works in the circulatory system, before the drug can reach the brain.

"This would be the first-ever treatment that does not work on the [opioid] receptor," Gage told Live Science.

What's in the vaccine?

To keep fentanyl from reaching the brain, the immune system must first recognize the drug. But fentanyl is a tiny molecule, not a pathogen like a virus, and immune cells don't naturally react to its presence.

To spur an immune response to fentanyl, the University of Houston's Colin Haile, an ARMR co-founder and scientific adviser, and his colleagues had to tie the opioid to something else.

They chose a deactivated diphtheria toxin called CRM197, a compound already used in vaccines on the market; once deactivated, the toxin is no longer toxic and instead helps rouse an immune response. To boost this immune response even further, they also added dmLT, a compound distilled from toxins produced by the Escherichia coli bacterium. This modified compound is not toxic itself, and it has also been tested in humans in trials of other, not-yet-approved, vaccines.

These two components are attached to a synthetic piece of the fentanyl molecule, which in and of itself cannot cause a high or pain relief.

When the immune system meets this combo of fentanyl fragments, CRM197 and dmLT, it builds antibodies that react to real fentanyl. These antibodies bind to the opioid, keeping it from crossing the brain's protective membrane — the blood-brain barrier — and then clearing it from the body.

In rat studies, the vaccine blocked fentanyl from entering the rodents' brain and also blocked the drug from depressing respiration and causing overdose.

How is the vaccine being tested?

So far, the studies on the vaccine have been in rodents, though dmLT and CRM197 have respectively been tested to some extent and are already used in other vaccines in humans. The protocol in rats is to give an initial dose of the fentanyl vaccine and then boosters three and six weeks out from the first dose, Haile told Live Science.

"The longest we've followed the animals in our studies is about six months and we saw complete blockade of fentanyl effects at six months post the initial vaccination," Haile said. It remains to be seen how that will translate to "human years," he noted, but lab rats live a couple of years in total, so the researchers think the vaccine will work for a long time in humans.

The initial human trials that will begin in early 2026 will enroll 40 people and will focus on detecting any safety issues with the vaccines, such as unwanted or dangerous side effects. Researchers will also draw blood samples from participants to make sure that the vaccine is spurring the creation of anti-fentanyl antibodies.

If these Phase I trials are successful, the next step will be Phase II trials to test the vaccine's efficacy — how well the vaccine blocks fentanyl's effects. In these trials, not only will antibody levels be tracked over time, but some participants will also be dosed with safe levels of fentanyl used for pain relief in medical procedures. This will be done under close supervision, to check that the vaccine works in the presence of the drug.

Are there potential drawbacks to the vaccine?

Fentanyl has legitimate medical uses as a painkiller, especially in emergency situations. One concern about the vaccine is that people who take it will lose this option for pain relief.

However, the antibodies created by vaccination do not bind to other opioids — such as morphine, oxycodone or methadone — or to other pain-relief options, Haile said. That means there are alternatives if people who get the vaccine need pain relief down the line.

The drug also does not interfere with buprenorphine, a drug used to treat opioid use disorder by reducing withdrawal symptoms and cravings. Haile said he and his team are currently testing the vaccine in combination with naltrexone, a non-opioid medication also used to block the effects of opioids in treatment of substance use.

In theory, it might be possible to take enough fentanyl to override the body's supply of anti-fentanyl antibodies, Haile said. However, given that the vaccine blocks fentanyl's euphoric effects, he expects people who want to quit will not be motivated to try to work around it.

"We want people who want to quit, want to not use the drug," he said. "That will give them a chance to realize that they won’t get high from this drug and there is no use in taking it any longer."

Who might benefit from the fentanyl vaccine?

Gage suggested that one market for the vaccine could be first responders concerned about accidental fentanyl exposure. (That concern has risen in recent years with the spread of misinformation about fentanyl.)

For clarity: if fentanyl gets on your skin via casual exposure — for example, if you touch an object that's been exposed to the drug — it will not absorb through the skin. Meaningful absorption through the skin requires direct contact to the drug over hours or days. That said, if an EMT or police officer gets the drug on their hands and then touches their mouth or eyes, they could feel some of the drug's analgesic, or pain-relieving, effects, Haile said.

The vaccine could also be "an extra tool in the toolset" for people with opioid use disorder, Gage said. Combining the vaccine with "robust" cognitive behavioral therapy, a type of talk therapy, and communal support could be "incredibly beneficial to people who are just looking for another lifeline to help themselves get better," he said.

Finally, the vaccine could be beneficial for people who use less-deadly drugs — such as cocaine, stimulants or painkillers — that they buy on the black market. That's because these drugs are increasingly cut with fentanyl, meaning people may overdose without even knowing they are taking the opioid.

"I had two close childhood friends who passed away from fentanyl overdose," Gage said. "Neither of them were seeking it out."

Over 48,000 people are estimated to have died of opioid overdoses in 2024 in the U.S., according to provisional data. Perhaps due to this high death toll, early research suggests that people with personal experience with opioid use disorder and the general public alike view a possible anti-fentanyl vaccine positively. Time will tell how the new vaccine will perform in human trials, but if eventually approved, it could be a first-of-its-kind tool against overdose deaths.

This article is for informational purposes only and is not meant to offer medical advice.

1. Secrets of the world's oldest woman

Maria Branyas Morera, once the world's oldest woman, died in 2024 at age 117. Live Science took a deep look at a study that examined Branyas' biology and uncovered key traits that may have protected her from disease in old age. Could lessons from the study help others lead longer, healthier lives?

2. What makes us human?

Many consider the brain to be a central feature of what makes us human — but how did the remarkable organ come to be? In an interview, science communicator Jim Al-Khalili discussed what he learned from shooting the new BBC show "Horizon: Secrets of the Brain," which tells the story of how the human brain evolved. And in a book excerpt and interview with Live Science, neuroscientist Nikolay Kukushkin described the evolutionary forces he believes were key to the formation of the human brain and consciousness as we know it.

3. Could lab-grown brains gain consciousness?

Miniature models of the human brain can be grown from stem cells in the lab, and they're getting more and more advanced. Some scientists have raised concerns that these "minibrains" could become conscious and feel pain. We investigated experts' concerns and hopes for future regulation of the research.

4. The promise of mRNA medicine

mRNA may be best known for forming the basis of the first COVID-19 vaccines, but it could also be used in revolutionary cancer therapeutics, immune-reprogramming treatments and gene therapies. The promise of these emerging mRNA medicines is staggering, but due to the politicization of COVID-19 shots in the U.S., mRNA research and development — even unrelated to vaccines — now hangs in precarious uncertainty. A Science Spotlight feature described emerging mRNA technologies and their wobbly status under the second Trump administration.

5. Cancer in young people

You may have heard that more young people are being diagnosed with cancer. But which types of cancer are driving this trend? And why are the rates going up in the first place? We looked at what may be driving this pattern, from underlying cancer triggers to better techniques for early detection.

6. Male vs female brains

Is there really a difference between male and female brains? And do we even have the data required to answer that question? A Science Spotlight explored the existing research on sex differences in the brain, finding the results murkier than one might expect. Headlines often proclaim that male and female brains are "wired differently," and that may be true in some subtle ways. But the biological consequences of those differences remain unclear, even to experts in the field.

7. AI is designing viruses

Artificial intelligence can now be used to design brand-new viruses. Scientists hope to use these viruses for good — for example, to treat drug-resistant bacterial infections. But could the technology usher in the next generation of bioweapons? An analysis probed this dual-use problem and what can be done to safeguard our biosecurity.

8. When pandemics are a "certainty," how do we prepare?

In a book excerpt, epidemiologist Dr. Seth Berkley explained how he and other health leaders orchestrated a massive vaccine rollout to poor countries during the COVID-19 pandemic, so that the shots wouldn't exclusively be hoarded by wealthy nations. Live Science also spoke with Berkley about the lessons learned from the pandemic and the ongoing fight for vaccine equity.

9. USAID cuts

The United States Agency for International Development (USAID), once the world's largest foreign aid agency, was hit by massive funding cuts under the second Trump administration. A few of its functions will reportedly continue, under the control of the Department of State. We looked at the predicted and devastating effects that the loss of USAID will likely have on HIV care worldwide. And in an interview with author John Green, who published a book on tuberculosis (TB) this year, we explored what the cuts could mean for TB patients.

10. Microplastics on the brain

A study went viral after suggesting that healthy human brains may contain a similar amount of plastic as the average plastic spoon. But should we really be concerned? Our analysis broke down what we know and what we don't about microplastics in the brain.

11. Dodging early Alzheimer's disease

A man genetically guaranteed to develop early Alzheimer's disease is still disease-free in his 70s. We explored the details of the man's case, digging into his genetic profile and the broader lessons it could teach scientists about dementia.

12. Mental health after weight-loss surgery

Weight-loss surgeries often come with improvements in mental health — but research revealed that this effect is less tied to the weight loss itself and more connected to the relief from stigma that people often experience post-procedure. We examined this finding and what it can tell us about the profound impact of weight stigma on people's health and well-being.

13. Measles makes a comeback

In 2000, the United States hit a public health milestone by eliminating measles. But now, there's been a sustained resurgence of the highly infectious disease, putting the country on the brink of losing that precious elimination status. This story explained how we got here and what's at stake. And in an opinion piece, several experts called out the anti-vaccine movement that drove down measles vaccination rates — a movement that health secretary Robert F. Kennedy Jr. has been spearheading for years.

14. Is America losing the war on cancer?

In a book excerpt, Nafis Hasan argued that the United States has been employing the wrong strategies to fight cancer for decades. While hyperfocusing on finding treatments for individuals with cancer, America has largely ignored population-level strategies that could help drive down cancer rates and cancer deaths across the board, he argued.

15. Threats to fetal tissue research

The U.S. federal government is threatening to restrict research conducted with human fetal tissue. In an opinion piece, cell biologist, geneticist and neuroscientist Lawrence Goldstein dispelled widespread myths and misinformation about this type of research.

16. "The Big One," a disaster to dwarf COVID-19

Epidemiologist Michael Osterholm predicts that the next pandemic could be even worse than COVID-19. In a book excerpt and interview with Live Science, Osterholm described the lessons we should have taken away from the coronavirus pandemic, and how recent changes in U.S. policy may have destroyed our capacity to handle serious outbreaks.

17. Climate change may drive up hyponatremia

As the planet warms, a dangerous condition called hyponatremia may be on the rise. The condition causes a dramatic decline in sodium in the body, which can potentially cause seizures, coma and death. A Live Science exclusive looked at the emerging trend.

18. Baby-making robots?

A viral story suggested that researchers in China were working on a "pregnancy robot" that could gestate a human baby from conception to birth. It turns out that the story was complete fiction — but, in theory, could such a technology be realized? Experts weighed in on the sci-fi-sounding idea and discussed whether, eventually, it could be feasible to build a bona fide pregnancy robot.

People with typical recognition capabilities are worse than chance: more often than not, they think AI-generated faces are real.

That's according to research published Nov. 12 in the journal Royal Society Open Science. However, the study also found that receiving just five minutes of training on common AI rendering errors greatly improves individuals' ability to spot the fakes.

"I think it was encouraging that our kind of quite short training procedure increased performance in both groups quite a lot," lead study author Katie Gray, an associate professor in psychology at the University of Reading in the U.K., told Live Science.

Surprisingly, the training increased accuracy by similar amounts in super recognizers and typical recognizers, Gray said. Because super recognizers are better at spotting fake faces at baseline, this suggests that they are relying on another set of clues, not simply rendering errors, to identify fake faces.

Gray hopes that scientists will be able to harness super recognizers' enhanced detection skills to better spot AI-generated images in the future.

"To best detect synthetic faces, it may be possible to use AI detection algorithms with a human-in-the-loop approach — where that human is a trained SR [super recognizer]," the authors wrote in the study.

Detecting deepfakes

In recent years, there has been an onslaught of AI-generated images online. Deepfake faces are created using a two-stage AI algorithm called generative adversarial networks. First, a fake image is generated based on real-world images, and the resulting image is then scrutinized by a discriminator that determines whether it is real or fake. With iteration, the fake images become realistic enough to get past the discriminator.

These algorithms have now improved to such an extent that individuals are often duped into thinking fake faces are more "real" than real faces — a phenomenon known as "hyperrealism."

As a result, researchers are now trying to design training regiments that can improve individuals' abilities to detect AI faces. These trainings point out common rendering errors in AI-generated faces, such as the face having a middle tooth, an odd-looking hairline or unnatural-looking skin texture. They also highlight that fake faces tend to be more proportional than real ones.

In theory, so-called super recognizers should be better at spotting fakes than the average person. These super recognizers are individuals who excel in facial perception and recognition tasks, in which they might be shown two photographs of unfamiliar individuals and asked to identify if they are the same person or not. But to date, few studies have examined super recognizers' abilities to detect fake faces, and whether training can improve their performance.

To fill this gap, Gray and her team ran a series of online experiments comparing the performance of a group of super recognizers to typical recognizers. The super recognizers were recruited from the Greenwich Face and Voice Recognition Laboratory volunteer database; they had performed in the top 2% of individuals in tasks where they were shown unfamiliar faces and had to remember them.

In the first experiment, an image of a face appeared onscreen and was either real or computer-generated. Participants had 10 seconds to decide if the face was real or not. Super recognizers performed no better than if they had randomly guessed, spotting only 41% of AI faces. Typical recognizers correctly identified only about 30% of fakes.

Each cohort also differed in how often they thought real faces were fake. This occurred in 39% of cases for super recognizers and in around 46% for typical recognizers.

The next experiment was identical, but included a new set of participants who received a five-minute training session in which they were shown examples of errors in AI-generated faces. They were then tested on 10 faces and provided with real-time feedback on their accuracy at detecting fakes. The final stage of the training involved a recap of rendering errors to look out for. The participants then repeated the original task from the first experiment.

Training greatly improved detection accuracy, with super recognizers spotting 64% of fake faces and typical recognizers noticing 51%. The rate that each group inaccurately called real faces fake was about the same as the first experiment, with super recognizers and typical recognizers rating real faces as "not real" in 37% and 49% of cases, respectively.

Trained participants tended to take longer to scrutinize the images than the untrained participants had — typical recognizers slowed by about 1.9 seconds and super recognizers did by 1.2 seconds. Gray said this is a key message to anyone who is trying to determine if a face they see is real or fake: slow down and really inspect the features.

It is worth noting, however, that the test was conducted immediately after participants completed the training, so it is unclear how long the effect lasts.

"The training cannot be considered a lasting, effective intervention, since it was not re-tested," Meike Ramon, a professor of applied data science and expert in face processing at the Bern University of Applied Sciences in Switzerland, wrote in a review of the study conducted before it went to print.

And since separate participants were used in the two experiments, we cannot be sure how much training improves an individual's detection skills, Ramon added. That would require testing the same set of people twice, before and after training.

Here are 12 of our most intriguing Diagnostic Dilemmas from the past year. (If descriptions of medical symptoms and procedures make you squeamish, proceed with caution.)

1. Boy spoke foreign language after surgery

A Dutch teenager got knee surgery to treat a soccer injury, and upon waking up from anesthesia, he spoke only English — a language he'd previously spoken only in language classes at school. He kept insisting he was in the U.S., did not recognize his parents, and could not speak or understand spoken Dutch, his native language. Exams turned up no neurological abnormalities, and the doctors didn't initiate any specific treatment to address the language issue. Within 18 hours of surgery, the boy could understand some Dutch but not speak it without struggling. But then suddenly, he could both understand and speak it as normal. The doctors described the event as a strange case of "foreign language syndrome."

2. Woman with no vaginal opening gets pregnant via oral sex

A teenager reported to a hospital with abdominal pain, and examinations soon revealed that she was nine months pregnant and that she was having contractions. When doctors examined the patient's reproductive tract, they found that she lacked a vaginal opening — a rare condition called distal vaginal atresia. Because of this, the medical team had to deliver the baby — a healthy, 6.2-pound (2.8 kilograms) boy — via cesarean section. The teenager had been seen at the same hospital about nine months prior, when an ex stabbed her after finding her fellating a new boyfriend. The wounds she incurred during the stabbing likely allowed sperm to escape her digestive tract and make their way to her reproductive tract, resulting in an unlikely pregnancy, her doctors theorized.

3. Man stabbed by huge fish

A man was brought to a hospital by boat and helicopter after incurring an injury while fishing. He'd caught a white marlin (Kajikia albida) — a large fish with a long, pointy "bill" — and when he leaned over the edge of his boat to release his hook from the fish, it jumped up and struck him. At the hospital, doctors found a fragment of the fish's bill lodged in the man's throat, spinal canal and base of his skull. With an emergency surgery and antibiotics to prevent infections, the man survived the encounter without any long-term symptoms.

4. Acupuncture led to joint injury

A woman with osteoarthritis of the knee began getting acupuncture regularly when her pain medications started causing bad stomach issues. But her knees then became very sore, and she went to a hospital to be examined. X-rays revealed areas of her joints and shinbones where the bone tissue had thickened and spurs had formed. Additionally, hundreds of tiny flecks could be seen around both knee joints. It turned out that the woman's acupuncturists had left golden threads inside her knees on purpose as part of her treatment. In other cases, these threads have caused cysts and tissue damage, which can happen when they migrate through the body.

5. Man experiences rare meat allergy

A man in Michigan went to an ER with swollen eyelids and an itchy rash, and he noted that he'd also been experiencing cramps, nausea, abdominal pain and vomiting over the preceding days. When doctors examined the patient, they uncovered signs of anaphylaxis, a severe allergic reaction, and his condition quickly progressed to shock. The medical team successfully stabilized the patient, but a few days later, his condition worsened again. At that point, the doctors spotted a pattern: The symptoms arose when the man ate red meat. An allergy to meat, a condition called alpha-gal syndrome, can be triggered by the bite of certain tick species. It turned out that the man was an avid deer hunter who likely encountered an adult tick or tick larvae while hunting, his doctors concluded.

6. Woman had XY chromosomes in her blood

A woman had her chromosomes checked following a pregnancy loss to see if there might have been an underlying genetic reason for the miscarriage. The test revealed that, at least in the woman's blood, her chromosomal profile (or karyotype) was 46,XY — the typical karyotype among males. Further tests revealed that across the rest of her tissues, her karyotype was 46,XX, the typical chromosomal profile of a female. The woman had a fraternal twin, so in this case of "chimerism," the doctors concluded that the XY chromosomes likely came from her brother in the womb but somehow assimilated them only into her blood cells. The doctors suspected the "veins and arteries of the two children became intertwined in the umbilical cord" at some point. The woman had no overt symptoms tied to carrying these chromosomes in her blood and later went on to carry a pregnancy that resulted in the birth of a baby boy.

7. Woman injects herself with black widow venom

A woman visited an emergency room with a headache, severe cramps and muscle pain, as well as an elevated pulse, breathing rate and blood pressure. She told doctors she'd attempted to get high by injecting a ground-up black widow spider (Latrodectus) into her veins in a suspension of distilled water. The doctors suspected the injected dose of black-widow venom was likely much higher than one would get from a bite, and its effects may have been exacerbated by the patient's allergic reaction to proteins in the venom. After the patient had been treated for several days in an intensive care unit, her symptoms resolved and she was discharged.

8. Nut allergy was triggered by ejaculate

A woman developed hives, swelling under her skin and trouble breathing after having sex with her partner. While receiving treatment at a hospital, she reported having a known allergy to Brazil nuts. She said that her partner ate them a few hours prior to sex but that he'd taken a bath and washed his hands thoroughly before intercourse. When the doctors conducted a skin-prick allergy test, using samples of the partner's semen, before and after he ate Brazil nuts, they found that the allergy triggers could indeed pass through the semen and set off the woman's allergy.

9. Rash mysteriously migrated

Following a cancer treatment, a man developed a red rash that started out near the anus and then spread rapidly to the trunk and limbs. The rash, which looked like wavy lines all over the patient's body, appeared to migrate, with the lines starting out in one spot and later moving across the skin. A stool test revealed Strongyloides stercoralis, a parasite that can cause an infection called strongyloidiasis in humans. These worms were migrating under the man's skin, and the infection likely arose because the patient's immune system was stunted by glucocorticoids used in his cancer treatment.

10. Rare tooth-in-eye surgery performed

A rare autoimmune disorder injured a man's corneas and extensively impeded his sight. To restore vision in one eye, doctors attempted an osteo-odonto-keratoprosthesis, or "tooth-in-eye surgery." The procedure involves removing one of the patient's teeth and implanting it in their eye socket, where it serves as a platform for a transparent, plastic lens. The lens stands in for the injured cornea and enables light to enter the eye. The man's successful procedure was the first of its kind in Canada.

11. "Muscle-plumping" injections cause calcium spike

A man went to a hospital because he was experiencing weakness and vomiting. There, tests revealed that his kidneys were failing and the calcium in his blood was too high. Physical exams and scans revealed abnormalities in his upper-arm and chest muscles — namely, areas of superdense calcification. It turned out that the man had previously gotten injections of silicone-like, oil-based substances to "plump" up the look of his muscles. In this case, the injections triggered a persistent foreign-body reaction, resulting in extensive scarring and calcification of the muscle that leached calcium into the bloodstream.

12. Scientist catches plague from defanged bacteria

A lab worker came down with an infection that, despite medical treatment, ended up being fatal. His doctors were informed that the patient had worked with a weakened strain of Yersinia pestis, the bacterium that causes the plague. This weakened form of the germ was thought to be noninfectious, but nonetheless, the man contracted it. Further tests revealed that the man had unusually high levels of iron in his blood. One way the plague bacteria had been weakened was that its key gene for absorbing iron had been removed — but the man's blood, which was chock-full of iron, may have enabled the germ to overcome this weakness and establish a deadly infection.

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

This article is for informational purposes only and is not meant to offer medical advice.

How many Diagnostic Dilemmas have you read — and can you guess the diagnosis? Take our quiz that draws from the cases we highlighted in 2025 and see if you can figure out each patient’s ailment. Tell us how you got on in the comments below.

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That's the question posed by a study published in November in the journal Cancer. Conducted by researchers at the cancer detection-test company Exact Sciences, the paper models how cancer care for five million U.S. adults might be changed by easy access to blood tests designed to spot many cancers — known as multicancer early detection (MCED) liquid biopsy tests.

The study suggests the tests could save lives by catching cancer at earlier stages, when it's more easily treated. It predicted that, over a decade of use, MCEDs could reduce stage IV cancer diagnoses in the U.S. by 45%, compared to the current standard-of-care.

But for now, liquid biopsies that test for multiple cancers still have unacceptably high false-positive rates. And even when they don't, there aren't clear guidelines for how to integrate them into the standard-of-care. That means they aren't going to make their way into the clinic in the near term, experts told Live Science.

Before the transformative effect predicted by the Cancer paper can be borne out, doctors will need to figure out how to best use these tests in the clinic.

The pitch for liquid biopsy

The idea behind liquid biopsy tests is that they enable clinicians to look for cancer without going anywhere near the tumor itself, Dr. Carolina Reduzzi, an oncologist and director of the liquid-biopsy platform at Weill Cornell Medicine, told Live Science.

"It's like translating a tissue biopsy into the blood," said Reduzzi, who was not involved in the Cancer report. These tests can detect various signs of cancer, including individual circulating tumor cells (CTCs), chunks of tumor genetic material floating in the bloodstream, and even tiny fragments of tumor cells.

Because they do not direct tumor sampling, liquid biopsy tests are comparatively simpler and less invasive. Additionally, the hope is that if clinicians regularly repeat liquid biopsies, they could build up a picture of how a tumor changes in response to treatment.

If a patient's tumors contain many genetically distinct cells, tissue biopsies that only sample one portion of the tissue may provide a biased view of their disease, said Reduzzi. Liquid biopsy, in contrast, should provide a broader picture of a patient's cancer by making it easier to analyze cells from multiple tumor sites.

Which tests are in use now?

To date, the U.S. Food and Drug Administration (FDA) has approved five liquid biopsy diagnostic tests, each for single types of cancer. These tests have been validated via assays that compared their ability to detect signs of cancer against tests that sample tumor tissue.

No MCED tests are currently approved or available through routine clinical care, although some, like Exact's Cancerguard and GRAIL's Galleri, are available in the United States as "laboratory-developed tests" (LDTs). LDTs exist in a regulatory gray area in which they are not formally approved by the FDA but are available to patients through their clinicians or independent telemedicine providers.

Dr. Iseult Browne, a clinical oncologist based at the Royal Marsden Hospital in London and the U.K. Institute of Cancer Research, said that progress in Europe is patchier. The U.K.'s National Health Service is conducting a trial of Galleri based on data from 140,000 participants. That data will be released next year.

Browne and Reduzzi noted that inertia in the field of oncology could delay the further rollout of liquid biopsies. Oncologists have, for decades, built diagnostic and treatment plans based on data from tissue-biopsy analyses. Shaking these entrenched practices, even with data showing the utility of liquid biopsies, is difficult.

Even with single-cancer tests, Browne says that standardization is an issue. "Everyone is using a different assay," so making head-to-head comparisons to decide which test is best can be confusing. Different trials have been analyzing different markers of cancer, at various timepoints in disease progression, she said.

'Less optimistic' predictions

Ruth Etzioni, a biostatistician at Fred Hutch cancer center in Seattle, leads a multi-institute effort to review emerging cancer treatment and diagnostics. Similar to the Cancer report, Etzioni's team has modeled the impact of MCEDs and predicts that they would allow cancers to be detected at earlier stages.

However, she added, "our numbers are a little less optimistic."

The tests' helpfulness varies by cancer type, because it hinges on how long different cancers remain in each stage of progression. If a cancer lingers longer in stage I and II, then MCED tests would be well-placed to diagnose it early. But if a cancer rapidly progresses to stage IV, then the test will be less useful, Etzoni explained.

The question of how long different cancers stay in each stage is still a matter of debate. The "dwell times" used in the recent Cancer report leaned more optimistic, assuming that cancers would progress slowly enough for an annual MDEC test to make a difference.

Another reason MCED tests are not ready to replace existing diagnostics is that some analyses will always require a tissue biopsy, and current medical guidelines advise doctors to make some clinical decisions based on tumor-tissue samples.

"Immunotherapy is given in some cases based on how much your tumor has leukocytes [immune cells] infiltrating the tumor," Reduzzi said. "You cannot get that in the blood." All the researchers interviewed for this article agreed that a positive on a liquid biopsy test would need to be followed up with further testing before any cancer treatment was initiated.

So, multicancer tests may diagnose cancer earlier, but whether that early diagnosis will lead to lower death rates will depend on whether those confirmation tests happen quickly, Etzioni said. And those follow-up tests also have to be up to the task of identifying early-stage cancer, she noted.

Fixing false positives

Emerging MCEDs also have issues with false positives, Browne said. Early, non-peer reviewed data from the ongoing trial shows that Galleri was extremely good at identifying people without cancer — correctly identifying people without the disease 99.6% of the time. But meanwhile, roughly 40% of the patients that the test diagnosed with cancer were actually cancer-free.

This number of false positives puts unnecessary worry on the patient, said Browne, and each false positive could trigger follow-up tests that people would not have gotten otherwise. If scaled up to the millions of people at elevated risk of cancer, it would significantly burden any health system that adopted the tests.

To reduce false-positive rates, future studies will need to find more reliable signals of cancer to detect. Detecting information from other cell types, like immune cells, has been shown to improve test specificity. Improvements to laboratory standardization could also help cut the false-positive rate.

Browne hopes that liquid biopsy could someday help patients avoid the sapping side effects that were once unavoidable parts of cancer treatment. For instance, an ongoing trial at the Royal Marsden Hospital is assessing whether a test could identify breast cancer patients who don't need post-operative chemotherapy. The test enables the doctors to assess a patient's risk even after their tumor has been removed because it looks for tumor DNA in the blood.

Reduzzi believes that optimized multicancer tests — which would identify a large fraction of people who have cancer while having a low false-positive rate — will transform cancer diagnostics, and that such tests are on the horizon.

"I don't think we have a test that is there," she said. "But I think we will. With time."

Editor's note: This story was updated on Jan. 5, 2026, to clarify a comment from Dr. Iseult Browne and correct the name of the ongoing Galleri trial.

This article is for informational purposes only and is not meant to offer medical advice.

The symptoms: The man went to the urology unit of a hospital after urine had been leaking out of small holes in his perineum — the skin between the penis and anus — for about two weeks. This condition is known as "watering can" perineum. The man had a history of various urinary problems, such as a poor stream, discharge from the urethra, urine dribbling, and a burning sensation while peeing.

What happened next: Because the man had a poor urinary stream — meaning his urine didn't flow as quickly or forcefully as usual — the doctors had to drain his full bladder before they could explore the cause of the leakage in his perineum.

The doctors attempted to insert a catheter through the urethra and into the bladder, creating a tunnel for urine to flow into a bag. However, as they tried to push the tube, they hit a wall. Something was blocking the catheter's path.

The doctors instead made an incision in his abdomen and inserted a catheter into the bladder that way, bypassing the urethra altogether. Once urine began to flow, they tested it for signs of infection and found Staphylococcus aureus bacteria. These bugs are an uncommon cause of urinary tract infections and usually appear only when there is a physical abnormality blocking urine flow, which allows this species to remain in the bladder and thrive.

The doctors referred the patient to the radiology department to get scans of his bladder and search for signs of such physical abnormalities. To visualize the bladder in X-ray scans, the radiologists administered an X-ray-sensitive dye through the abdominal catheter. This revealed that the bladder had inflated at its base, leaving a pointy tip.

The diagnosis: This condition is known as a "Christmas tree" or "pinecone" bladder, owing to its appearance.

The X-rays confirmed that urine had been blocked from leaving the organ. Yet a closer inspection of the bladder revealed no issues with the organ itself, such as an obstructing mass or bladder stones. This led the doctors to wonder if an obstruction was located elsewhere.

Further X-ray imaging revealed that the urethra had narrowed significantly about halfway up its length, cutting off urine flow. This condition is called a urethral stricture and has a multitude of causes.

Often, it arises following a pelvic injury or physical trauma, such as from falling onto a bicycle's crossbar. It can also stem from sexually transmitted bacterial infections or appear if a tumor presses against the tube. Sometimes, the condition has no identifiable cause. (The exact reason for this man's condition wasn't noted in the report of his case.)

The treatment: The doctors treated the man's staph infection with antibiotics and performed an operation to restore the urethra's channel. Surgery can offer some respite from the condition, but urethral strictures often reoccur, the doctors noted in the report.

What makes the case unique: A urethral stricture is an unusual cause of Christmas tree bladder. Normally, a bottleneck in the urethra slows urine flow, leading to some degree of distension in the bladder, but not so much that the organ would widen at the base into a tree-like shape.

The "Christmas tree" swelling is usually caused by a problem with the nerves that control bladder contractions, thus preventing it from emptying properly. Often, this occurs following nerve damage from a spinal cord injury, stroke or neurodegenerative disease, such as multiple sclerosis. Alternatively, it can arise if the neck of the bladder becomes constricted or choked, such as by an inflamed prostate in men.

This article is for informational purposes only and is not meant to offer medical advice.

The minimally invasive wireless device, which is placed under the scalp, receives inputs in the form of light patterns, which are then conveyed to genetically modified neurons in brain tissue.

In the new study, these neurons activated as if they were responding to sensory information from the mice's eyes. The mice learned to match these different patterns of brain activity to perform specific tasks — namely, to uncover the locations of tasty snacks in a series of lab experiments.

The device marks a step toward a new generation of BMIs that will be capable of receiving artificial inputs — in this case, LED light — independent of typical sensory channels the brain relies on, such as the eyes. This would help scientists build devices that interface with the brain, without requiring trailing wires or bulky external parts.

"The technology is a very powerful tool for doing fundamental research," and it could address human health challenges in the longer term, said John Rogers, a bioelectronics researcher at Northwestern University and senior author of the study, which was published Dec. 8 in the journal Nature Neuroscience.

Bypassing the sensory system

The device, which is smaller than a human index finger, is soft and flexible, so it conforms to the curvature of the skull. It includes 64 tiny LEDs, an electronic circuit that powers the lights, and a receiver antenna. Additionally, an external antenna controls the LEDs using near-field-communications (NFC) — electromagnetic fields for short-range communications as is done for contactless card payments.

The compact device is designed to be placed under the skin, rather than being implanted directly into the brain. "It projects light directly onto the brain [through the skull], and the response of the brain to that light is generated by a genetic modification in the neurons," Rogers told Live Science.

Brain cells don't normally respond to light that is shone on them, so gene editing is required to make that happen.

"The genetic modification creates light-sensitive ion channels," Rogers explained. When activated by light, these channels allow charged particles to flow into brain cells, tripping a signal that then gets sent to other cells. "Through that mechanism, we create light sensitivity directly in the brain tissue itself," he said. The genetic modification of the brain cells was done using a viral vector, a harmless virus made to deliver the desired genetic tweak into specific cells in different regions of the brain.

The use of light to control the activity of genetically modified cells is called optogenetics, and it's a relatively new science. In past work, the researchers used a similar approach to activate just one group of brain cells, but the new device enabled them to toggle the activity of many neurons across the brain.

"[The genetic modification] is not just stimulating the part of the brain that's naturally responsible for visual perception, but across the entire surface of the cortex," Rogers said. Thus, sending different patterns of illumination creates a corresponding distribution of neural activity. "It's like we can project a series of images — almost like play a movie — directly into the brain by controlling [the] sequence of patterns."

The researchers tested the implant in the mice by wirelessly instructing it to produce various patterned bursts of light. The mice were trained to respond to each pattern with a specific behavior, indicating that they could distinguish between the patterns transmitted. With each type of signal, they had to go to a specific cavity in a wall, and for choosing correctly, they'd get sugar water as a reward.

Bin He, a neuroengineering researcher at Carnegie Mellon University who wasn't involved in the study, called it a novel technique for using light to tune circuits across the brain. "It may have various applications in neuroscience research using animal models … and beyond," he said.

For instance, the researchers see potential for this device in future prosthetics. Applications could include adding sensations, like touch or pressure, to prosthetic limbs, or sending visual or auditory signals to vision or hearing prostheses.

"Optogenetic techniques are just beginning to be used with humans," Rogers said. "There are tremendous advantages [to using light] because you don't need to disrupt the brain tissues. You can use different wavelengths of light to control different regions of the brain."

Rogers said that from a technology standpoint, the platform could scale to cover much larger areas of the brain and contain more micro-LEDs. However, they would have to rethink the power-supply requirements to support a larger device. It should technically work in humans as it does in mice, but further research will be needed before any tests are attempted in humans.

"The biggest hurdle is around the regulatory approval for the genetic modification," he said.

Brain quiz: Test your knowledge of the most complex organ in the body

Items like cameras, binoculars, and telescopes aren't impulse buys, and certainly not stocking fillers. They are also very personal purchases, and often expensive. Trusting someone else to make the right choice on your behalf is a gamble, and frankly, we wouldn't always recommend it.

If you're a skywatcher, you'll have a preference for what you like to look at; some telescopes will be more suitable for deep space explorations, and others will be best for planets. Similarly, photographers will know the subject matter they want to capture, which will dictate what the camera needs to be good at. Handling ISO well, a reliable autofocus? Mirrorless or DSLR? 12MP versus 61MP?

Nature spotters and birders will know what magnification and objective lens size they need for their binoculars, whether they need a waterproof or nitrogen-purged model, and whether they prefer coated or multi-coated lenses or Bk7 or BaK-4 glass. The list goes on.

There's a good chance someone buying a pair as a gift won't consider what you would if you were buying for yourself. But skywatching and camera equipment are often expensive, and deserve careful consideration. This is why self-gifting makes sense. Besides, we all like to splurge on a "me-to-me" every now and then!

That is why we created this self-gifting guide, which lists the binoculars, telescopes and cameras that we are more than happy to recommend this season. Each item below links to an in-depth review conducted by our staff writers or experienced freelance contributors.

We do, of course, have individual guides to the best cameras, best binoculars, and best telescopes, but this guide has been curated based on what our editors would buy for themselves — and have, in some cases — in each of the categories below.

Binoculars

This first section is for skywatchers who don't want a telescope, as well as wildlife watchers and birders. Other people might think they know what you want, but it really pays to do the research for yourself. Binoculars aren't just about how powerful they are.

Binoculars vary depending on their purpose. Stargazing, birding, wildlife spotting and sports viewing will all require different objective lens sizes, have more suitable fields of view, and require different quality glass and coatings. For example, a pair that is ideal for astronomy might be too heavy and impractical for long walks, while compact travel binoculars might fall short under dark skies.

Comfort is also a crucial consideration. Weight, balance, eyecup design, interpupillary distance (will you use them whilst wearing spectacles?) and grip all affect how long you can comfortably use a pair of binoculars for. These are things only you can judge.

Comfort aside, optical preferences are personal, too. Some people might prioritize brightness, whereas others prefer edge-to-edge sharpness or excellent colour accuracy.

Binoculars are typically a long-term investment. A well-chosen pair can last decades. It’s worth making sure they suit your needs now and into the future. Here is a list of binoculars that we believe strike the perfect balance between performance, versatility, and ease of use. Each one is a standout choice in its category.

Telescopes

Next up, we have telescopes — and as previously touched on, which is the right telescope for you depends on exactly what you want to observe.

Do you want to see local planets and the moon, or deep-sky objects? Do you want to use it for astrophotography? Do you need to move it from A to B often? Do you have space to store it in your house, assembled or not? There are lots of things to consider. Things which others might not think of.

Telescopes also have different experience requirements. Some are usable right out of the box, whereas others are reserved for advanced users. A well-meaning gift can be too complex, causing the recipient frustration, or too basic, making it difficult for a budding astronomer to advance. Only you know your experience and/or patience level.

When so much money is being spent on telescopes, whether it is your own or not, there should be no compromises. You want something that will provide enjoyment on every clear night you can be outside. Here are some of our recommendations.

Cameras

A camera is another (and probably the most important) purchase in this guide that is best made by you, rather than guessed at by someone else. You want something that matches your skill level and ambition. Plus, photography is intensely personal, and it is difficult to buy a camera for someone else.

Each style of camera, and even each manufacturer, will have its own particular strengths. Ergonomics also matter. Button layouts and menu styles are a matter of personal preference. Specs like autofocus systems, number of megapixels and ISO handling will depend on the style of shooting. Even questions like how your computer handles image files are things only you will know the answer to (and the frustration of your computer not being able to cope!). If you're already a photographer with an ecosystem of lenses and accessories, you don't want to have to change that because someone thought they were doing the right thing by getting you an "upgrade".

Finally, it goes without saying that cameras are expensive. Buying your own camera gives you the exact tool to suit your vision as a photographer. Here are some of our recommendations for self-gifting.

Surprisingly, no: The teenage growth spurt is only the second fastest that humans can grow.

"We've been tracking children's growth from birth all the way through to adulthood, and the fastest period of growth is clearly the first couple of years during infancy," Sean Cumming, a professor in the Department for Health at the University of Bath in the U.K., told Live Science. "That's when children are growing most rapidly."

Babies can add nearly 1 foot (25 to 30 centimeters) of height per year — more than double the rate of even the most dramatic teenage growth spurts.

In fact, for girls, "at 18 months, they will be 50% of their adult size," Adam Baxter-Jones, a professor in the College of Kinesiology at the University of Saskatchewan in Canada, told Live Science. Boys reach 50% of their adult size at 24 months, he said.

Then, things slow down. "When we get into late infancy and childhood, physical growth is put on the back burner," Cumming said.

Growth drops to about 2 to 2.5 inches (5 to 6 centimeters) per year from age 4 until puberty, according to Baxter-Jones. That's when humans hit their second-fastest period of growth.

At their peak during puberty, girls grow an average 3.5 inches (9 centimeters) per year, and boys grow an average of 4 inches (10 centimeters) per year, according to a study in the Journal of Adolescent Health.

But those average peak growth rates are just that — averages.

"If we measure regularly enough, what we see is these periods of really, really intense growth, and then the body adapts afterward," Cumming said. "We can see rates of anywhere up to about 20 centimeters [nearly 8 inches per year] in some of the studies that we've looked at … of course, if you average that over a period of time, [you get] 10 to 12 centimeters [4 to almost 5 inches] per year."

Just as they did when they were babies, girls go through their growth spurts earlier — around 11 years old, while boys usually enter puberty around two years later.

"Boys will typically have a slightly more intense growth spurt," Cumming said. "That's because they produce more growth hormone, but also testosterone, which is also contributing to bone length."

The pubertal growth spurt stops at around age 16 for girls and 18 for boys — and because boys both have that more intense growth and grow for around two years longer, they end up taller on average.

The age at which someone hits their growth spurt doesn't affect their final height — someone who matures early stops growing sooner than someone who matures later, so someone who matures late has more time to grow, Baxter-Jones said.

Growth spurts and body shape

Growth spurts happen from the outside in. "First it's the feet and the hands, and then it's the long legs and the long arms. That's why you see kids just at the start of puberty, they look like baby giraffes. They've got these big clown feet, these legs that go on forever," Cumming said.

The torso grows last — and if a child develops late, sometimes the torso never quite catches up with the rest of the body. As a result, in sports like ballet and gymnastics, teams select for late developers because they have a more linear physique and longer legs, according to Cumming. However, early developers have their own athletic advantages.

"If you get a puberty growth spurt early, you're bigger, stronger. Those are the kids that get selected for all the top positions and into the top academies," Cumming said. "In the Scottish Academies we surveyed over a thousand kids beyond 14 years of age. We didn't find any late developers at all."

But that rapid growth comes at a cost. During growth spurts, bones are weaker and more susceptible to damage.

"Your bones grow, and then they mineralize. There's about a nine month gap there," Baxter-Jones said. "The peak fracture rate is during that adolescent growth spurt."

Muscles and tendons also take up to nine months to catch up with the growing bones, which can lead to growth-related injuries, especially around the heel, knee and lower back.

However, monitoring growth spurts carefully can help prevent more serious problems. "If we do that in the Premier League academies, we can reduce those non-contact injuries by about 70%," Cumming said.

For parents wondering if their child's growth pattern is normal, both experts emphasized that wide variation is expected.

"It's normal to grow quickly, but it's also normal to grow slowly," Baxter-Jones said. Final adult height comes down to genetics. There are also rare conditions in children, such as pituitary gigantism, that lead to excessive production of growth hormone. Children with this condition can grow up to 6 inches (15 cm) a year, and one report documented a 13-year-old boy growing 7.5 inches (19 cm) a year. But even this fast growth is less than the rate at which babies grow.

So what's the fastest a human can grow? The answer isn't when you're stretching out of your jeans as a teenager — it's when you were too young to remember it happening at all.

Previous studies suggested that the body's internal clock, the circadian rhythm, can influence how well immune checkpoint inhibitors work. These drugs help the immune system recognize and attack cancer cells by blocking tumors' ability to shut those immune responses down.

In several cancers — such as kidney, liver, stomach, esophagus, and head and neck cancers, as well as melanoma — giving this treatment in the morning has been associated with better outcomes than giving it in the late afternoon or evening.

Now, the new study, published Dec. 8 in the journal Cancer, shows that the time of day a drug is delivered also affects extensive-stage small cell lung cancer (ES-SCLC) — a fast-growing cancer that is typically associated with a poor prognosis and accounts for about 15% of new lung cancer cases.

This study is "very important," said Dr. Francis Lévi, a medical oncologist and founder of the Chronotherapy Group at Warwick University, who was not involved in the work. It extends earlier research he did with the same team, which involved different lung cancer types and different immune checkpoint inhibitors but produced similar results.

"Early time of day of immune checkpoint inhibitors, as single agents or combined with chemotherapy or antiangiogenics [drugs that starve tumors of blood], significantly improves treatment efficacy compared to later dosing times," Lévi told Live Science.

Other experts not involved in the study agreed that the results were impressive. In a joint statement, oncologist Dr. Pasquale Innominato and circadian biologist Robert Dallmann, both at Warwick University, and oncologist Dr. Seline Ismail-Sutton at the Ysbyty Gwynedd Hospital in Wales, told Live Science they were "impressed by the large effect of time-of-day of immunotherapy administration on overall survival," calling it "a very meaningful difference."

Tweaking treatment timing "represents a simple, low-cost adjustment with the potential to deliver meaningful improvements in patient outcomes … without adding new drugs or complex interventions," they said.

Earlier treatment, longer survival

In the study, researchers from the Affiliated Cancer Hospital of Xiangya School of Medicine at Central South University in China analyzed data from nearly 400 patients with ES-SCLC, a cancer with a median survival rate of 14 months. All the patients received a standard, initial immunotherapy in combination with chemotherapy between May 2019 and October 2023.

Each patient's average treatment time of day was calculated based on the first four therapy cycles. The researchers then compared survival outcomes for patients treated at different times of day, between 11 a.m. and 4:30 p.m. They matched the patients to ensure that the main thing that differed between them was the treatment timing, not baseline characteristics, such as age or sex.

3 p.m. marked a critical cutoff point. Patients who generally received treatment before 3 p.m. survived significantly longer without their cancer progressing. They also had longer overall survival over the next five years, compared with those treated later in the day.

Even after accounting for other factors that could influence the patients' outcomes, this earlier treatment time remained a strong, independent predictor of better survival.

The study findings align with laboratory studies that suggest killer T cells — immune cells that can directly kill cancer — tend to migrate into tumors in the morning, said Dr. Chi Van Dang, a professor of cancer medicine at Johns Hopkins University, who was not involved in the study. Therefore, aligning immunotherapy with this migration may help it work better, he told Live Science.

Personalized 'chronotherapy'

The large sample size of the study was a strength, but the research has some caveats.

Lévi pointed out that most patients were men, for example. The pronounced timing effects did not seem to extend to the women in the study, but this may come down to there being few women included, the study authors wrote, so it bears exploring in larger studies.

The study found that patients who received immunochemotherapy before 3 p.m. lived nearly twice as long as those treated later in the afternoon. However, this picture isn't completely clear, Lévi said, because the study doesn't pinpoint the best cutoff time for care. "This results in an uncertainty regarding the most appropriate cut off time, that actually could be located between 11:30 and 15:00," he said.

Additionally, because the study looked back at past patient data, stronger evidence will still need to come from randomized clinical trials, in which different treatment timings are explicitly tested and compared against one another. Most evidence of the benefits of early treatment "comes from retrospective studies," Innominato and colleagues said, "with only one prospective trial completed and additional trials now in development."

Assuming trials show positive results, there could still be logistical hurdles to overcome. "If treatment were restricted to a single time window, such as the morning, clinical units could quickly become overwhelmed," Innominato and colleagues said.

It's important to note that the "optimal window" for treatment may not be universal among patients, they added. It may partially depend on each individual's biological rhythms and lifestyle characteristics.

Chronotyping — categorizing people as "morning larks" or a "night owls” — could "align therapy with each patient's internal clock, accounting for individual variability and thus boosting efficacy while easing pressure on clinical units by distributing treatments across the day," they suggested. "The challenge now is to develop quick, reliable ways to identify chronotype and scale this approach, and dedicated studies are already underway."

This article is for informational purposes only and is not meant to offer medical advice.

The symptoms: The man suddenly developed numbness on his left side, as well as unsteadiness.

What happened next: Upon the man's admission to a hospital, his blood pressure was found to be 254/150 millimeters of mercury (mm Hg), according to a report of the case. That extremely high reading indicates a hypertensive crisis. A neurological exam confirmed that he had numbness across the entire left side of his body and that he had trouble coordinating movements with his left arm and leg.

A CT angiogram — a scan that details the blood vessels, including blockages and damage — showed signs that the man may have experienced a sudden spasming and narrowing of the cerebral arteries, an event known as reversible cerebral vasoconstriction syndrome (RCVS). Additionally, an MRI showed tissue death in the thalamus, which acts as a relay station for motor and sensory information; specifically, he had damage in the thalamus located on the right side of the brain.

There were no other notable findings on the patient's exam, and his medical history lacked any history of smoking, alcohol use or substance abuse. The report describes him as "normally fit and well."

The diagnosis: The man was diagnosed with a right thalamic lacunar stroke. A lacunar stroke happens when a blood vessel that carries blood to one of the brain's deep structures gets blocked. Right-sided strokes affect the sensation and movement on the left side of the body, and vice versa.

The treatment: The man was treated with a combination of physiotherapy and occupational therapy while at the hospital, and he began taking blood thinners to help prevent another stroke. He also began taking a cholesterol-lowering drug and blood-pressure-lowering medications.

The man had several follow-up appointments over the next three months. "He appeared to have made an excellent functional recovery, although the sensory symptoms [of numbness] were persistent and deteriorated throughout the day," his doctors noted. His blood pressure had also remained persistently high, so he began taking additional blood-pressure drugs.

At that point, the doctors asked the patient more questions about his lifestyle and learned that he consumed an average of eight cans of a "high-potency" energy drink each day. Each can contained 160 milligrams of caffeine per 16 fluid ounces, adding up to about 1.2 grams of caffeine a day. (Less than 400 milligrams is considered a safe daily dose of caffeine.)

The patient was advised to stop consuming energy drinks, and his blood pressure quickly fell to normal levels. He was able to stop taking all of his prescribed medications within three weeks of quitting the drinks.

"Further follow-up at 3 and 6 months showed complete resolution of hypertension and a complete recovery from the stroke with full return to work," his doctors reported. Eight years later, he had had no further strokes, though he still had lingering sensory issues on his left side from the first stroke.

What makes the case unique: Although he was otherwise healthy, the man's excessive consumption of energy drinks appeared to have driven his high blood pressure and subsequent stroke.

The case report authors noted that the high caffeine levels were likely a big culprit, but they hypothesized that other common ingredients in energy drinks may have contributed to the stroke risk. For instance, when combined with caffeine, taurine and guarana may amplify the stimulant's blood-pressure-boosting effects and its effects on blood-vessel constriction, they theorized. Taurine, an amino acid, is often added to energy drinks for its purported ability to increase exercise capacity, while guarana is a plant that is similarly perceived to have health benefits and whose seeds contain caffeine.

Additionally, the high sugar content of many energy drinks may further raise the risk by causing inflammation and dysfunction in the lining of blood vessels.

The authors cited a handful of published medical case reports in which the excessive consumption of energy drinks or of individual energy drink ingredients was tied to cardiovascular issues, including dangerously high blood pressure.

They concluded that "both acute and chronic intake" of energy drinks may increase the risk of cardiovascular disease and stroke.

"Healthcare professionals should consider specific questioning related to ED [energy drink] consumption in young patients presenting with stroke or unexplained hypertension," they concluded. Importantly, the risk seems to be reversible, they added, given that quitting energy drinks appears to resolve the related problems.

For the patient's part, he said, "I obviously wasn't aware of the dangers drinking energy drinks were causing to myself. [I] have been left with numbness [in my] left hand side hand and fingers, foot and toes even after 8 years."

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

This article is for informational purposes only and is not meant to offer medical advice.

There are many theories as to why daytime heart attacks are more harmful; some point to daily fluctuations in stress hormones and blood pressure as possible culprits. But the role of the immune system has remained less clear.

Earlier research showed that immune cells called neutrophils, which act as first responders to injury, cause more inflammation and collateral tissue damage at injury sites during the day. They are relatively calmer at night.

Now, in the new study, published Dec. 12 in the Journal of Experimental Medicine, scientists connected the dots between daytime heart attacks and aggressive neutrophils.

More damaging by day

By analyzing clinical records from more than 2,000 heart attack patients, the team found that patients admitted during daytime hours showed higher neutrophil counts and greater heart damage, suggesting neutrophils themselves might play a role in worsening the injury. They then confirmed the same pattern in experiments with mice.

The researchers split their lab mice into two groups: one with normal neutrophil levels and one whose neutrophil levels were depleted with an antibody treatment. Then, they induced heart attack in the mice at different times of the day and night.

In the first set of mice, they observed a pronounced rhythm of greater heart injury in the morning than at night, similar to what was seen in the human data. However, in the mice with low neutrophil counts, this rhythm disappeared and the heart attacks caused less damage overall.

To test the idea further, the researchers genetically disabled a gene that helps control the circadian clock, a regulator of 24-hour cycles in the body. As they expected, the rhythm again disappeared and the overall heart damage was reduced in these modified mice.

Importantly, although depleting neutrophils hobbles the immune system, deleting just the clock gene didn't impair the mice's ability to fight infections, the scientists found.

"This makes the study really interesting," Tim Lammermann, an immunologist at the University of Münster in Germany who was not involved in the work, told Live Science. That's because it was always believed that immune protection and inflammatory damage caused by neutrophils "cannot be disconnected from each other."

Putting neutrophils in 'night mode'

Next, the scientists wanted to test whether there might be another way to control this gene and mimic the body's natural nighttime calming of neutrophils without diminishing the cells' numbers. They focused on a receptor on neutrophils called CXCR4, which typically responds to signals that slow down neutrophil activity at night.

They genetically engineered mice to carry really high concentrations of this receptor. This calmed the cells down even during the daytime, so the heart injury was again alleviated and the rhythmic pattern disappeared.

Finally, using a drug that activates this receptor, the researchers toned down neutrophil activity during the day, pushing the cells into their nighttime state. Treatment with this drug prior to heart attack reduced tissue damage and improved heart function weeks after the event, they found.

What's more, in mouse models of sickle cell disease, in which neutrophils clog blood vessels and trigger rampant inflammation, the drug reduced blockages and improved blood flow.

It's surprising that controlling just one type of immune cell offered significant protection against these inflammatory injuries, senior study author Andrés Hidalgo, an immunologist at Yale University, told Live Science.

Lammermann noted that the experiments with the drug were particularly significant, providing evidence that the compound reduced the inflammatory response of neutrophils while keeping their defense mechanisms intact.

The researchers also uncovered an interesting pattern behind the neutrophil action: In skin wounds and heart tissue alike, daytime neutrophils tend to spread into neighboring uninjured areas, enlarging the injury site, Hidalgo explained. Calmer, nighttime neutrophils, on the other hand, stay confined to the center of the damaged zone.

The findings suggest there could be ways to fine-tune neutrophils and tone down their aggressiveness without compromising their defense capability. However, translating this approach to humans will require careful study. The ways in which CXCR4 signaling affects other types of cells would also need to be carefully considered, Lammermann cautioned.

A drug that calms down inflammation without compromising immunity would be the holy grail of immune therapy. However, human trials for such a drug would need to assess many factors, such as the timing of when it should be given in the event of a heart attack, and if there are any potential risks involved, he added.

This article is for informational purposes only and is not meant to offer medical advice.

Imagine you're walking a well-worn route home, but you accidentally take a wrong turn. It doesn't take long for your brain to sound alarms to tell you that you've gotten lost.

The new study, published Dec. 4 in the journal Nature Communications, combined high-powered brain imaging and virtual reality (VR) to reveal what happens in the brain when we explore both familiar and unfamiliar environments.

"When you move to a new city or travel somewhere, it doesn't happen that you just become familiar," study co-author Deniz Vatansever, a neuroscientist at Fudan University in China, told Live Science. "You have to explore your environment to become familiar with it." Vatansever and his team aimed to re-create this experience in VR.

They recruited 56 healthy volunteers ages 20 to 37, each of whom navigated a virtual world while inside a scanner. They explored the virtual environment — a grassy field surrounded by mountains — while looking for six "items" hidden throughout it. Vatansever's team monitored the volunteers' brain activity with functional MRI, a technique that tracks blood flow through the brain, as they explored familiar and unfamiliar areas of this world.

The team zoomed in on the hippocampus, a brain region that's important for memory and navigation. The seahorse-shaped hippocampus is rich with place cells, which light up in response to specific locations. Previous research had shown that one end of the hippocampus contains cells that fire when we think about location in a broad sense, such as where landmarks are in a nearby city. At the other end, place cells activate when we think about specific locations, like where we keep a box of cereal in our kitchen.

Between the "head" and "tail" of the hippocampus seahorse is a gradient of activity linking these broad and fine-tuned representations of locations. But no one had previously examined the organization of cells that respond to the newness or familiarity of a place.

Vatansever's team found that the head of the hippocampus contains cells that fired when their participants explored areas they had been in previously. Cells at the tail responded to new locations. And the whole region was arranged in a gradient, from familiar to unfamiliar.

"You could see that there's this shift in level of novelty versus familiarity as you go from one end to the other," Vatansever said.

Previous research produced mixed results on which areas of the hippocampus respond to novelty or familiarity in the environment, said Zita Patai, a cognitive neuroscientist at University College London who was not involved with the research. "What they're showing is that [the discrepancy] might partially be due to the fact that it's a gradient," she told Live Science.

Other brain areas also responded differently to new and familiar locations. A region in the cortex — the brain's higher-thinking hub — had a cone-shaped gradient. "At the very center of it are bits that 'prefer' more familiarity. And as you move out, then there is greater and greater preference for being active for novelty," Vatansever said.

The team also probed whether navigating familiar and unfamiliar areas activated broader brain networks, or groups of cells spread throughout the brain that often activate in sync. Familiar areas activated networks previously linked to motor control and memory, whereas novel areas activated networks associated with focus and perception.

This division may help the brain adapt to new environments by focusing on and absorbing relevant details, Vatansever said. Then, memory and motor control combine to help navigate familiar areas, he proposed.

The findings may explain some of the earliest signs of dementia, Vatansever suggested. The cells within the gradients in the cortex and hippocampus happen to be among the first brain areas affected by Alzheimer's disease. Both the front and rear regions of the hippocampus are equally vulnerable in the condition's early stages.

Louis Renoult, a cognitive neuroscientist at the University of East Anglia who was not involved with the research, said the paper demonstrated the strong links between navigation and memory.

The brain areas that help us navigate are also key for episodic memory, which relates to specific events in our lives rather than to factual knowledge, Renoult told Live Science. Episodic memory is also especially vulnerable in the early stages of Alzheimer's.

A better understanding of how navigation is encoded in the brain could reveal measurable signs of dementia's earliest stages, when the ability to navigate begins to falter.

"If you wanted to enhance people's ability to be independent, you'd want them to be able to go to new places and understand new things," Patai said. "In that sense, the link between spatial novelty and memory is really interesting."

Rather than cluttering your bathroom with multiple gadgets, this clever device combines high-frequency sonic brushing and powerful water flossing into a single unit. The result is a system that looks good and performs well.

We've been using this sonic toothbrush meets water flosser for around a month, and we've already given our separate flosser away — no, really. Our last water flosser was a novel idea at first, but in reality, after a couple of days' use it was sent to the cupboard — probably when the battery first died — where it stayed gathering dust, bar the odd occasion when we remembered we had one! With the Soocas NEOS II, we found it much easier to maintain a consistent routine.

For us, it replaced the electric toothbrush and separate water-flossing combo, and now the NEOS II sits proudly on the sink, always charged and ready to go. There are some drawbacks but overall, we were pleasantly surprised by this unique bit of kit.

Soocas NEOS II 2-in-1 toothbrush review

Soocas NEOS II 2-in-1 toothbrush review: Design

• IPX8 Waterproof rating
• Available in two colorways
• Packaged in recycled sugarcane

The first thing we'll acknowledge is the packaging, which is made from recycled sugarcane — something we hope to see more of across the board. Sugarcane husk is an existing waste product: it's the dry, fibrous pulp left over after sugarcane stalks are crushed to extract their juice. A natural, plant-based material, it doesn't require extra land or deforestation, requires less energy than paper and cardboard made from wood pulp, and biodegrades in around 90 days.

A great first impression, even though the toothbrush itself isn't made from recyclable materials (as the SURI is, for example).

The Soocas NEOS II looks like a normal, albeit chunky, electric toothbrush. That's because a 50 ml water tank built into the handle feeds the flosser. Sure, this isn't as compact as having a "regular-sized" electric toothbrush, but it certainly beats having a separate brusher, flosser and a different charger for each.

The only thing we will say about the water tank is that we wish it were accessible from the front. A couple of times, we loaded up our toothbrush with toothpaste, forgetting to fill up with water. You can guess what happened when we turned the toothbrush upside down to fill the tank.

We tested the Deep Violet version of this toothbrush, though we'd consider it more like a navy blue. It also comes in Pearl White. Both designs are discreet and would blend with any decor, but the noticeably large handle does make it stand out; you'll likely get questions from house guests who haven't seen one before.

Soocas decided to build the NEOS II to IPX8 waterproofing, meaning it can be submerged to a depth of 6.5 feet (2 meters). So if you really want to multitask your way through your morning routine, you can safely use it while showering.

Soocas NEOS II: Features

• Built-in water flosser
• Two modes with three pressure modes each
• No smart features

Obviously, the main feature of this 2-in-1 water flosser is that it combines a sonic toothbrush and a water flosser. One handheld device that does both jobs, so you only need one charger and one step in your teeth-cleaning routine.

There isn't an accompanying app or any particular smart features, but there are two programs.

The first, Quick Floss, is described as a 60-second "brush and flush" cycle with a fixed intensity, and is recommended for quick refreshes after mealtimes or snacks. The other mode is Deep Clean, which provides two minutes of brushing time, followed by a one-minute brush and flush. You can adjust the intensity of this mode from one to three. It is recommended that new users start on the gentle setting and gradually build up to the most intense setting as their gums adjust to the new routine.

The best way to use this toothbrush is to let it do all the hard work. Move it slowly along your teeth. Vibration reminders remind you when to move to a different part of your mouth, then a more intense vibration reminder alerts you when the flosser is about to start. You can pause the program by quickly pressing any button, then press it again to restart, or you can long-press any button to turn the toothbrush off.

The standard Soocas NEOS II ships with a water tank cleaner, two brush heads (so you can share immediately if you wish) and a magnetic charger. There is no plug adapter (the bit that goes into the wall), but we didn't mind — we have plenty around the house. There is also an "Ultimate" set that ships with two extra heads and a handy travel case. Replacement heads cost around $30 for a pack of two, and it is recommended that you replace them every three months.

We were quite happy with the functionality of this toothbrush, and we felt it did a good job – without needing an app to tell us exactly where we've brushed and flossed and where we might have missed, though perhaps some users would like this functionality. We typically brushed for as long as each program lasts (three minutes or one minute), so there's no need to use a separate timer.

Soocas NEOS II: Performance

• More than 30 days of battery life
• No brush-only mode
• Noticeable results after a short amount of use

The Socas NEOS II has a built-in, rechargeable 2600mAh lithium-ion battery that lasts more than 30 days. At around 28 days in, we're still using it on its first charge, and the battery indicator is still showing a breathing green light, which means there's still somewhere between 30% and 100% charge.

When it changes to a breathing red light, we know there is less than 30%. A constant flashing red light means there's less than 10%, and we need to plug it in. It takes about 8 hours to fully charge, so it's best to do this overnight, ready for the morning.

We were very happy with the Soocas NEOS II's brushing performance, and noticed a change in the feel of our teeth after just a few days. Remember, we went from not flossing very often, or only when we remembered, to flossing every time we brush thanks to the convenience.

There is no brush-only mode. Instead, you have to stop the deep clean program partway through, before the flosser kicks in. Sometimes you just want to give your teeth a good old-fashioned scrub, so it might be worth keeping a manual toothbrush aside for these occasions, but overall, your teeth will definitely feel like they're getting extra care and attention, and they will feel and look cleaner in the gaps, too!

Sooca NEOS II toothbrush: User reviews

There were 688 global ratings on Amazon at the time of writing, and the NEOS II scored an admirable 4.5 out of 5, with over 74% of users awarding it 5 stars.

The worst ratings weren't particularly helpful, with one being "rubbish that's all I can say" and someone else saying they "didn't feel like it does a good job at cleaning or flossing."

On the other hand, there were plenty of reviews raving about the toothbrush. One user said: "This 2-in-1 toothbrush is a game-changer for oral hygiene." Another claimed, "It’s perfect for my busy lifestyle," while a third said, "The built-in water-flosser makes my teeth feel extra clean without needing a separate device."

Should you buy the Soocas NEOS II toothbrush?

✅ Buy it if: You want to improve your dental hygiene routine but keep things simple. With one device to brush and floss, there's no excuse for skipping flossing, as we often did before.

❌ Don't buy it if: You want something with app functionality. Some users want visual feedback from an accompanying app, but you won't get that with the NEOS II.

If this product is not for you

If you want a toothbrush with smart features, the Oclean X Pro Digital Sonic gives you detailed feedback on brushing coverage. During our review, we were impressed by its brushing efficiency and by how immaculately clean our teeth were, which is ultimately what we strive for in any toothbrush.

If you'd prefer visual and vocal feedback over using an app, consider the Oclean X Ultra S. The world's first talking toothbrush, it is also customizable to a wide range of brushing needs and offers an impressive 40-day battery life.

For a great value-for-money option, have a look at the Bitvae R2. This oscillating toothbrush costs just $34.99 and is often further discounted during sales events like Prime Day and Black Friday. It comes with seven spare brush heads, features five cleaning modes and includes a pressure sensor, a feature usually only found on more expensive models.

Soocas NEOS II Toothbrush: How we tested

We spent almost a month testing the Soocas Neos II toothbrush daily. We wanted to see how easy it would slot into or change our morning routine, and considered the design, brushing performance, battery life, functionality and value for money. We also tested its IPX8 waterproof rating by submerging the toothbrush for the full three-minute deep clean cycle.

The study found that 14 psychiatric disorders can be classified into five major groups, depending on the genetic variants associated with them. For instance, the findings group together anorexia nervosa, obsessive-compulsive disorder (OCD) and Tourette's syndrome according to their shared genetic profile.

The findings, published Dec. 10 in the journal Nature, suggest that disorders within the same group may stem from shared biological mechanisms. An understanding of these common pathways could help scientists develop treatments that work across multiple mental health conditions, the team said.

Chunyu Liu, a professor of psychiatry and behavioral sciences at SUNY Upstate Medical University who was not involved in the study, said the findings make sense based on existing research.

"Even before seeing the results, this is generally expected," Liu told Live Science in an email. "The shared genetics between schizophrenia and bipolar disorder pointed us in this direction [as a field]."

He agrees with the study authors' conclusion that shared genetics point to shared biological mechanisms. However, Liu noted that the study does not explain why clinical symptoms vary so widely between these disorders, even when the underlying genetics overlap.

"It is an important paper, but still a small step toward understanding the disorders," he said.

Genes aren't the whole story

The study showed that many of the genetic variants linked to psychiatric disorders are also linked to other traits, including intelligence; sleep problems like insomnia; personality; social behaviors like aggression; and socioeconomic status.

"Not all of these links are negative," Abdel Abdellaoui, a geneticist at the University of Amsterdam who was not involved in the study, wrote in a commentary article for Nature. For example, the genetic overlap between schizophrenia and bipolar disorder is also associated with traits that can support academic success, such as creativity and persistence.

This nuance matters because embryos used for in vitro fertilization (IVF) are sometimes screened for psychiatric risk factors, which are measured via the embryo's genetics. Parents-to-be then have the option to select embryos with lower "risk scores" for psychiatric disorders. But this choice isn't necessarily clear-cut, Abdellaoui argued. Carrying certain genetic traits doesn't guarantee a disorder will emerge, and the same genes can influence positive traits, such as creativity or resilience, he noted.

Abdellaoui said psychiatric disorders often appear at the extreme ends of a natural range of genetic variation, especially when combined with certain life experiences. In other words, a person can have a genetic predisposition for a given disorder but not ultimately develop it unless they encounter certain adverse events, whether trauma or environmental hazards.

"This should reframe mental illness not as defective biology, but as the unfortunate intersection of natural variation and environmental stress," he said.

The five groupings

To study which genetic variants are unique to each disorder and which are shared across disorders, Andrew Grotzinger, an assistant professor at the Institute for Behavior Genetics at the University of Colorado Boulder and his colleagues analyzed genetic information from more than 1 million people who primarily had European ancestry.

Disorders that share many genetic variants were dubbed "genetically correlated." Using these correlations, the scientists found that the 14 disorders fell into five genomic factors:

Five genomic factors

• Compulsive: Anorexia, OCD, Tourette's
• Neurodevelopmental: Autism, ADHD
• Internalizing: Depression, PTSD, anxiety
• Substance use: Alcohol, cannabis, nicotine and opioid dependence
• Schizophrenia-bipolar

Each genetic factor showed a unique biological pattern, in terms of how the associated genes behave in the brain. For example, genes linked to the schizophrenia-bipolar factor are strongly active in excitatory neurons, which push other neurons to activate, and in brain areas involved in interpreting reality.

Genes linked to the internalizing factor are associated with glia, the brain's support cells. Glia serve as immune protection and maintain connections between neurons, among other roles. This implies that these disorders may relate more to these support cells than to neurons, Abdellaoui said.

The substance-use factor included gene variants that encode the enzyme responsible for breaking down alcohol, and others that encode the receptors that respond to nicotine.

Liu cautioned that these genetic links to psychological disorders should be interpreted carefully. "Genes or biological pathways statistically associated with a disorder should not be interpreted as causal without additional evidence supporting a direct mechanistic role," he said. In short, correlation does not imply causation.

"There are multiple alternative explanations for why a gene is associated with a disorder," he said, "or why two disorders exhibit overlapping genetic signals."

This article is for informational purposes only and is not meant to offer medical advice.

While this is a budget fitness tracker, that doesn't mean it's lacking in features. You can do more than just track your workouts with this smart band: you can also track your sleep, stress levels, heart rate and so much more. There's also no shortage of sports modes — with 150+ to choose from, you're bound to find the workout you want on this watch.

While the Xiaomi Smart Band 10 has a few features the Xiaomi Smart Band 9 doesn't, such as underwater real-time heart rate monitoring, running courses and a larger screen, there are also plenty of similarities between the two. Both offer three weeks of battery life, and neither has its own built-in GPS, for a start. But how does the Xiaomi Smart Band 10 perform compared to its predecessor, which we placed in our best budget fitness trackers guide?

Xiaomi Smart Band 10 fitness tracker review

Xiaomi Smart Band 10 fitness tracker: Design

• Strap is difficult to put on alone
• Charger is USB-A – we'd prefer USB-C
• Comfortable to wear, day and night

The Xiaomi Smart Band 10 is a small yet surprisingly well designed fitness tracker. Unlike other smartwatches, with huge watch faces that protrude from your wrist, the Xiaomi Smart Band 10 is nice and sleek. With a face that measures only 1.72 inches (44 millimeters) diagonally, ultra-thin bezels of just 0.07 inches (2 mm) and a weight of 0.56 ounces (15.95 grams), this fitness tracker is barely noticeable when it's being worn.

The screen is an AMOLED display and performs well in direct sunlight — not once did we struggle to see the details on the screen in any light. But while the slender screen is a welcome relief from bulkier fitness trackers, we did find the strap rather annoying to put on alone.

Our sample was the Midnight Rose variation and came with a light pink TPU strap, where you need to press the button into the strap. However, due to the strap's flexibility, it's hard to tighten the strap and push the button in without losing tightness, and we found it easier to have someone help us. After a while, we managed it alone, but this was frustrating at first.

Saying that, you can change the strap if you find this irritating. There's a quick-release button on the back, which you can press with a fingernail and release the strap with no fuss. There are many alternative options, including leather, metal and silk knitted straps, as well as the option to turn it into a pendant.

We liked how many watch faces there are for you to download for free on the Mi Fitness App, and there are even more if you are happy to pay a little. This means you can personalize your watch and change things up if, like us, you get bored with the same image as your watch background.

As we've already mentioned, the watch face is slender and unobtrusive. There are also no buttons that can be accidentally pressed during mid-workout, or that will interfere if you have your wrist bent in a Pilates, yoga or exercise class, for example. With other fitness trackers we have sometimes found the buttons an irritation during classes, or they have caught on long-sleeve tops. You don't have this issue with the Xiaomi Smart Band 10, so you can trust your data will be not be ruined by accidental presses.

Apart from our slight irritation with the strap at the start, the only other annoying thing about the design of this watch is that the charger is a standard USB-A connector rather than USB-C. For some, this might not be an issue, but we had to hunt around the house to find a charging plug with a USB port — most other items in our home require USB-C, so receiving a new fitness tracker with what we'd call an outdated port was surprising. This meant we couldn't easily charge it while at our laptop, for example, which would have been nice.

This is only a minor issue, but it's something to be aware of if you're thinking of buying one.

Xiaomi Smart Band 10 fitness tracker: Performance

• Accurately recorded most health stats
• Incredible battery life for a budget tracker
• Location tracking performed poorly

Let's start with some of the basic requirements of a comfortable and reliable fitness tracker. The screen was durable and didn't mark during a testing period in which we wore it every day for two weeks (plus many other days after this, on and off, mainly because we liked it). There is not a single scratch or mark to be found — impressive for a fitness tracker that only costs a little over $45.

However, the light colored pink TPU strap did start to look a bit dirty, mainly around the loop where the strap slides together. This isn't very noticeable but there's a slight color change towards a gray. But, seeing as you can personalize this watch with other straps, this isn't a huge problem.

Our main negative was the comfort of this watch — we loved the slender screen, but you need to have this watch done up really tight to get it to stay in place. Tightness also aids the accuracy of the stats, but it felt too tight to be comfortable sometimes. When we chose to wear it on the looser notch, this inevitably meant the tracker would slide down our wrist during exercise, sacrificing the accuracy of the data. Of course, it could just be that our wrists were of a size in-between the available notches, and perhaps a different strap would have worked better.

But let's look at the positives of this amazing budget fitness tracker. The battery life is utterly astounding. We only needed to charge it once in three weeks. That's two weeks of testing the watch every day and night — we did one form of exercise every day, sometimes two, plus we wore it to bed every night — and then a last week when it was on and off our wrist on an "as and when" basis. That's incredible battery life and something that astounded us, given this watch's low price.

Another positive aspect of this watch's performance is related to the sleep tracking. We found it satisfyingly accurate in capturing when we fell asleep and when we woke up, plus any times we were disturbed during the night. The Mi Fitness app provides detailed information, capturing your sleep and wake times, quality of sleep, length of sleep, stages of sleep you experienced and for how long, and your average heart rate. Plus, there is the sleep improvement plan you can do to help improve the quality of your sleep.

However, where the Xiaomi Smart Band 10 fell a bit short was on its location tracking. While we didn't need to know the location of the walks we took with our dog, for example, we noticed the location tracking struggled as soon as we were in the countryside. And when we say countryside, we mean not the middle of nowhere but on the edge of a large town.

Seeing as the Smart Band 10 doesn't have its own GPS and relies on your smartphone's GPS, you will not be able to track your runs or walks if you lose phone signal. However, when walking around our local high street or neighbourhood, the smartwatch could locate us accurately.

Aside from this, we thought the Smart Band 10 did a good job of capturing our health stats, including BPM (when stationary and when exercising), max BPM when exercising and the start and end times of our workouts. We had no way of knowing if the calories burned were accurate, but when using the watch during walks, the step counts appeared to be accurate for the length of the walks we did, as did the average pace.

Xiaomi Smart Band 10 fitness tracker: Functionality

• Easy-to-use interface
• 5ATM water resistance
• 150+ sports modes for every form of exercise

There are so many functions to this fitness tracker that we're sure it will take you a while to get your head around everything it has to offer. Some functions you will find useful and come back to often, and some you may use once or twice and then forget about.

There is a wealth of data you can capture on this fitness tracker, but the interface itself is easy-to-use, and you'll be navigating around the watch within minutes. The only thing we found tricky at first was locating where the 150+ sports modes were — some are placed in obvious categories whereas others were hidden.

One clever thing this watch does, though, is that once you've located your training or sports mode a few times, it pops it into the menu you first see when clicking on the 'workout' tile on the main menu. So, realistically, you only have to go rooting around once or twice — after that, your most-used workouts are just a press away.

The Smart Band 10 has 5ATM water resistance, making it suitable for swimming. Plus, there is now real-time underwater heart rate monitoring, something the Smart Band 9 does not have.

While there are many things this watch can do, you can also monitor your stress levels, your oxygen levels and heart rate whenever you feel like it. Not only this, but with every workout you do, the watch can calculate your vitality score and training state, offering personalized recovery times in between your workouts. This will be useful if you are trying to return to fitness and an exercise routine, as well as for those training for a specific purpose, so you don't end up overdoing it.

For those looking for some guidance on runs, this watch has various running courses you can follow, from basic to advanced. These are easy to locate from the main menu, and once you've selected the one you would like to do, the watch gives you guidance on how long to run/walk for, helping you to slowly build your stamina. This is great for those looking to start running, allowing them to pace themselves to avoid overexertion.

One thing this watch lacks is the ability to detect when a workout has ended. This meant that a few times, our data was skewed as we forgot to stop our workout at the end of a class. Sometimes we ended up with data covering the walk back to the car, for example. While this isn't a huge problem — and understandable for a budget fitness tracker— it's important to remember to stop the watch whenever you finish working out.

The problem was that we often forgot we had it on in the first place, due to how lightweight it is!

Should you buy the Xiaomi Smart Band 10 fitness tracker?

We loved this budget fitness tracker, which would suit those starting out on their fitness journey, or those who aren't into tech and want to keep things simple. The interface is easy to navigate, the data and stats are digestible and we could not fault the battery life, which reduced any faff around having to remember to charge it regularly. The watch did a good job of capturing our health data after workouts, and we particularly liked the sleep data and sleep improvement plan. For beginners, the running courses and guidance are a fantastic way of building stamina.

There were a few things we may have changed if we were designing it, such as the strap and charging cable, but these are things others may not have an issue with. Overall this fitness tracker performed well, especially for the price.

If this product isn't for you

If you want a budget fitness tracker with a larger, squarer screen, the Amazfit Active may suit. Offering a 1.75 inch (4.4 cm) screen, the same water resistance of 5ATM, built-in GPS and 27 days of battery, this is a strong rival to the Xiaomi Smart Band 10.

If a larger screen is a priority for you, the Redmi Watch 5 offers a 2.07 inch (5.3 cm) colorful display.

If you're a runner, the Garmin Forerunner 165 will provide everything you need to sufficiently track your runs. Plus, being part of the Garmin family means you'll be getting quality without breaking the bank.

Alternatively, if you have the money to spend, the Garmin Vivoactive 6 may be a good option: we rated it the best for beginners in our best fitness trackers guide, as it offers guided walking workouts.

Traumatic tattoos are formed when everyday materials, like graphite, dirt or gravel; or metal pieces, like shrapnel, become lodged beneath our skin, leaving a visible (and often long-lasting) mark.

"It's when foreign particles like dirt, asphalt, metal, sand, etc become embedded into the skin's … dermis," Dr. Mara Weinstein Velez, a dermatologist at the University of Rochester Medical Center, told Live Science in an email. "And it happens more often than you'd think! Events like car accidents, scrapes and falls can cause this."

These residual marks don't always cause pain or even discomfort in the long term, but their appearances can last a lifetime. While some are born from truly traumatic events, like a motorcycle crash that ends in road rash, leaving gravel or asphalt trapped under the skin, or a gunshot wound that isn't fully cleaned, others originate from common experiences, like the poke of a pencil in an elementary school classroom.

Sometimes the material itself becomes unlodged naturally over time, and sometimes it travels nearby within the body. For instance, one child had a pencil lead in their hand travel to their wrist. But in these cases, particles sometimes remain at the original entry spot, which is why a dark-colored scar can be left behind, under the skin.

Although the presence of an old traumatic tattoo isn't necessarily harmful or worthy of a trip to the doctor on its own, experts say it's best to seek medical advice when you're first wounded. The biggest risk is usually the possibility of infection, as harmful bacteria can enter the body along with the foreign object. However, surgery may also become necessary if the object has migrated under the skin to a more risk-prone location or if it has become uncomfortable. Always consult a doctor if you experience this type of injury.

"It's very important to seek medical help right away to avoid infection, since it is a foreign object," Weinstein Velez said. "Treatments like minor surgeries, laser and dermabrasion can help safely remove the foreign matter from the skin."

People who work in physically demanding industries, like mining and construction, are more likely to develop traumatic tattoos in the workplace, as they're exposed to fast-moving foreign materials like silt and rock more often during their day-to-day life.

But the traumatic tattoos we're perhaps more familiar with are small, barely noticeable scars from pencils. Pencils are made with graphite, which is a soft mineral held together with clay and wax, and is considered nontoxic and safe. However, "a doctor will probably need to see deep stab wounds that go further than the skin and any that are close to the eyes," according to Missouri Poison Control.

Traumatic tattoos also appear frequently in the military, often from the enmeshment of gunpowder and ammunition under service members' skin after explosions or gunshots — and even during weapon malfunctions during live drills, as seen in one study conducted by researchers with the Department of Oral and Maxillofacial Surgery at the Womack Army Medical Center in North Carolina.

Even if not otherwise treated, traumatic tattoos can be addressed from a cosmetic standpoint. To disguise or cover these marks, dermatologists employ the same types of lasers that are typically used to remove professional tattoos, matching the color of the trapped pigment to the appropriate wavelength of light. The pigment fragments into smaller pieces when targeted by these lasers. However, because some tattoo colors are able to absorb a wider range of wavelengths than others, meaning they can be broken into even smaller particles that the immune system can then target, dermatologists use different tools on different marks depending on color and placement.

The laser "breaks up the pigment, and then your body's immune cells, called macrophages, clear out the pigments," said Dr. Anna A. Bar, a professor of dermatology and co-director of Mohs micrographic surgery at Oregon Health and Science University. "It's not an instant result — you have to wait like a month for the tattoo to fade."

Even though a traumatic tattoo may take time and multiple sessions to address, because there is usually less pigment involved, "they're often easier to remove than professional tattoos," she added. "Usually, it's a bit easier to remove amateur tattoos or traumatic tattoos."

This article is for informational purposes only and is not meant to offer medical advice.

Suze Lopez, a 41-year-old emergency room nurse from Bakersfield, underwent a procedure to have both the cyst removed and her baby delivered at the same time. The effort involved about 30 medical professionals at Cedars-Sinai Medical Center in Los Angeles.

Lopez began hemorrhaging after the baby was delivered but was stabilized by the medical team, who used 11 units of blood to do so, according to a statement from Cedars-Sinai. (For context, a typical blood donation is about one pint of blood, which is one unit.)

The baby, who weighed 8 pounds (3.6 kilograms) at birth and had a full head of hair, was quickly transferred to the neonatal intensive care unit (NICU) after birth. All things considered, he was remarkably healthy, his physicians said.

"I was amazed by this little guy," Dr. Sara Dayanim, a neonatologist with Cedars-Sinai Guerin Children's, said in a video accompanying the announcement. "He's defied all odds," she said.

How the pregnancy went undetected

The baby, named Ryu, was discovered because Lopez was scheduled to have a 22-pound (9.9 kg) ovarian cyst removed. The cyst was noncancerous, but it had been growing for years by the time Lopez was scheduled to undergo the surgery.

Lopez was used to experiencing irregular periods and abdominal discomfort, so she didn't expect to get a positive result on the pregnancy test prior to the surgery. She surprised her husband Andrew with news of the pregnancy while at a Dodgers baseball game in Los Angeles; the pair snapped a selfie together while holding up a Dodgers-branded onesie.

However, later at the game, Lopez started to have intense abdominal pain, and they immediately went to Cedars-Sinai.

Lopez arrived at the hospital with very high blood pressure, and as medical staff set about treating it, they also ran blood work and body scans, including an MRI and ultrasound. That's when they discovered that Lopez was carrying a rare abdominal ectopic pregnancy. The baby was situated near the liver, with his back half resting on top of the uterus.

"It was the baby growing in her abdomen behind the mass that was pushing everything out," Dr. John Ozimek, medical director of Labor and Delivery and the Maternal-Fetal Care Unit at Cedars-Sinai, said in the video. "So that's the reason she didn't know she was pregnant."

He added that "a pregnancy this far outside of the uterus that is living is pretty much unprecedented."

Ectopic pregnancies occur outside the uterus and account for roughly 2% of all pregnancies. All forms of ectopic pregnancy, in any location in the body, are life-threatening, as they can rupture organs and cause catastrophic bleeding and, potentially, shock due to blood loss. Ectopic pregnancies cannot be transferred into the uterus, and as such, medical guidance is to treat the condition by ending the pregnancy, either with medication or surgery.

The vast majority of ectopic pregnancies — about 95% — occur in a fallopian tube, a tube that shuttles eggs from an ovary to the uterus. Abdominal ectopic pregnancies, by comparison, occur in only about 1% of ectopic pregnancy cases.

If an ectopic pregnancy escapes notice — as in this case — it's very improbable that the fetus would develop normally outside the uterus. Thus, fetal death is likely.

That said, the medical literature includes a handful of unusual cases in which abdominal ectopic pregnancies were discovered very late in gestation and ultimately resulted in the birth of healthy babies.

In Lopez's case, "we had to figure out how to deliver the baby with a placenta and its blood vessels attached in the abdomen, remove the very large ovarian mass and do everything we could to save mom and this child," Dr. Michael Manuel, a gynecological oncologist at Providence Cedars-Sinai Tarzana Medical Center, said in the statement. And in the end, they were successful.

Lopez, who has a teenage daughter, had been hoping for a second pregnancy for years.

"I could not believe that after 17 years of praying, and trying, for a second child, that I was actually pregnant," she said in the statement. "I appreciate every little thing. Everything. Every day is a gift and I'm never going to waste it."

This article is for informational purposes only and is not meant to offer medical advice.

In a new study, published Dec. 10 in the journal Frontiers in Immunology, researchers zeroed in on a type of immune cell called natural killer (NK) cells that may play a key role.

The research was partly inspired by a 2022 national screening study conducted in Saudi Arabia that showed generalized anxiety order (GAD) was on the rise, and that the trend was most pronounced in women. People with GAD experience constant, uncontrollable worrying, and their concern is typically more intense than the situation calls for; this can cause an array of related symptoms, including sleep problems.

This finding led immunologist and lead study author Renad Alhamawi at Taibah University in Medina, Saudi Arabia, to explore how anxiety might affect immunity among women.

Alhamawi and her colleagues recruited 60 female students between ages 17 and 23 and asked them to fill out a questionnaire about their mental health. The responses showed that 75% reported symptoms consistent with GAD — such as feeling nervous, being so restless that it's hard to sit still, or becoming easily irritable— including 13% with severe symptoms. (Although the participants were screened for GAD symptoms, none were officially diagnosed as part of this study.)

About 53% of the cohort, or 32 students, reported not getting enough sleep.

Next, the researchers took blood samples from the participants and surveyed the levels of various immune cells, which revealed that those who experienced anxiety-like symptoms had 38% fewer NK cells than those without symptoms.

NK cells are one of the first types of immune cells to respond to an infection or to the presence of cancer in the body, and immunologists split them into two subsets. The first subset secretes enzymes that break down and "kill" diseased cells. The second subset works by secreting protein signals, called cytokines, that regulate other immune cells. A reduced abundance of these dual-action cells could potentially predispose individuals to disease.

The participants who reported anxiety symptoms had reduced levels of both subsets of NK cells, while people reporting insufficient sleep had 40% fewer of the immune-regulating subset of cells only.

Importantly, this study found only a correlation between these anxiety symptoms, sleep and reduced NK cell levels; the researchers have yet to explore a causal link, let alone investigate whether this drop in NK cells could lead to markedly higher rates of disease.

It is not yet clear what factors might be behind this change in NK cell abundance in the bloodstream. For example, it could be that the cells die off or that the body renews them at a slower rate.

Also, "focusing on circulating NK cells [in the blood] does not allow investigation of NK cells infiltrating the nervous system," Stefano Garofalo, an immunologist at the Sapienza University of Rome who was not involved with the work, told Live Science in an email. He speculated that the drop in NK cells could happen if they migrate from the bloodstream into nerve tissue in people who have anxiety or insomnia. His research focuses on how NK cells help regulate brain function and shape behavior in mice.

These findings are consistent with those from other research, such as a study on chronic tinnitus, wherein participants who reported higher stress levels had fewer cell-killing NK cells. Alhamawi said that the stress hormone cortisol may drive down NK cell populations because it is known to exert other immune-suppressing effects. For instance, cortisol can hinder antigen-specific T cells, a type of immune cell that recognizes features of specific threats, like viruses.

"Anxiety increases the level of cortisol, so we think it might affect the number of NK cells in an indirect way," Alhamawi said.

The current research has a few caveats. "The main limitation of the study is the very small participant group, consisting exclusively of women under 25 years of age and belonging to a single ethnic background," Garofalo said. Future studies could determine if the correlation is more generalizable, using a larger mixed-sex population of individuals from different backgrounds.

Alhamawi noted that she would like to perform a long-term study, in which researchers track how anxiety, sleeping patterns and NK cell levels change over time in the same cohort of participants. That could provide a clearer picture of the relationship between these psychological factors and immunity, as well as the incidence of disease.

"We can see if there is [an] effect by testing if they develop more infectious disease or chronic disease," she added.

This article is for informational purposes only and is not meant to offer medical advice.

Confused? Do not worry. We have curated a list of the 23 best fitness gifts, blending practicality, innovation, and a touch of luxury to help your favorite athlete level up their training routine in the New Year. You can trust us here — we have worked in the fitness industry for more than a decade now, and know a thing or two about what constitutes a great fitness gift. With these ideas, you can skip the guesswork and give your loved one something they will truly make use of.

• Related: The best gifts for nature lovers and outdoor explorers

Massage guns and recovery tools

Forget basic foam rollers — the real game changers for post-exercise stiffness and muscle knots are percussion massage guns. These powerful handheld devices deliver targeted percussive therapy (rapid pulses or vibrations to the muscles), helping to alleviate soreness, increase blood flow and improve range of motion after intense workouts. If your loved one trains hard for a sporting event and/or tends to struggle with DOMS (Delayed Onset Muscle Soreness), giving them one of the best massage guns will show that you care just as much about their rest and well-being as you do about their effort.

• More buying advice: Theragun vs Hypervolt: Which is best?

Running headphones and sports earbuds

Every fitness buff knows that the right soundtrack can turn a good workout into a great one. Noise-cancelling headphones are a perfect gift for a gym lover — they will block out the clanging weights, distracting conversations and underwhelming gym playlists, immersing them fully in their own auditory zone and helping them achieve their best. Make sure that the headphones are fully sweatproof, with a customizable fit and a good battery life, and, most importantly, are compatible with your intended recipient's phone.

Mind you, if your fitness lover is more of an outdoor than an indoor exerciser, they may prefer one of the best bone conduction headphones instead. They have an open-ear design that allows for situational awareness, making them a better choice for runners and hikers. They are also the only headphone type that can be used underwater — if your loved one is a swimmer or triathlete, they will surely appreciate it.

Gym essentials: Gym duffle bags, water bottles and towels

An active lifestyle is not cheap, and not just because of the steep gym membership costs. The devil is in the details: you may need a reusable water bottle to keep you hydrated between sets, a towel to wipe out your sweat from the cardio machines, an ultra-grippy yoga mat to help you step up your Pilates sessions, a gym bag to keep all your bits and pieces in one place... The list goes on. This is why gym essentials make for fantastic gifts. If you can give your fitness-obsessed loved one something that will help them cut the costs of keeping fit, they will not be disappointed.

Fitness trackers: Smartwatches, skipping ropes and swimming goggles

It is not just Garmin watches and smart rings — these days, fitness trackers come in all shapes and sizes, from innovative digital skipping ropes that count your jumps to smart goggles that measure your stroke rate and other vital stats when doing laps in a pool. Choosing the best fitness tracker for your loved one can be a daunting task, but it is worth the effort. Gym lovers love to keep track of their workout endeavours, and they will always appreciate a gift that helps them make sense of their fitness stats and identify areas for improvement.

• More buying advice: How to choose the best smartwatch for your loved one, according to an expert: The ultimate Christmas gift guide

Fun fitness gifts: Games and trinkets

Fitness gifts do not have to be serious, quite the opposite. The tongue-in-cheek presents are a particularly good option if your loved one already has every possible gym item available, or if they are in dire need of workout inspiration. This Christmas, bring a smile to their face with a fun music boxing machine, fitness board game or a set of coasters shaped like weight plates.

The symptoms: The man received a left kidney transplant in an Ohio hospital, and about five weeks later, he began experiencing tremors, weakness in his lower extremities and urinary incontinence, as well as confusion.

What happened next: About a week after these initial symptoms emerged, the man was hospitalized with additional health problems, including fever and difficulty swallowing. He also developed hydrophobia, or an irrational fear of water. Once hospitalized, he required breathing support with a ventilator.

The diagnosis: The man's doctors suspected that his signs and symptoms indicated a rabies infection, so they consulted the Ohio Department of Health and U.S. Centers for Disease Control and Prevention (CDC) about the case. Various clinical samples from the patient were sent to the CDC for testing and ultimately came back positive for rabies RNA, the genetic material of the virus, as well as antibodies against the virus.

The treatment: Within a week of being hospitalized, the patient died of his infection. Once a rabies infection is established, there is no effective cure available. There are only about 30 reports of people surviving symptomatic rabies in the medical literature, and doctors can't yet reliably replicate this outcome. As such, rabies is nearly always fatal.

(People who suspect they may have been exposed to rabies — for example, after being bitten by an animal — can be treated with anti-rabies antibodies or vaccines to help prevent the virus from triggering an infection in the first place. This preventative treatment is very effective.)

What makes the case unique: This man's rabies infection — the first reported in Michigan in about 15 years — was suspected to be potentially linked to his organ transplant, according to a report of the case. Investigators had ruled out direct animal exposure as the source of the infection.

Upon learning about the suspected infection, the CDC and state- and local-level partners launched an investigation into possible contamination of the donor kidney. The donor had been from Idaho and the investigators got in touch with the donor's family.

It turned out that "in late October 2024, a skunk approached the donor as he held a kitten in an outbuilding on his rural property," the report says. "During an encounter that rendered the skunk unconscious, the donor sustained a shin scratch that bled, but he did not think he had been bitten. According to the family, the donor attributed the skunk’s behavior to predatory aggression toward the kitten."

Five weeks after being scratched, the donor began experiencing symptoms consistent with rabies, including confusion, difficulty swallowing, hallucinations and a stiff neck, a family member said. He then fell unconscious at home and didn't wake up, though he was resuscitated and hospitalized. He was declared brain dead and removed from life support five days later.

Notably, hospital staff members who treated the donor were initially unaware of the skunk scratch and attributed his symptoms to chronic conditions, not to rabies. That said, they took various clinical samples from the patient that the CDC then retroactively tested for the virus.

A biopsy from the donor's right kidney tested positive, but there wasn't a big enough sample from the left kidney to test. Nonetheless, this supported the idea that the donor kidney was likely the source of the Michigan man's rabies.

"This was the fourth reported transplant-transmitted rabies event in the United States since 1978," the case report noted. "However, the risk for any transplant-transmitted infection, including rabies, is low." In short, this chain of events is very unlikely, and hospitals follow extensive protocols to safeguard against transplanting infected organs into patients.

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

This article is for informational purposes only and is not meant to offer medical advice.

It's known that people who get kidney transplants are three times more likely to develop bladder cancer than the general population. Researchers have hypothesized that because transplant patients are immunosuppressed, dormant viruses lurking in the body are given the opportunity to reactivate.

These sleeping pathogens include BK virus (BKV), also called human polyomavirus type I, a common cold virus that 95% of people pick up as children. After an infection, the virus then lies dormant in the kidney. This introduces a question: Can the BK virus cause cancer years after it infects someone?

In a study published Dec. 3 in the journal Science Advances, researchers showed that the virus can cause the type of DNA damage that is also seen in bladder cancer that occurs later in life. But instead of finding DNA mutations directly caused by the virus, the researchers found that the culprit was the body's own immune system.

"This is a nicely-done laboratory study to show a possible way that BKV could have a larger role in bladder cancer than previously thought," Dr. Patrick Moore, a tumor virology researcher at the University of Pittsburgh who was not involved in the study, told Live Science in an email.

Connecting the dots

There are several types of viral infections that can lead to cancer. Some viruses, such as HPV, hijack the host cells of the infected person and insert their viral genetic material into the human genome, which causes the host cell to become cancerous. However, in some cancers, like those originating in the bladder, no detectable virus is present —but nonetheless, there are genetic signs of a previous viral infection.

"The long-running narrative since the 1950s has been that smoking and industrial exposures are the big cause of bladder cancer," said senior study author Simon Baker, a cancer researcher at the University of York in the U.K. But the patterns of DNA mutation seen in bladder cancers are different from those resulting from chemical carcinogens.

Instead, the cancers bear mutational signatures known to be caused by a family of enzymes called APOBEC. Normally, these enzymes help form the body's first-line defense against viruses and other pathogens. "They have these signatures from APOBECs, and we know APOBECs are part of the antiviral host defense," Baker explained.

Baker and his team took healthy human bladder cells and infected them with the BK virus in lab dishes. They found that the cells not only exhibited mutations similar to those seen in bladder cancer but also boosted the activity of APOBEC3, an enzyme that damages viral genomes in response to infection.

When the scientists turned off APOBEC3 and then infected the cells with the BK virus, the DNA damage didn't occur. This finding suggests that the enzyme made by the host cell was causing the damage, not the virus itself.

Additionally, the researchers found increased APOBEC3 expression and cancer-like genetic mutations in nearby "bystander" cells that hadn't been infected with the virus. So, a cell doesn't have to contain the actual virus to accumulate genetic mutations caused by an infection elsewhere in the body.

"That was a surprise," Baker said. "But the reason it makes perfect sense is that … bladder cancers don't have viruses in them." This finding starts to unravel the connection between early-life viral infections and cancers diagnosed decades later.

A starting point

Although these initial data are impactful, Moore said he would like to see whether patients with bladder cancer are infected more often with the BK virus than people without the cancer.

"It is intriguing," he said, "but only a starting point and work needs to be done to show its actual importance to human cancer."

When a person contracts the BK virus in childhood, they generally experience common cold symptoms before recovering. The virus then stays inactive, or dormant, in the kidney, bladder and tubes between the two organs. For most people, it never becomes an issue, and it's not routinely tested for outside of hospital settings.

For those about to have a kidney transplant, however, the immunosuppressants that prevent the rejection of their new kidney can also result in the reactivation of the BK virus, possibly damaging the kidneys, ureter and bladder in the process.

Tim Tavender, a kidney transplant patient from Southampton, developed a BK virus infection following his procedure and eventually had bladder cancer.

"Seeing this research makes me hopeful," Tavender told The Independent. "If scientists like Dr. Baker can find new ways to control BK virus, it could spare other people from going through what I did — and that would be life changing."

This article is for informational purposes only and is not meant to offer medical advice.

Cancer-causing triggers, such as ultraviolet (UV) light or certain chemicals, activate a natural defensive pathway that leads to premature graying but also reduces the incidence of cancer, the research found.

The researchers behind the study tracked the fate of the stem cells responsible for producing the pigment that gives hair its color. In mouse experiments, they found that these cells responded to DNA damage either by ceasing to grow and divide — leading to gray hair — or by replicating uncontrollably to ultimately form a tumor.

The findings, reported in October in the journal Nature Cell Biology, underline the importance of these sorts of protective mechanisms that emerge with age as a defense against DNA damage and disease, the study authors say.

Graying hair as cancer defense

Healthy hair growth is dependent on a population of stem cells that constantly renews itself within the hair follicle. A tiny pocket within the follicle contains reserves of melanocyte stem cells — precursors to the cells that produce the melanin pigment that gives hair its color.

"Every hair cycle, these melanocyte stem cells will divide and produce some mature, differentiated cells," said Dot Bennett, a cell biologist at City St George's, University of London who was not involved in the study. "These migrate down to the bottom of the hair follicle and start making pigment to feed into the hair."

Graying occurs when these cells can no longer produce sufficient pigment to thoroughly color each strand.

"It's a sort of exhaustion called cell senescence," Bennett explained. "It's a limit to the total number of divisions that a cell can go through, and it seems to be an anti-cancer mechanism to prevent random genetic errors acquired over time propagating uncontrollably."

When the melanocyte stem cells reach this "stemness checkpoint," they cease to divide, meaning the follicle no longer has a source of pigment to color the hair. Ordinarily, this occurs with old age as the stem cells naturally reach this limit. However, Emi Nishimura, a professor of stem cell age-related medicine, and colleagues at the University of Tokyo were interested in how this same mechanism operates in response to DNA damage — a key trigger for cancer development.

In mouse studies, the team used a combination of techniques to track the progress of individual melanocyte stem cells through the hair cycle after exposing them to different harmful environmental conditions, including ionizing radiation and carcinogenic compounds. Intriguingly, they found that the type of damage influenced how the cell reacted.

Ionizing radiation caused the stem cells to differentiate and mature, and ultimately activated the biochemical pathway responsible for cell senescence. As a result, the melanocyte stem cell reserves were rapidly depleted over the hair cycle, thus halting the production of further mature pigment cells and leading to gray hair.

Meanwhile, by essentially switching off cell division, this senescence pathway prevented the mutated DNA from passing into a new generation of cells, thus lowering the likelihood of those cells forming cancerous tumors.

Exposure to chemical carcinogens — such as 7,12-dimethylbenz[a]anthracene (DMBA), a tumour initiator widely used in cancer research — appeared to bypass this protective mechanism. Instead of switching on senescence, it toggled on a competing cellular pathway.

This alternative chemical sequence blocked cell senescence in the team's mouse studies, enabling the hair follicles to retain their stem cell reserves and the ability to produce pigment, even after DNA damage. That meant that the hair retained its color, but in the long term, the unchecked replication of damaged DNA led to tumor formation and cancer, the team said in a statement.

These findings reveal that the same stem cell population can meet opposite fates depending on the type of stress they're exposed to, lead study author Nishimura said in the statement. "It reframes hair graying and melanoma [skin cancer] not as unrelated events, but as divergent outcomes of stem cell stress responses," Nishimura added.

The next step will be to translate this understanding into human hair follicles, to see whether these observations in mice carry over to people, Bennett said.

This article is for informational purposes only and is not meant to offer medical advice.

In 1954, researchers described a new drug that sent children with acute leukemia into remission. It would become one of the first chemotherapy drugs and would later form the basis for a new, "rational" approach to designing drugs.

Gertrude Elion had earned a master's degree in chemistry in 1941, but she was turned down for many graduate research posts, which were not available to women. So she worked as a high school chemistry teacher and a food quality tester for a supermarket company, according to an autobiographical sketch she wrote in 1988.

But by 1944, she had found a job in the lab of George Hitchings at the Burroughs-Wellcome pharmaceutical company (now GSK). Hitchings was developing a novel way to make new drugs that eschewed the trial-and-error approach that had previously dominated drug design.

"One of the deciding factors may have been that my grandfather, whom I loved dearly, died of cancer when I was 15. I was highly motivated to do something that might eventually lead to a cure for this terrible disease," Elion wrote in 1988.

Hitchings and Elion reasoned that, because all living cells need nucleic acids, which make up DNA, to reproduce, then fast-growing cells, like invasive bacteria and tumor cells, would need even more of these compounds to fuel their insatiable growth. So, they rationalized, finding compounds that inhibit the synthesis of nucleic acids could squelch cancer growth.

In 1950, when Elion was 32, the team discovered a compound derived from purine, called 6-mercaptopurine (6-MP), which could inhibit the growth of both bacterial cells and leukemia cells in a lab dish. Over the next two years, they tested the drug in tumors in animals, finding that it slowed tumor growth. In 1952, researchers began trials in 107 patients with various types of cancer, including 45 children and 18 adults with acute leukemia. Prior to this, there was no good treatment for these children, who would usually die months after their diagnosis.

There had been a few earlier chemotherapy drugs, but many were based on highly toxic compounds, such as war gases. By contrast, the children who took 6-MP seemed to tolerate it fairly well, and 15 children went into complete remission for a few weeks to a few months. It wasn't a huge increase, but it was more than had been possible before. Elion was elated when the children got better, and crushed when they got sick again.

Hitchings and Elion were determined to pursue other, related compounds that could create a more durable remission. In the late 1950s, they hit upon a regimen that combined methotrexate — another chemotherapy drug, developed by Dr. Jane Wright and colleagues — with 6-MP to create a longer-lasting, stable remission in some kids with acute leukemia.

Over a decades-long career, Elion would go on to develop many more drugs, including azathioprine, a rheumatoid arthritis and transplant anti-rejection drug; acyclovir, an antiviral that treats genital herpes, chickenpox and shingles; and AZT, the first drug that worked against HIV/AIDS. In 1988, she earned the Nobel Prize in physiology or medicine, along with Hitchings and James Black for her work on "important principles in drug design," including her work on 6-MP.

The Advisory Committee on Immunization Practices (ACIP), which steers the CDC's vaccine policy, was recently overhauled by Health and Human Services Secretary Robert F. Kennedy Jr. Its members now include prominent vaccine skeptics who have sown doubt in the established childhood vaccine schedule.

The vote came Friday (Dec. 5) after a dysfunctional meeting and a series of delayed votes. The vote overturns a 30-year-old recommendation that newborns in the U.S. be vaccinated against HBV. This rollout has been a public health success story, having dramatically reduced the rate of hepatitis B infections among children, as well as adults up to 39 years old, who were among the first to get the vaccine as infants.

The proposed changes have been widely criticized by medical associations, including the American Academy of Pediatrics.

"No rational science has been presented" to support the new recommendations, Dr. Joseph Hibbeln, ACIP committee member and former Chief of the Section on Nutritional Neurosciences at the National Institutes of Health, said in the meeting.

"This has a great potential to cause harm, and I simply hope that the committee will accept its responsibility when this harm is caused," Hibbeln said in the meeting when the votes were cast.

During its chaotic, multi-day meeting, the committee rolled out four different versions of language, so multiple ACIP members expressed uncertainty as to what they were voting for.

What is Hepatitis B?

Hepatitis B, a viral infection, can easily go undetected because it doesn't always cause overt symptoms. However, when the infection becomes chronic, it can cause liver damage and raise the risk of liver cancer. The infections contribute to about one-third of liver cancer deaths globally.

The permanent infection must be managed with medications for life, and the organ damage can lead people to need liver transplants. Up to 1 in 4 four newborns infected with hepatitis B die prematurely of liver disease as adults.

This chronic form of the disease is especially common among people who are infected as kids. In about 95% of cases, hepatitis B contracted in early childhood becomes chronic, according to the World Health Organization (WHO). That's why the hepatitis B vaccine, first licensed in 1971, has been recommended to newborns in the U.S. since 1991.

According to the WHO, in countries where the virus is endemic and infects people in high numbers, the most common routes of transmission are from mother to child at the time of birth or from an infected person to an uninfected child in the first five years of the child's life — they can pick the infection up from a biting incident at daycare or from accidentally touching a friend's scraped knee, for instance, as the virus can be spread via contact with small quantities of blood. In the U.S., vaccinating babies at birth heads off these two common routes of transmission.

A second dose of the vaccine was recommended to be given at 1 to 2 months old, and then a third at 6 to 18 months old. This three-dose series in childhood also later protects against the types of transmission that are common in adults, such as unsafe intravenous drug use and sexual activity.

Historically, anti-vaccine advocates have argued that the shot is unnecessary for kids because these latter two routes of transmission presumably aren't relevant to them. As with other vaccines given in early childhood, anti-vaxxers have claimed that the safety of the schedule hasn't been studied — which it has — and that the vaccines cause autism spectrum disorder — which they do not.

The risk-stratified approach of only vaccinating children of mothers known to be positive has been tried in the past and found to be ineffective. In 1990 — when children had started to be vaccinated for hepatitis B but newborn vaccination had yet to be introduced — acute hepatitis B infections affected 3 per 100,000 people ages 19 and under in the U.S. Compare that to 2023, when that rate fell to 0 per 100,000. The rate of chronic infections fell, in turn, with only 0.4 per 100,000 people under 19 diagnosed in 2023.

In the meeting, the committee also voted to recommend that after the first dose, patients should consult with doctors to see whether they should test for certain levels of antibodies against HBV before giving the second and third shots.