People with obesity are 70% more likely than those without the condition to be hospitalized with or die from severe infections, according to a new study of over half a million people.

The research found that 1 in 10 deaths attributed to infections worldwide were in people with obesity. This link persisted even in people with obesity who did not have metabolic syndrome or diabetes. And it showed up regardless of socioeconomic status or physical activity levels, researchers reported Feb. 9 in the journal The Lancet.

"People with obesity may find it harder to fight off infections," study senior author Mika Kivimäki, an epidemiologist at University College London, told Live Science. "Extra body fat can affect the immune system in several ways, including impairing lymphatic function, reducing lung function, and increasing long-term low-grade inflammation." The lymphatic system helps to maintain a balance of fluids in the body, as well as to train and ferry immune cells around.

An earlier study by different researchers, published in August 2025, found that using semaglutide — the active ingredient in drugs like Ozempic and Wegovy — reduced users' risk of severe infections by 10%. That finding might also hint that obesity and infection susceptibility are linked and, perhaps, suggest that the risk can be lowered.

The connection between obesity and the dangers of infection were made prominent during the COVID-19 pandemic, the new study found. In 2021, 15% of all infection hospitalizations and deaths were linked to obesity. That connection between obesity and COVID-19 severity motivated Kivimäki and his team to investigate whether the coronavirus was uniquely dangerous for people with obesity or whether the danger extended to all types of infections.

They turned to the UK Biobank, a large database of genetic sequencing and linked medical records from U.K. adults, as well as two similarly large studies from Finland: the Finnish Public Sector study and the Health and Social Support study. Together, these databases included over 540,000 people.

In the Finnish cohorts, participants self-reported their heights and weights, which could be used to calculate a body mass index (BMI). BMI is a rough estimate of body composition often used in large-scale population studies. The UK Biobank participants had more precise measurements done with a body-composition device, and they also had their waist circumferences measured. (Some researchers have argued that these types of metrics should replace BMI, as they're more useful for predicting health outcomes.)

In the study, people with obesity included those with a BMI of 30 or higher; a waist circumference of over 40 inches (102 centimeters) in men or over 35 inches (88 cm) in women; or a waist-to-height ratio of 0.6 or more. Obesity was linked to a 70% greater chance of hospitalization with or death from infection, once adjusted for age and sex. This relationship held across different definitions of obesity and across all bacterial, viral, fungal and parasitic infections.

The results also showed that the greater the degree of obesity, the greater the risk.

People with a BMI of 30 to 34.9 had a 50% higher risk of infection, hospitalization or death, compared with people with BMIs under 30. But people with a BMI of 35 to 39.9 had twice the risk, and people with a BMI of 40 or above had three times the risk. In participants with follow-up measurements of obesity after their first baseline measurement, those who lost or gained weight saw their severe infection risk drop or rise in turn.

The nature of the study did not enable the researchers to prove causation or tease out precisely how obesity might raise these risks, Kivimäki said.

That said, evidence suggests that fat tissue and the immune system are enmeshed; the precursor cells that can turn into fat cells can act like immune cells, and some fat cells also excrete pro-inflammatory substances, said Nikhil Dhurandhar, a professor of nutritional sciences at Texas Tech University who was not involved in the new research.

Previous studies have found not only that weight can influence infection risk but also that certain pathogens are linked to the development of obesity, Dhurandhar told Live Science. The evidence that certain germs drive increases in fat has mostly been gathered in lab animals so far, while the human data is less conclusive.

Obesity can contribute to immune dysfunction that makes it harder for the body to fight infection, Dhurandhar added. Because of this dysfunction, people with obesity may not respond as well to vaccination as do people with weights categorized as overweight or normal, leaving them vulnerable. Obesity is tied to a lack of sensitivity to the hormone leptin, which helps regulate body weight and appetite and also has an immune-protective role, he said.

Dhurandhar said the 1 in 10 infection deaths linked to obesity in the study shouldn't be considered easily preventable by weight loss, because it is very difficult to lose weight and keep it off.

"Obesity is a disease," he said. "It's a chronic disease. It's not a matter of willpower; it’s not a matter of discipline."

However, the emergence of drugs like semaglutide, collectively known as GLP-1 agonists, may make weight loss easier for some people. The effect of these medications on risks from infection remains to be seen, Kivimäki said.

While trials hint that these medications reduce the risk, people taking these drugs also often lose muscle mass along with fat, which could have negative effects on the immune system. Muscle tissue provides an amino acid called glutamine that powers some immune cells, and also produces the anti-inflammatory compound interleukin-6.

"In our future research, we want to better understand why obesity raises the risk of severe infections," Kivimäki said, "and, importantly, what can be done to reduce that risk."

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

Just over 40% of Americans are obese based on their BMIs, and that number has been on the rise since the mid-1970s. But a few new statistics suggest that the obesity rate is now plateauing, or even declining.

Could this mean America has hit its heaviest weight on the scale? Experts aren't so sure.

The apparent plateau is short-term, the data incomplete and the share of people with severe obesity still rising. The childhood obesity rate also continues to rise. In addition, nutrition data suggests that Americans are still eating large amounts of ultraprocessed foods, which can fuel obesity.

For researchers, none of this news points to a change in the obesity trend.

"It's not a moment to relax," Niyati Parekh, a professor of public health nutrition at New York University, told Live Science.

The latest numbers

Obesity is defined as a body mass index (BMI) of 30 or higher, while "severe" obesity, also called Class III obesity, is defined as 40 or higher. This measure of body fat based on height and weight is imperfect for diagnosing individual health — for instance, someone with a very muscular build might qualify as overweight or obese despite having a healthy body composition. But it is used by public health officials to get a sense of how much of the population is overweight and obese.

Obesity, in turn, is linked to chronic health problems such as sleep apnea, cardiovascular disease, liver disease and diabetes.

The rate of obesity began rising in the U.S. across all groups starting in the late 1970s, according to data collected by the Centers for Disease Control and Prevention (CDC). In 1980, 13.4% of U.S. adults were obese. By 2008, 34.3% were. The latest data, collected between 2021 and 2023, shows that 40.3% of adults are obese.

That recent age-adjusted increase was not a statistically significant change compared with the decade prior, suggesting that the obesity rate is no longer rising. But the National Health and Nutrition Examination Survey (NHANES) from which these numbers emerge is limited, said Barry Popkin, a nutrition professor at the University of North Carolina whose work focuses on evaluating policy related to food labeling and obesity.

While the survey is a national sample, the North is surveyed in the summer and the South in the winter, making regional and seasonal comparisons impossible, Popkin said. More importantly, the survey compares the 2021-2023 numbers to a decade ago, which is only two data points.

"We have seen some short-term plateaus earlier at different points," Popkin said. There was a pause in the rise between 2009 and 2012, for example, that turned out to be a temporary bump in a continuing upward trajectory.

The most recent Gallup National Health and Well-Being Index, released Oct. 28, found an overall obesity rate of 37% in U.S. adults in 2025, down from a high in the same surveys of 39.9% in 2022. But there are questions about this data, too, said Justin Ryder, an associate professor of surgery and pediatrics at the Northwestern Feinberg School of Medicine and vice chair of research for the department of surgery at Lurie Children's Hospital in Chicago.

Gallup surveys about 5,000 adults each quarter, but it's not clear how many individuals in that sample have BMIs in the obese range, given that the participants are not chosen to be nationally representative by weight status.

Small sample sizes can skew the picture, Ryder said. Over a decade ago, he said, there was data suggesting the obesity rate was dropping in 2- to 5-year-old children. But that trend turned out to be based on only 700 children, and in the next year of data collection, the findings evaporated. Ryder told Live Science he was skeptical of the Gallup data for a similar reason.

"I don't believe it," he said.

The role of GLP-1s

In reporting the results of the survey, Gallup suggested that new medications that target the glucagon-like peptide 1 (GLP-1) receptor might be making an impact on America's obesity rate. These medications, known by brand names such as Ozempic and Zepbound, help regulate blood sugar levels and slow the emptying of the stomach, leading to weight loss.

In Gallup's nationally representative sample, 12.4% of adults reported currently using one of these GLP-1 drugs, up from 5.8% in February 2024. The biggest reductions in obesity rates in Gallup's numbers were in people ages 40 to 64, matching the highest uptake of GLP-1 medications.

Overall, though, it's early to say whether these medications are having a nationwide impact, Popkin said. Gallup's data is not a comprehensive look at the number of people using GLP-1s, nor does it cover whether the treatment was successful, how long they used the medication, or if the users dropped enough weight to move between weight categories. Because of off-label prescriptions and the drugs' use in controlling diabetes, it's also difficult to know if people reporting taking GLP-1s are obese, overweight, or a healthy weight, per their BMI category.

Until recently, more affordable, compounded versions of some of the most popular GLP-1 medications were widely available from local pharmacies because some brand-name medications were in shortage. Those shortage rules have now been lifted, making it harder to get inexpensive versions.

Because of lack of insurance coverage and cost, only a small percentage of people eligible to use the medications are on them, Ryder said. Looking at the situation beyond the Gallup numbers suggests the number being successfully treated is not likely enough to move the needle on national obesity numbers, he said.

The latest NHANES data raises another question: why is the severe obesity rate still rising if GLP-1s are reducing obesity, overall? The data suggests that 9.4% of the population has a BMI of 40 or higher, a number that rose from 7.7% in 2013-2014. In addition, the diagnosis of diabetes is at an all-time high according to Gallup's numbers, at 13.8% of the population.

People with BMIs over 40 and those with diabetes should be the ones most likely to be prescribed a GLP-1, according to medical criteria. There's a question as to why those numbers aren't going down as the number of people prescribed GLP-1s goes up, Popkin said, again raising questions about the data's limitations.

Medicare and Medicaid only cover the medications for patients with diagnosed diabetes or with obesity along with cardiovascular disease. On Nov. 4, the Trump Administration announced a deal to enable Medicaid and Medicare coverage of some GLP-1s for weight loss, alone for people with obesity and no related conditions. But whether this move will expand access will depend on the ultimate out-of-pocket cost for consumers, Ryder said.

"While I'm very hopeful that we'll start to see obesity prevalence decrease," he said, "that's going to coincide with better access to medications."

Changing the environment

Also adding to experts' skepticism about a turn in the obesity rate is the fact that little has changed about the food system in America. Policies put the onus on consumers to avoid prepackaged snacks high in sodium, saturated fat and added sugars, Parekh said.

"It's much cheaper to be unhealthier and buy unhealthy foods," she said.

For many, it's also a challenge to buy healthier foods. The U.S. Department of Agriculture estimates that 18.8 million Americans live in "food deserts" where it is difficult to access a full-service supermarket.

According to CDC data, 55% of the calories Americans consumed between 2021 and2023 were ultraprocessed, a somewhat nebulous category encompassing foods that are formulated from substances derived from foods — such as pure starch or fat — but that contain very little in the way of whole ingredients. These foods also tend to include additives not found in home kitchens, such as stabilizers and preservatives. They initially became a larger part of the American diet in the late 1970s, when the obesity rate started its rise.

Clinical and observational studies link high consumption of ultraprocessed foods to the development of obesity. This may be in part because they are hyperpalatable — in other words, very tasty — and thus encourage overconsumption, said Filippa Juul, an epidemiologist at SUNY Downstate Health Sciences University in New York. It may also be because the body may more easily break down these foods and use all their fats and sugars, compared to whole and less-processed foods that take more energy to digest.

"Even though you may think you're eating the same calories in almonds and potato chips, according to the label, you're actually eating less calories when you're eating the almonds, because you're not digesting it all," Juul told Live Science.

The Make America Health Again (MAHA) movement spearheaded by health secretary Robert F. Kennedy Jr. has drawn attention to ultraprocessed foods. But experts say there is little chance that MAHA will make major changes to how such foods are regulated.

There was initially interest from Trump's Food and Drug Administration (FDA) in looking at new labeling requirements for ultraprocessed foods, said Popkin, who was part of those conversations. However, when the administration released its MAHA Strategy in September, there was only one reference to labeling, which committed only to exploring the issue.

Popkin and his colleagues have found that clear warning labels can change real-world consumer purchases by alerting consumers to high levels of saturated fat, sodium, or sugar on the front of a product. Labels that use a red-yellow-green color-coded system to convey information about healthfulness are also effective, they have found.

But "instead of using our approach, which was valid and used in other countries, they are going back and saying we need more research," Popkin said. That position suggests it's unlikely that the U.S. will put new labeling regulations into play anytime soon, he said.

Meanwhile, the fate of the long-running NHANES survey that allows federal researchers to track the obesity rate is in the balance given ongoing cuts at the CDC. On Oct. 10, the team that runs the survey was fired. The next day, the decision was reversed for half of that team. A federal judge later blocked the remaining layoffs because they occurred during a government shutdown.

When it comes to ultraprocessed foods, "the MAHA movement is toothless," Popkin said. "Lots of talk, no policies or laws."

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

Abandoning the biannual switch to daylight saving time could prevent more than 300,000 strokes and slash over 2 million obesity cases a year, a new model using data from over 300 million Americans suggests.

Adopting permanent standard time (ST) takes less toll on our circadian rhythm — the body's rough 24-hour pacemaker — than daylight saving time (DST) or flicking between the time policies twice a year, the researchers found.

As a result of this reduced burden on our body clock, staying in ST year round could prevent almost 900,000 more cases of obesity and around 85,000 more strokes a year than remaining in DST year-round, the scientists concluded in a study published Sept. 15 in the journal PNAS.

"We can't propose public policy without data," study co-author Jamie Zeitzer, a professor of psychiatry and behavioral sciences at Stanford University, told Live Science. The data from this research marks "the beginning of a conversation," he said.

Time for a change?

DST, which makes clocks wind forward by an hour every spring, was first introduced in the U.S. in 1918 to save fuel during World War I. It was later made federal law by the Uniform Time Act of 1966.

Our circadian rhythm regulates and coordinates the functioning of each cell in the body. This internal pacemaker is highly sensitive to light exposure, and disruptions to it — for instance, when people must wake up or stay awake during dark hours — creates a "circadian burden" that has been associated with a measurable increase in negative health outcomes, including heart attacks, strokes and car accidents around the time of the switchover.

Insufficient sleep and a circadian burden are also metabolic stressors associated with reduced energy expenditure and excess food intake — risk factors for weight gain and obesity. As such, the position of the American Academy of Sleep Medicine is to scrap DST altogether and permanently stick to ST. Although the health risks of biannual switching are low for individuals, the effects are noticeable at the population level, Zeitzer said.

"You're really looking at lottery ticket kind of risk. But if 350 million people are doing it on the same day, someone's going to win the lottery," Zeitzer told Live Science. "[It's] just not one that you want to win."

To model the health impacts of a mismatch between circadian rhythm and the environment, Zeitzer and colleague Lara Weed, a bioengineer at Stanford University, calculated the circadian burden associated with each time policy: permanent ST, permanent DST and biannual shifting.

To do this, they simulated artificial light and sunlight exposure for the people in every U.S. county across a year under all three time policies. They assumed regular sleep routines (10 p.m. to 7 a.m.), and regular work schedules in a well-lit office (9 a.m. to 5 p.m., Monday to Friday).

The team found that biannually flicking between time policies created the largest disruptions to circadian clocks and therefore the largest circadian burden.

The researchers then used data on county-level prevalence of chronic diseases to determine how the different circadian burdens predicted eight health outcomes: arthritis, cancer, chronic obstructive pulmonary disease, coronary heart disease, depression, diabetes, obesity and stroke. They controlled for various socioeconomic and health factors that could also determine disease prevalence, such as high blood pressure, health insurance status and unemployment.

Sticking to ST would prevent around 2,602,866 cases of obesity and 306,988 strokes compared to a biannual shift. Permanent DST prevented obesity and strokes to a lesser degree, with 1,705,437 fewer predicted obesity cases and 220,092 fewer strokes on average, compared to the biannual switch.

Their model found neither policy led a statistically meaningful reduction in the six other health outcomes.

However, the research is based on simulations which deliberately included unrealistic assumptions, including universal regular light exposure and sleep, and it also did not consider seasonal variations in behavior. Moreover, the health outcomes dataset relied on self-reported information, such as for body mass index (BMI) and whether they'd had a past stroke or not.

Also, they did not include race in their model, despite there being persistent racial and ethnic disparities in sleep in the U.S. This exclusion "doesn't necessarily change the results of the study," said Karin Johnson, a professor of neurology at UMass Chan School of Medicine-Baystate and a spokesperson for the American Academy of Sleep Medicine, who was not involved in the research.

It does mean, however, that the increased risks of stroke and obesity are likely to be felt most keenly by people [namely, Black and Hispanic or Latino populations] that are "already at risk for sleep disparities from other causes," Johnson told Live Science in an email.

Even before kindergarten, Autumn Lloyd feared other kids wouldn't like her because she was twice their size.

In high school, she lost more than half her body weight through a punishing and unsustainable regimen of diet and exercise, which was celebrated by her peers and even featured in a local newspaper.

"Even though I excelled academically, I feel like it never quite mattered as much as this vanity piece," Lloyd told Live Science.

When the weight later returned, as research shows it often does, Lloyd felt scrutinized, which led to her obsessively monitoring her eating and exercise in public, while binge eating in private. A dietician suggested she track her food intake, but it became an obsession, and the pressure to lose weight contributed to self-injury and depression.

By college, she'd been hospitalized twice for suicidal thoughts, with her weight deeply tied to her mental health. She continued a grueling exercise regimen — even running the Chicago marathon twice — before reaching her lowest adult weight. Then the weight returned.

After further weight gain, Lloyd underwent bariatric surgery in 2022, dropping a substantial amount of weight but less than the median. She felt judged by others. "If you appear to be obese, and didn't hit your weight goal, you look [to some] like a failure," she said.

Lloyd's experience of being scrutinized and negatively judged for her weight is not unique. The negative mental health consequences Lloyd faced are also not rare. A growing body of evidence suggests that weight stigma itself leads to poorer mental, physical and economic health for people with higher body weights.

"It really is the norm," Larissa McGarrity, a clinical psychologist at University of Utah Health who studies mental health after weight-loss surgery.

Lloyd's experience of facing weight stigma even after surgery — and that affecting her mental health — is also common.

New research by McGarrity and colleagues suggests that this stigma affects how patients fare after bariatric surgery. Their study, which was published June 5 in the journal Health Psychology, found that shedding weight stigma — rather than the weight itself — may explain why some people report better mental health and less disordered eating after weight-loss surgery.

On the flip side, people who underwent weight-loss surgery but still faced stigma afterward were at higher risk for depression, anxiety and disordered eating compared to their less-stigmatized peers, the study found. These findings suggest that the stigma, not just body size, presents a major barrier to better health for those with obesity.

Related: Childhood obesity should be treated early and aggressively, new guidelines say. Is that safe?

What is weight stigma?

Bias against people who are overweight often stems from the misconception that a person's body weight is entirely within their personal control and can be managed with diet and exercise alone. Research, however, shows that weight is shaped by a complex mix of genetic, physiological, psychological and social factors. Studies show that for most, losing weight and maintaining that weight loss long-term is very difficult without proper medical assistance.

Weight stigma is pervasive, with over 40% of U.S. adults reporting that they've experienced it personally at some point in their lives. Growing evidence shows that weight stigma does not help with weight loss, and what's more, it can worsen health. It's associated with increased stress, inflammation and mental health issues, including depression and disordered eating behaviors, according to the World Obesity Federation.

"There's considerable evidence that societal weight stigma is prevalent and has harmful health consequences for people with obesity," said Rebecca Puhl, deputy director for the Rudd Center for Food Policy and Health at the University of Connecticut, who was not involved in the new study.

However, there's little data about what happens to people after they lose weight through surgery — the most effective intervention for severe obesity and one that's become more common in recent years.

"This new study begins to address this research gap," Puhl told Live Science.

Losing weight doesn't make you "immune"' to stigma

Past research showed that while bariatric surgery improves mental health for most, some people see their mental health worsen afterward. Previous work has also hinted that weight stigma could play a role in the amount of weight lost or regained after surgery.

To understand the effect of weight stigma in this dynamic before and after weight-loss treatment, McGarrity and her colleagues recruited 148 patients who underwent bariatric surgery. They collected data before surgery and 1.5 to three years afterward, measuring patients' experiences of weight stigma in the week prior to survey, alongside measures of their mental health and eating behaviors.

More than 90% of the patients reported experiencing stigma before the procedure, and most — about 60% — experienced significantly less weight stigma post-surgery.

Those who experienced less stigma afterward saw notable improvements in mental and physical health. They were more likely to have a lower weight at that time point compared to patients who continued experiencing stigma post-surgery. However, weight loss itself was not associated with the improvement in mental health.

Related: Weight-loss surgery is becoming more common among US teens

About 40% of participants reported regularly experiencing weight stigma following their procedures, and these people were at increased risk for mental health problems compared to their peers. The higher the level of weight stigma reported post-operatively, the higher the risk for poor mental health, eating behavior and weight outcomes. Again, these effects appeared to be tied to the perception of stigma rather than to any weight loss they had after the surgery.

The study suggests "bariatric surgery patients are not immune to the effects of weight stigma, even years after surgery, even after significant amounts of weight loss," McGarrity said.

She emphasized that the study design has important limitations: the patients' experience of weight stigma was self-reported, and for obvious ethical reasons, the study didn't assign people to face differing levels of weight stigma. As such, it cannot directly establish cause and effect. Moreover, the patients were drawn from only one region and their perceived stigma was only measured at one time point after surgery.

Puhl added that it would also have been helpful to get a more detailed picture of the patient's experience over time. And more research is needed to understand how much this bias affected patient health.

The takeaways

The findings highlight how important it is to address weight stigma at every stage of a patient's weight journey, and not assume it will resolve after surgery, Puhl said.

McGarrity said public health and policy officials, as well as members of the media, should examine whether the public conversation around weight could be harming people's health. On an individual level, she said that everyone can "do better with the people in our lives who struggle with weight — to not just be one more person that conveys the [message of] 'just eat less and exercise more.'"

That jives with Lloyd's experience. "If you're in a world where weight stigma is hitting you from every side, I think that will directly hinder your progress," Lloyd said.

Lloyd says she's learned to tackle the aspect of weight stigma she can control: her own perception of her weight. To people who live with a higher weight, she says to be kind to themselves.

"The journey is very difficult. There's a lot of noise to filter through, and there's some fights that we just don't have the bandwidth to get into," Lloyd said. "You're not broken. You're not failing because you haven't reduced your weight."

Editor's note: This story was updated on June 11, 2025, to adjust Autumn Huett's name to Llyod, her married name. The article was first published June 10.

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

Disease name: Prader-Willi syndrome

Affected populations: This genetic, multisystem disorder affects an estimated 1 in 30,000 to 1 in 10,000 people worldwide. Most cases of the syndrome occur sporadically, meaning the genetic changes behind the condition appear randomly in early development rather than being passed down through generations. Only in rare cases is the genetic trigger inherited.

The syndrome affects males and females at equal rates, as well as people of different racial and ethnic backgrounds. Approximately 10,000 to 20,000 people in the United States have Prader-Willi syndrome.

Causes: The syndrome occurs when specific genes on chromosome 15 lose their function, either because they are missing or because they've been turned off. The portion of chromosome 15 that's affected in Prader-Willi syndrome is called 15q11.2-q13, and it's also known as the Prader-Willi syndrome/Angelman syndrome (PWS/AS) region.

Human cells typically carry 46 chromosomes, including 22 pairs of non-sex chromosomes, numbered 1 through 22, and one pair of sex chromosomes. Each parent contributes one-half of each pair of non-sex chromosomes — so one copy of chromosome 15 comes from the mother and another comes from the father, for example. Because cells carry two copies, every gene on each chromosome does not need to be active. Through a process called "genetic imprinting," certain genes on either the mother's or the father's copy get switched off.

Prader-Willi syndrome affects the paternal copy of chromosome 15, and in most cases — around 60% or 70% — the PWS/AS region is randomly deleted during development. Meanwhile, the maternal PWS/AS region is switched off in everyone. Thus, the deletion leaves people without a working set of those genes.

For about 30% to 40% of people with the syndrome, they inherit two copies of the maternal chromosome 15, so they're missing the paternal copy altogether.

More rarely, a person carries the paternal chromosome 15 but the relevant genes do not work properly. This happens due to either a small genetic mutation — a "microdeletion" — or changes in epigenetics, which are modifications to DNA that don't change its code but can turn a gene on or off. Even more rarely, the syndrome may be triggered by translocation, in which a portion of chromosome 15 breaks off and then reattaches to a different chromosome.

Symptoms: Prader-Willi syndrome affects many parts of the body, and its symptoms can vary from person to person. Many of the genetic changes that underlie the syndrome are thought to affect the hypothalamus, a key hormone-making region of the brain that helps control many basic bodily functions, including body temperature, hunger and sleep.

Hypotonia, or low muscle tone, is seen in nearly all infants with the syndrome, making them feel "floppy" when held. There can be signs of this symptom before birth, in that the fetus will not move as much as expected or will end up in unusual positions. After birth, hypotonia can contribute to the baby having a poor sucking reflex, which hinders feeding and weight gain in early life. Developmental delays are also common.

Infants can also have distinctive features, such as almond-shaped eyes; a thin upper lip; a downturned mouth; and a long, narrow head. Many patients have short stature, in part due to growth hormone deficiency. A percentage of people with the syndrome lose a gene called OCA2, which is involved in making pigment in the skin and hair. These individuals have very fair skin and light-colored hair.

Later in childhood, around age 2 to 8, children's appetite often increases dramatically, and these individuals tend to not feel full after meals. This can subsequently lead to hyperphagia, or excessive eating, which can result in obesity and related complications, such as type 2 diabetes, heart issues and gastrointestinal problems. It's thought that this voracious drive to eat is triggered by issues with the hormones that normally regulate appetite, as well as by differences in brain areas involved with processing rewarding stimuli (like food).

Additional symptoms of Prader-Willi syndrome include cognitive impairment, ranging from mild to moderate; genital underdevelopment; sleep problems; nearsightedness; and underactive thyroid.

With adequate treatment and support, people with Prader-Willi syndrome can live into their 70s. But complications such as diabetes and heart failure can limit their lifespan if these conditions are not adequately controlled, and they can cause death by a person's 40s.

Treatments: There is no cure for Prader-Willi syndrome. Treatments vary depending which symptoms a person has, when those symptoms began and how severe they are.

To help patients feed in infancy, doctors may recommend high-calorie formula and special feeding methods, including tube feeding. Replacing missing hormones — with testosterone, estrogen or growth hormone, for example — can help offset symptoms related to low hormone levels. Growth hormone therapy was approved as a Prader-Willi syndrome treatment by the Food and Drug Administration (FDA) in 2000, and it's been shown to help boost muscle tone and growth while lowering body fat.

Physical, behavioral, occupational and speech therapies can help with motor skills, intellectual disabilities, and speech and language development. Medications might be recommended to help with sleep issues or psychiatric disorders that can be associated with the syndrome, such as psychosis.

The FDA also approved the first-ever treatment for hyperphagia in Prader-Willi syndrome in 2025. It's approved for patients ages 4 and older. The exact mechanism of this drug is unknown, but it's thought to help decrease the production of certain hunger-triggering signals from the hypothalamus.

Especially in childhood, patients with Prader-Willi syndrome should be kept on carefully controlled diets and eating schedules, the Mayo Clinic advises. Dietitians can help advise patients and their families on what to include in a healthy diet and whether supplemental vitamins or minerals might be necessary.

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

An experimental pill may work just as well as injectable, Ozempic-style drugs at treating type 2 diabetes, early trial results suggest.

The oral medication, called orforglipron, belongs to a class of drugs called glucagon-like peptide 1 (GLP-1) agonists. This class also includes Ozempic, which is made by Novo Nordisk and approved as a blood-sugar control aid in type 2 diabetes, as well as a treatment for people with type 2 and either heart disease or kidney disease. It also includes Wegovy, which has the same active ingredient as Ozempic but is approved for chronic weight management.

GLP-1 agonists are best known as weight-loss drugs, and likely drive weight loss in part by slowing digestion and curbing appetite by messing with hunger signals in the body. In diabetes, the drugs help lower blood sugar by boosting levels of insulin, the hormone responsible for shuttling sugar out of the blood.

However, as of yet, GLP-1s are all injectable medications that require refrigeration, The New York Times reported. It's possible that introducing a daily pill that can achieve the same results could potentially increase the availability and use of the medications, Lilly, the drug's maker, suggests.

Related: Ozempic-style drugs tied to more than 60 health benefits and risks in biggest study-of-its-kind

"Injections cannot be the solution for billions of people around the world," Dr. Daniel Skovronsky, chief scientific officer of Lilly, told The New York Times.

In a statement published Thursday (April 17), Lilly shared the topline results of a late-stage trial of orforglipron. The trial's results have not yet been published in a scientific journal but will be in the future, and the results will also be presented at the American Diabetes Association's 85th Scientific Sessions, the statement noted.

The trial included 559 adults with type 2 diabetes whose blood sugar was not adequately controlled with diet and exercise alone. For just over nine months, the participants took either orforglipron or a placebo pill daily. Those taking orforglipron got one of three doses: 3 milligrams, 12 mg or 36 mg.

After 40 weeks, the trial runners checked everyone's blood sugar levels using an A1C test, which can reveal average blood-sugar levels from the preceding three months. The test gives results as a percentage, with 6.5% or higher typically indicating diabetes and 5.7% to 6.4% signaling prediabetes. The participants in the trial started out with an average A1C of 8%.

After 40 weeks, the groups who took orforglipron saw their A1C drop by 1.3% to 1.6%, on average, while the placebo fell only 0.1%. That effect is about the same as what was seen in separate trials of Ozempic and Mounjaro, another GLP-1, The New York Times reported.

Around two-thirds of those who took the highest dose of the drug had their levels fall to less than or equal to 6.5%, the threshold for diabetes. The high-dose group also lost an average of 16 pounds (7.3 kilograms) each. The other dosing groups lost about 10 to 12 pounds (4.4 to 5.5. kg), while the placebo group lost about 3 pounds (1.3 kg).

"Given that participants had not yet reached a weight plateau at the time the study ended, it appears that full weight reduction was not yet attained," the Lilly statement noted.

The most common side effects were mild to moderate and were similar to those seen with other GLP-1s. For example, diarrhea, nausea, indigestion, constipation and vomiting were more common in the treatment groups than the placebo. Between 3% and 8% of the participants in each treatment group opted to stop taking the medication, compared to 1% of the placebo.

Lilly said it would seek approval from the Food and Drug Administration later this year to market orforglipron for obesity and early in 2026 for diabetes, The New York Times reported. In addition to the diabetes trial described above, the company is also testing the pill in adults with obesity or who are overweight with at least one weight-related medical problem. They're also investigating its use as a treatment for high blood pressure and sleep apnea in people with obesity.

The price of the pill has not yet been announced.

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

Five scientists who helped develop Ozempic-style drugs have been awarded a $3 million prize nicknamed the "Oscars of Science."

The Breakthrough Prizes are annual awards that aim to recognize "the world’s top scientists working in the fundamental sciences," according to the official website for the prizes. Six awards are given, in total, covering accomplishments in fundamental physics, mathematics and the life sciences.

This year, Dr. Jens Holst, Dr. Daniel Drucker, Dr. Joel Habener, Lotte Knudsen and Svetiana Mojsov have been announced as joint winners of one of three Breakthrough Prizes in Life Sciences for 2025.

"When something [like this award] drops in completely unexpected, that's nice, that's wonderful," Holst, a professor of medical physiology at the University of Copenhagen, told Live Science.

Related: Scientists behind tech in mRNA vaccines snag 2nd prestigious prize — is a Nobel next?

Holst and his colleagues received one of the life-science awards this year "for the discovery and characterization of glucagon-like peptide 1 and revealing its physiology and potential in treating diabetes and obesity," read an official statement.

Glucagon-like peptide 1, or GLP-1, is a hormone that the gut secretes after eating. The hormone stimulates the release of insulin, which lowers blood sugar levels, and it also slows down digestion, making people feel full. It's a key player in how the brain regulates appetite.

Drugs like Ozempic and Wegovy are examples of "GLP-1 receptor agonists" — they mimic the action of the GLP-1 hormone in the body to treat type 2 diabetes and obesity, respectively.

These drugs have garnered significant popularity over the past decade, and they are now being investigated as potential treatments for many other health conditions, ranging from substance-use disorders to Alzheimer's disease. In 2024, Wegovy also got regulatory approval in the United States to treat heart disease, although questions remain regarding how it actually treats the condition.

However, despite their success, GLP-1 receptor agonists have also faced considerable scrutiny. For instance, there have been reports of some patients experiencing nasty side effects, such as persistent vomiting and stomach paralysis.

Additionally, a large study published in 2025 revealed that these drugs may reduce the risk of developing 42 health conditions but may increase the chances of experiencing 19 others, including abdominal pain, low blood pressure and arthritis. This study was correlational, so it's unknown if GLP-1 agonists are actually driving these conditions, but it still raises questions about the drugs' long-term effects.

Even with these concerns, though, many believe these drugs have revolutionized the treatment of cardiometabolic disorders. In the U.S., 1 in 8 adults have reported using a GLP-1 drug at some point in their lives.

Holst and colleagues originally discovered the GLP-1 hormone back in the 1980s. Piece by piece, they gathered data showing that the hormone stimulated insulin secretion, and that it inhibited food intake and the emptying of the stomach after a meal, Holst said.

Over the years, the researchers further examined these physiological effects within the context of diabetes and obesity, which eventually led to the development of the widely used drugs that are household names today.

There is likely a huge interest around these drugs because they offer an alternative, and very effective, route to weight loss for people with obesity who might not have found success with other interventions, Holst said. However, as a doctor, he is more interested in their ability to treat the knock-on health concerns tied to obesity, such as certain cancers and atherosclerosis, which can lead to coronary artery disease, he added.

"What we know is that obesity is associated with a hell of [a lot of] complications," he said. "The important thing is that with these compounds, you can prevent that."

Holst and colleagues are now investigating how the body regulates its own GLP-1 hormone levels and whether this process can be manipulated. For instance, they want to see whether patients with obesity or diabetes could be given a drug that increases the secretion of their own GLP-1 hormone, rather than being given a drug that just mimics the action of GLP-1, Holst said.

In addition to the prize awarded to GLP-1's developers, the other two life sciences awards this year went to Dr. Stephen Hauser and Dr. Alberto Ascherio, for their work on multiple sclerosis, and David Liu for developing two common gene editing technologies known as "base editing" and "prime editing."

This year's winners will receive their awards at a ceremony in Los Angeles on April 5, 2025.

Scientists have spotted unique subtypes of fat cells in the human body, and by unraveling their functions, they found that the cells may play a role in obesity.

The research, published Jan. 24 in the journal Nature Genetics, could theoretically open up avenues for new therapies to mitigate downstream effects of obesity, such as inflammation or insulin resistance, the scientists said.

"Finding these [fat] subtypes is something very surprising," study co-author Esti Yeger-Lotem,a professor of computational biology at Ben-Gurion University of the Negev, told Live Science. "This opens up all kinds of potential future work."

The findings suggest fat cells "are more diverse and complex than we previously thought," Daniel Berry, a professor of nutritional sciences at Cornell University who wasn't involved in the study, told Live Science in an email.

Related: Fat cells have a 'memory' of obesity, study finds

Over the past few decades, research has shown that fat tissue does a lot more than simply store excess energy in the body. For example, fat cells, also called adipocytes, and immune cells work in concert to communicate with the brain, muscles and liver. This, in turn, helps to regulate appetite, metabolism and body weight, and it's also involved in related diseases.

"If something is wrong there," within the fat tissue, "it affects other places in the body," Yeger-Lotem said.

Not all fat is created equal

Scientists have also long known that carrying excess fat is linked with a risk of health conditions. However, one of the many aspects of obesity that have left scientists puzzled is that not all fat is created equal.

Visceral fat — fat cells that reside in the abdomen close to the internal organs — is linked to a greater risk of various health problems than fat under the skin, known as subcutaneous fat. For example, excess visceral fat comes with a heightened risk of heart attack, stroke, diabetes, insulin resistance and liver disease. Studies also suggest visceral fat is more "proinflammatory" than subcutaneous fat, which could potentially contribute to the ill health linked to obesity.

To better understand what might be happening inside fat tissues, Yeger-Lotem and her colleagues charted a "cell atlas" of adipocytes as part of the Human Cell Atlas, a global project that aims to map all the cells in the human body.

The researchers built this map using single-nucleus RNA sequencing (snRNA seq), which measures which genes are active and to what degree by looking at RNA, a molecular cousin of DNA. RNA molecules act as blueprints for proteins, shuttling instructions from the DNA in the cell's nucleus out to its protein-construction sites. By measuring RNA in the nuclei of cells extracted from fat tissue, the team gathered clues as to what each cell does inside the tissue.

Yeger-Lotem and colleagues examined samples of subcutaneous and visceral fat collected from 15 people during elective abdominal surgeries. Most adipocytes were fairly "classical" — meaning storing excess energy was their main purpose. But a small proportion of the fat cells were "non-classical," as their RNA suggested they carried out functions not typically associated with fat cells.

Among these cells were "angiogenic adipocytes," which carried proteins usually used to promote blood vessel formation; "immune-related adipocytes," which make proteins related to immune cell functions; and "extracellular matrix adipocytes," which are related to scaffold proteins that help support cells' structures. These cell subtypes, found in both visceral and subcutaneous fat, were also confirmed under the microscope.

This "state-of-the-art application" of snRNA seq suggests these cells may play a role in "remodeling" fat tissues, Niklas Mejhert, a professor of endocrinology at the Karolinska Institute in Sweden who wasn't involved in the study, told Live Science in an email. Remodeling here refers to the way fat tissues change in response to weight fluctuations or metabolic changes. "Healthy" remodeling would help maintain metabolic balance, but if dysregulated, it could spur inflammation and other drivers of poor health in obesity, Mejhert said.

Related: In a 1st, scientists reversed type 1 diabetes by reprogramming a person's own fat cells

The study also spotted differences in the newly described cell types depending on which tissue they were taken from. Unconventional adipocytes from visceral fat seemed more likely to communicate with the immune system than those found in skin fat, Yeger-Lotem said. This link to immune cells suggests the cell subtypes might play a role in triggering visceral fat's proinflammatory nature, which could help explain why belly fat is worse for health.

The data also hinted that the fat-tissue donors with higher insulin resistance tended to have a higher concentration of these unconventional cells in visceral fat than did people with lower insulin resistance. However, Mejhert noted that the authors did not prove causation, so it's not clear whether the cells might drive the insulin resistance in any way. It's too early to know.

If these fat subtypes can be linked to human disease, understanding how they work could "help us fight inflammatory processes," Yeger-Lotem said. That could potentially help doctors predict the risk of insulin resistance in people with obesity, assuming all the dots connect, she added.

Berry cautioned that the study used a relatively small sample size and that, at this stage, it only suggests rather than definitively demonstrates that the fat cells have these unusual functions. Still, "these insights highlight the importance of understanding fat depots' unique behaviors to develop targeted treatments for obesity and related diseases," he said.

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

Weight-loss drugs like Ozempic may decrease your risk of developing 42 health conditions, but increase your chance of experiencing 19 others, according to one of the most comprehensive studies-of-its-kind to date.

Glucagon-like peptide 1 receptor agonists (GLP-1RAs) have become increasingly popular over the past decade for the treatment of type 2 diabetes and obesity, with versions like Ozempic and Wegovy becoming household names.

These drugs help treat diabetes by promoting the release of insulin and helping to reduce blood sugar levels. But they have also been linked to weight loss, potentially by slowing down the digestion of food and curbing appetite. In 2024, Wegovy also received regulatory approval in the U.S. to treat heart disease, although the exact mechanism-of-action is unclear.

Evidence is additionally emerging to suggest that GLP-1RAs may help prevent the onset of conditions such as Alzheimer's disease and help patients to manage others like substance-use disorders. However, concerns have also been raised regarding the negative side effects of taking GLP-1RAs, including reports of gastrointestinal issues.

Related: Ozempic-like meds linked to higher risk of pancreatitis, 'stomach paralysis' than other weight-loss drugs

Now, in a new study, scientists have compiled what they say is the clearest ever picture of the effectiveness and risks associated with taking GLP-1RAs.

In the study, researchers assessed the impact of taking GLP-1RAs on the health of 215,000 people with type 2 diabetes over around four years. They then compared these effects to a control group of more than one million individuals who received different types of anti-diabetic drugs. Data on all participants was obtained from the U.S. Department of Veteran Affairs.

Overall, the researchers found that GLP-1RAs have many beneficial effects, some of which were previously recognized. For instance, those who took GLP-1RAs had a 9%, 8% and 12% reduced risk of having a heart attack, deep vein thrombosis and Alzheimer's, respectively, compared to controls. They were also less likely to develop substance-use disorders, including alcohol-use disorders and cannabis-use disorders (both an 11% lower risk), as well as having a 12% lower risk of experiencing bacterial infections.

These effects may somehow be linked to both the health benefits of physically losing weight, as well as other effects of GLP-1RAs in the body, such as reducing inflammation and influencing reward signaling in the brain, Dr. Ziyad Al-Aly, study co-author and an assistant professor of medicine at Washington University, said during a Jan. 16 news conference.

However, these benefits did not come without risks, the researchers observed. For example, GLP-1RAs also increased people's odds of developing gastrointestinal issues such as abdominal pain (12%), plus low blood pressure (6% higher risk) and arthritis (11% higher risk).

"We tend to think of drugs as being surgically designed to do only one thing, but the reality is, it's almost never like this," Al-Aly said.

The study, which was published Monday (Jan. 20) in the journal Nature Medicine, mainly used data from older, white males, meaning that the findings may not apply to other demographics.

Nevertheless, the hope is that healthcare providers could use the findings to decide whether patients should take these drugs, depending on their medical history, Al-Aly said.

"This [study] is a great example of the value of large databases of medical records data enabling not only a study to assess safety profile but also potential new uses for an increasingly widely used therapy for diabetes and obesity," Dr. Penny Ward, a visiting professor in pharmaceutical medicine at King's College London who was not involved in the research, told Live Science in an email.

The study was observational, therefore it cannot prove that GLP-1RAs cause these effects. To do this, a randomized controlled trial is needed, whereby the effects of GLP-1RAs are tested against a control group in a tightly-regulated way.

Fortunately, such trials are currently underway with results potentially available in the next one to four years, said Dr. Naveed Sattar, a professor of cardiometabolic medicine at the University of Glasgow in Scotland, who was not involved in the research.

"Such trials will lead us much closer to the truth," he told the U.K. Science Media Centre.

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

Weight-loss drugs that work like Ozempic can help users shed pounds. Now, a new study suggests the medications could also help people with alcohol use disorder.

The research, published Nov. 13 in the journal JAMA Psychiatry, adds to a growing body of work hinting these drugs could help people manage drug and alcohol addiction.

In the study, researchers used data from more than 227,000 people in Sweden's patient data registry, a national database of health records. The study's subjects were diagnosed with alcohol use disorder between 2006 and 2021. Among these, 4,321 people used semaglutide, the drug branded under the names Ozempic and Wegovy, and 2,509 people used liraglutide, another drug in the same class. Broadly, these drugs are called GLP-1 agonists because they mimic a hormone called GLP-1 that helps regulate appetite and hunger.

The analysis found that the people using the drugs were less likely to be hospitalized for problems linked to alcohol use disorder, such as intoxication and withdrawal symptoms like delirium, than the patients who weren't using the drugs. Semaglutide use was associated with a 36% lower risk and liraglutide with a 28% lower risk.

Related: Childhood obesity should be treated early and aggressively, new guidelines say. Is that safe?

Furthermore, the risk of hospitalization due to any substance use disorder was 32% lower in those taking semaglutide, while liraglutide was associated with a 22% lower risk.

The researchers also looked at naltrexone, a drug approved to treat opioid and alcohol use disorder. They found it was associated with a 14% reduction in the risk of hospitalization for issues related to alcohol and substance use.

"One of the most striking findings was that GLP-1 medications had a lower risk than alcohol-use disorder medications we use," study co-author Markku Lähteenvuo, a docent of forensic psychiatry at the University of Eastern Finland and Niuvanniemi Hospital, told Live Science.

That said, Lähteenvuo emphasized that this kind of study can't conclusively show that the drug directly treated a person's addiction. "These are associations, and we need to verify them in clinical trials," he said.

Still, he added, "the effect sizes were pretty big, so we are hopeful that these results are real."

Lorenzo Leggio, clinical director of the National Institute on Drug Abuse Intramural Research Program in Baltimore, said the work is "an interesting study that adds to the growing evidence" that GLP-1 agonists could help treat alcohol use disorder and addiction in general."It's important to note that alcohol use disorder and addictions are leading causes of hospitalizations, morbidity, and mortality," Leggio, who was not involved in the study, told Live Science in an email. "This study investigated important outcomes (hospitalizations) that are very relevant from a clinical and public health standpoint — another important strength of the study."

A growing body of work

Lähteenvuo and his colleagues aren't the first to spot the link between GLP-1 drugs and addiction.

"A few years ago, there was quite a buzz about these medications, and clinicians noticed their patients seemed to be reducing their alcohol intake," he said. "It was kind of a chance finding."

Since then, early research in the lab and some real-world studies have supported this observation. Studies on mice and rats found that semaglutide reduced the rodents' binge drinking episodes and dependence on alcohol, after they'd been provided with alcohol for some time. In addition, some observational studies in humans — including one published Wednesday (Nov. 26) in the journal JAMA Network Open — have found that GLP-1 agonists were linked to lower alcohol use in people with alcohol addiction.

And it's not just alcohol — previous studies found a link between Ozempic-like drugs and a lower risk of opioid overdose and cannabis-use disorder relapse.

These recent findings "offer the first real hope for the treatment of substance use disorder in decades," Patricia "Sue" Grigson, chair of the Department of Neural and Behavioral sciences at Penn State College of Medicine, told Live Science in an email.

Still, Grigson and Leggio noted that clinical trials are needed to show that the drugs are actually driving this change in addictive behaviors. The safety of using the drugs in this context also needs to be confirmed, Grigson added.

"These clinical trials are being conducted, and some have been completed," Grigson said. The emerging data is promising, but "we must await completion of further work to draw firm conclusions," she added.

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

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Losing weight can be a lot of work, which makes it all the more frustrating when, little by little, the weight creeps back. Now, a study suggests that fat cells retain a memory or past obesity, which may prime the cells to grow when exposed to high-fat foods.

The research "might add to the growing body of evidence that disproves lack of willpower as the underlying force behind 'weight cycling,'" said Dr. Katherine H. Saunders, an obesity physician at Weill Cornell Medicine and co-founder of FlyteHealth, a software and clinical services company for medical obesity treatment, who was not involved in the study.

Without weight-loss medications or bariatric surgery, most people will return to their original body mass within a few years of losing weight through a diet. This can lead to "yo-yo dieting." Scientists don't know why this happens, but genetics, environment and health history likely all play a role. Now, a study published Nov. 18 in the journal Nature adds an essential piece to this puzzle. Chemical modifications on DNA, or epigenetic markers, may help the cells retain a memory of their past state.

Related: Does it really take 20 minutes to realize you're full?

While DNA stays mostly the same throughout life, the way the body reads its DNA code is dynamic, thanks to epigenetic modifications: By tightly packing some sections of DNA and covering other parts of the molecule with chemical tags, these modifications change how a cell uses the DNA and, consequently, how the cell functions.

In the new study, scientists observed mice that were given a high-fat diet before switching back to a normal diet to return them to their starting weight. Once they dropped the extra weight, the mice were metabolically indistinguishable from mice that were never fed a fatty diet. However, when the researchers looked at the mice’s fat cells, they found that despite their weight loss, the cells still carried epigenetic changes that had arisen during the weight gain.

To check whether this also happens in humans, the team then analyzed cells from people who had undergone bariatric surgery. There, they found patterns of gene activity that suggested epigenetic changes took place and persisted after weight loss, said study co-author Laura Hinte, a doctoral student of nutrition and metabolic epigenetics at ETH Zurich.

"Adipocytes [fat cells] are known to go through a kind of identity crisis in obesity — they kind of forget who they are and what they are supposed to be doing," Hinte told Live Science. This work showed those changes remained "long after the mice had lost weight," she said, and a similar identity shift might be happening in human fat cells, the data suggest.

Further evidence came from a closer look at the mice's fat cells. When removed from the formerly obese mice and bathed in glucose and palmitate — high-sugar and fatty ingredients — the fat cells enlarged more quickly than those taken from control mice. The formerly obese mice also gained weight more quickly when provided a high-calorie diet, compared with the controls.

"The epigenetic changes didn't have consequences for the mice as long as they were in a healthy environment," Hinte said, referencing when the mice were given a standard diet.

Other mechanisms are likely involved in weight rebound, Hinte added. For instance, it's "very likely" that this memory exists in other cell types in the body, such as neurons, where these modifications may affect appetite in people who have lost weight.

The study doesn't prove that epigenetic changes directly cause weight rebound. However, it strongly suggests that these mechanisms may play a role in the complex interplay of forces that drive obesity.

Dr. Fatima Cody Stanford, an associate professor of medicine and pediatrics at Harvard Medical School, who was not involved in the study, said it "offers valuable insights into why maintaining weight loss is challenging."

She noted, however, that the observations in lab mice "may not fully represent the complexity of human obesity." Another major caveat to this study is whether it has practical applications, she said. To date, scientists haven't found many molecules that can tweak the epigenetics of DNA in a cell's nucleus.

The work also "strengthens the argument for early intervention when it comes to both weight gain and weight regain," Saunders told Live Science.

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

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Some modern Japanese people may have a higher body mass index, or BMI, thanks to DNA they inherited from prehistoric hunter-gatherers.

In a new study, researchers analyzed the genomes of more than 170,000 people living across Japan, from Hokkaido in the northeast to Okinawa in the southwest, and compared this modern DNA with 22 prehistoric Japanese and Eurasian genomes from a previously compiled dataset.

Specifically, the researchers examined how DNA inherited from the Jōmon people, a cultural group of hunter-gatherer fishers who lived in Japan up to 16,500 years ago, may be associated with 80 different complex traits in modern Japanese people. Complex traits are those encoded by multiple genes and include traits such as height, BMI and the amount of oxygen-carrying cells in the blood.

The scientists found that, on average, Japanese people have inherited around 12.5% of their DNA from Jōmon hunter-gatherers. Of all the traits studied, BMI was the only trait significantly associated with Jōmon DNA — meaning individuals with more genetic evidence of Jōmon ancestry were significantly more likely to have a higher BMI than those carrying less of this prehistoric DNA.

Therefore, this DNA may put the individuals who carry it at a higher risk of obesity, the researchers wrote in the paper.

Related: Papua New Guineans, genetically isolated for 50,000 years, carry Denisovan genes that help their immune system, study suggests

BMI is an imperfect measure of body fat, partly because it doesn't distinguish between fat and lean body mass. It's also mostly based on data from white populations, so its health implications don't always generalize to other demographics. Nonetheless, high BMI has been tied to various health risks, such as type 2 diabetes, and the metric is still in widespread use in medicine.

In addition to analyzing DNA from people in Japan, in separate analyses, the researchers focused on people with Japanese ancestry living abroad, including 2,200 East Asian people living in the U.K. These groups showed similar links between Jōmon ancestry and BMI, underscoring the far-reaching effects of this genetic legacy.

The researchers described these findings in a paper published Nov. 12 in the journal Nature Communications. They said the study is a demonstration of natural selection — the driving force behind organisms evolving useful traits over time. What may have been a positive trait in the past can negatively influence disease risk in a modern context, they concluded.

"It is a really important discovery that ancient hunter-gatherer ancestry is likely to play a key role in the health of modern day populations," study co-author Shigeki Nakagome, an assistant professor in genomic medicine at Trinity College Dublin, said in a statement. "The link to an increased BMI could also help to explain some of the disparities in obesity prevalence among Asian populations residing in Western countries."

The researchers found that Jōmon genes were very active in skeletal muscle cells, which enact voluntary movements. Some of these genes had previously been tied to a higher BMI. The team theorized that this DNA may have helped prehistoric hunter-gathers adapt to the high physical demands of their lifestyle.

Previous research has also shown that several of these Jōmon genes may increase bone mineral density, or the concentration of calcium and other minerals in bone. This is a sign that a person exerts elevated levels of physical activity. Having larger muscles and denser bones might bump up a person's BMI.

The new study also provides further evidence to support an emerging theory in population genetics.

For about three decades, many scientists have hypothesized that modern Japanese people originate from two ancestral groups: Indigenous Jōmon hunter-gatherers and migrants from Northeast Asia. However, recent evidence, including data from this new study, is beginning to turn this theory on its head, suggesting that a third ancestral group from East Asia also left their genetic imprint on modern Japanese people.

"I am sure there is much left to discover, both in Japanese populations, and in others across the globe," Nakagome said in the statement.

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The drive to eat may be controlled by a very simple circuit in the brain, new research in mice suggests.

Just three types of brain cells collaborate to suppress or enhance appetite, driving mice to eat less or more food, the study found.

First, specialized neurons detect "hunger-signaling hormones" that say whether an animal is full or hungry. These neurons then control the activity of neurons in a different part of the brain, which in turn, controls a third set of neurons in the jaw: These final nerve cells direct the movements needed for chewing.

The three-part circuit acts like a reflex, without needing conscious thought to direct it — similar to yanking your hand away from a hot object. In this case, the stimulus that sets off the reflex is a hunger-signaling hormone, and the resulting action is moving the jaw to chew.

Related: 'This is largely uncharted territory': Scientists reveal the brain's 'fear circuit' works differently than we thought

The new study, published Oct. 23 in the journal Nature, included only mice, and the three-part circuit has yet to be identified in humans. However, if it is found in people, this discovery could "change the narrative" on obesity, the authors behind the study argue.

"The control of how much we eat and when we eat is not so much based on your decision process, it just happens — it's a simple circuit," Christin Kosse, lead study author and a research associate at The Rockefeller University in New York, told Live Science.

In recent decades, medical organizations have characterized obesity as a chronic disease with an array of causes, including genetics. Previously, it was considered to be simply a consequence of personal decisions around eating. The new study adds evidence to the idea that physiological differences underlie obesity.

The new research also helps tie a number of existing theories about hunger together.

The first is known as "set point theory." Some scientists think that people generally have a body weight set point determined by their genetics and their environment. As the theory goes, a person's body tries to keep weight constant, even if they eat more or less food than they need — as such, there are various physiological mechanisms that help adjust for these fluctuations in calories.

But if these mechanisms fail, people may gain or lose weight.

For instance, after a filling meal, fat cells and cells in the gut release hunger-controlling hormones that signal to the brain that you should stop eating. These signals kick in approximately 20 minutes after you eat enough to be satiated. However, if this hormone signaling is disrupted for some reason, people can become extremely hungry even when they've eaten enough. In some cases, this can drive people to overeat to the point of becoming severely obese.

Previous research has shown that neurons in part of the brain called the hypothalamus play a role in regulating appetite, and they are targeted by weight-loss drugs in the same class as Ozempic. In addition, reductions in a protein called brain-derived neurotrophic factor (BDNF) in the brain are associated with obesity in both animals and humans.

The new study connects the dots between these findings.

In their experiments, Kosse and colleagues discovered that neurons in the hypothalamus that make BDNF are activated in the brains of mice who became obese after being fed a high-fat diet. This implies that these BDNF-making neurons activate in response to weight gain in order to suppress the rodents' appetites.

To test this hypothesis, the team switched these BDNF neurons on and off. When the neurons stopped working, the mice ate about 1200% more food than they normally would, and they made chewing movements even when there wasn't any food available to them. In some cases, they even started attempting to eat objects, such as wooden blocks, suggesting that this response was automatic.

Conversely, when the neurons were turned on, the opposite effect happened: The mice stopped eating and also didn't make any chewing movements. Once the team realized these BDNF neurons flip a key switch in the brain, they identified the two other types of neurons involved in this circuit.

Kosse believes that it is likely that we humans have a comparable control system for hunger in our brains.

Moving forward, the team now wants to see if this circuit changes in the context of different emotional states, such as anxiety.

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Retrievers are known to be food-motivated dogs, but a gene mutation found in some of these pups causes them to have not only an insatiable appetite but also lower metabolism, a combination that can lead to obesity, a new study finds.

This "double whammy" is caused by a mutation in the POMC gene, which plays a role in satiety by alerting the brain of hunger, according to a statement.

This genetic anomaly affects 25% of Labrador retrievers and 66% of flat-coated retrievers, and can cause the dogs to feel hungry even when their stomachs are full, according to a study published Wednesday (March 6) in the journal Science Advances.

"We found that a mutation in the POMC gene seems to make dogs hungrier," Eleanor Raffan, an assistant professor in systems physiology at the University of Cambridge in the U.K., said in the statement. "Affected dogs tend to overeat because they get hungry between meals more quickly than dogs without the mutation."

In the study, researchers analyzed 87 adult pet Labrador retrievers that were either a healthy weight or were slightly overweight. The researchers fed each dog a can of food every 20 minutes until the canines were stuffed. All of the dogs "ate huge amounts of food," but those with the POMC mutation ate the same amount as those without it, showing "they all feel full with a similar amount of food," according to the statement.

Related: How long do dogs live?

However, on a separate day, the researchers conducted what they called the "sausage in a box test." Three hours after feeding the dogs a basic breakfast, they tempted them with a meaty tidbit inside a clear plastic box with a partly cut open lid, so that the dogs could smell but not access the delectable treat. 

The dogs with the mutation "tried significantly harder" to nab the sausage versus those without it, indicating that they were more motivated to snag the snack due to higher hunger.

After the test, dogs slept in chambers that measured the gases they exhaled, as an approximate measure of their metabolic activity. This revealed that the POMC canines burned about 25% fewer calories than the other dogs when at rest.

The team also found that the POMC mutation changes a pathway in the dogs' brains that is linked to body-weight regulation. In effect, the mutation drives a starvation signal that tells the body to eat more food and to conserve energy by slowing down the metabolic rate even though the dogs are not actually starving.

Interestingly, the POMC gene and its effect on brain pathways is similar in humans, and mutations in the gene can also lead to obesity.

"People are often rude about the owners of fat dogs, blaming them for not properly managing their dogs' diet and exercise," Raffan said. "But we've shown that Labradors with this genetic mutation are looking for food all the time, trying to increase their energy intake."

She recommended that retriever owners space out food rations, for instance, by putting their dog's food in a puzzle feeder or by spreading it around a yard so it takes the dogs longer to eat it.

"It's very difficult to keep these dogs slim, but it can be done," Raffan said.

When you scarf down a massive dinner, your stomach will stretch to fit each morsel, activating receptors that ping the brain to let it know when you are "full."

A group of engineers has developed a vibrating pill that could help trigger that filled-up sensation sooner, which may one day help treat obesity. When the ingestible pill was given to pigs 20 minutes before eating, they ate roughly 40% less than pigs without the vibrating device, according to a study published Dec. 22 in the journal Science Advances.

"For somebody who wants to lose weight or control their appetite, it could be taken before each meal," Shriya Srinivasan, an assistant professor of bioengineering at Harvard University and lead author on the study, said in a statement. "This could be really interesting in that it would provide an option that could minimize the side effects that we see with the other pharmacological treatments out there."

Related: Common weight-loss surgery for teens may weaken their bones

Past studies have shown that vibration can create the illusion of stretching in skeletal muscle fibers. With this in mind, Srinivasan and her colleagues developed a pill to mimic this phenomenon in stomach muscles "that could modulate hormones and eating patterns," she said. To prevent the pill from vibrating before it reaches its destination, they coated it in a gelatinous membrane that dissolves only when submerged in gastric fluid, or the acidic juices that slosh around in the stomach to break down food. Once the pill's outer layer dissolves, it releases a spring-loaded pin that activates a vibrating motor, which runs for about 30 minutes. The pigs eventually poop out the pills.

After developing the pill, the researchers performed multiple experiments to test its safety and effectiveness in 12 Yorkshire pigs. For their main feeding test, the scientists separated the pigs into two groups, with one cluster receiving the vibrating pill and another given an inert placebo pill. Over the next two weeks, the pigs were given 108 meals and overall, animals with the device ate significantly less than the other group.

Additionally, the researchers took blood samples from the pigs before and after they were given the device, and found that the vibrating-pill-popping swines had lower levels of ghrelin, also known as "the hunger hormone," than the control group.

"The strong hormonal response to the vibrating capsules surprised me. It seems the body might be truly tricked into thinking it has just consumed a satisfying meal," Benjamin Terry, an associate professor of mechanical engineering at Brigham Young University who was not involved in the study, told Live Science in an email.

After the feeding experiment, an endoscopist assessed the lining of the pigs' stomachs and found that there were no abrasions, irritation or inflammation, suggesting that the vibrating pill does not harm the stomach muscles. Now, the researchers are planning to scale up the manufacturing of the pill, a step required to launch clinical trials in humans.

While these results are promising, "it remains to be seen if the results from this work will translate to humans," Terry said. Currently, the device is the largest allowed capsule size by the Food and Drug Administration, which might be "prohibitively large" if it eventually hits the consumer market, he said.

And while the pill might trigger some of the physical mechanisms that contribute to fullness, people overeat for many reasons "unrelated to satiety," including stress, distraction, social pressure and environmental cues, Terry said. "It's not clear that any of these eating pressures will be diminished by the vibrating capsules," he added.

However, the authors say that this vibrating pill could eventually offer a cost-effective and less invasive alternative to other obesity treatments, such as surgeries or intragastric balloons, a medical implant designed to reduce the volume of your stomach.

"For a lot of populations, some of the more effective therapies for obesity are very costly," Srinivasan said. "I'd love to see how this would transform care and therapy for people in global health settings who may not have access to some of the more sophisticated or expensive options that are available today."

"Inflammation is the new evil. Let me explain."

"You might think inflammation isn't really THAT big of a deal…but trust me when I say it is." 

Scan social media and you'll easily find content that portrays inflammation as a villain. 

In every bookstore you'll find at least one anti-inflammatory diet recipe book, and in your local drug store, an array of products parading their magical anti-inflammatory ingredients. 

But inflammation has evolved over millennia to protect us, says Ruslan Medzhitov, a Sterling Professor of Immunobiology at Yale University School of Medicine and Investigator at the Howard Hughes Medical Institute in Maryland who studies inflammation in the context of autoimmune disease and allergies. 

Related: 'If you don't have inflammation, then you'll die': How scientists are reprogramming the body's natural superpower

So if not all inflammation is bad for us, how do we know the difference between "good" and "bad?" 

Live Science spoke with Medzhitov about how inflammation is the body's response to a system out of equilibrium, how chronic inflammation results from a mismatch between our evolutionary environment and the modern one, and whether there's any evidence for specific "anti-inflammatory" diets.

Emily Cooke: What is inflammation?

Ruslan Medzhitov: Inflammation is an essential part of our defense system. It evolved to protect us from a variety of challenges, including many challenges that come from the outside world, such as infection or injury or toxins. Without inflammation, we would quickly succumb to infections and die and that would be the end of it. 

Mostly what we know about inflammation is what happens at the extreme, when there is an infection or injury and then there is swelling and redness and fever and things like that. But inflammation plays an important role in a variety of settings, including when we don't diagnose it clinically as inflammation, including when we may not even feel it, it's asymptomatic. 

Under the hood, it plays an important role in coordinating metabolism, different physiological functions and so forth. Those functions of inflammation are much, much less appreciated and much less studied. And just to give one quick example of the reach of inflammation throughout biology is that it controls our metabolism, controls adaptation to the environment in terms of thermogenesis [heat production] and [even controls] aspects of behavior. And that last part is what's particularly interesting, where inflammation can for example, control mood. It can control avoidance behaviors, and anxiety behaviors. And these are all presumably by design, meaning that these are meant to be protective phenomena, they're beneficial in certain settings. When this response becomes dysregulated in some way, it can lead to particular types of pathologies and disorders and so forth that inflammation unfortunately is more famous for. 

Related: Brain inflammation may drive mood changes in Alzheimer's

EC: Is there such a thing as "good" and "bad" inflammation?

RM: Yes, and there are two ways to divide between good and bad inflammation. 

So, good inflammation operates within the normal range. What is "normal" is decided not by us, by how we feel. It is decided by millions of years of evolution and calibrated by, on average, if you have this type of response, on average you have a better chance for survival. But that was in a very, very different setting. Throughout our evolutionary history, of course, our environment was very different. But the genes that evolved under those conditions, we still have them and they still operate as if nothing [has changed], because dramatic change in the environment happened only very recently. 

Good inflammation will be the one that operates with the right magnitude, that provides maximum benefit and lowest possible cost. 

But that line is very fuzzy and one can shift into what would be now called "bad" inflammation, which is a protective response but in overdrive. 

Phenomena like cytokine storms [when chemical signals associated with inflammation go haywire], sepsis [an over-reaction to infection], anaphylactic shock [a severe allergic reaction], these are all examples of inflammation that went way too far in magnitude, so it's induced too strongly. 

Again, what is a good magnitude versus too much? The logic of it is decided by evolution. 

So one delineation of good inflammation [versus] bad inflammation is just the magnitude of the response. 

The second type is when inflammation may be induced in the right magnitude, but it's induced for the wrong reasons. And that is what often leads to chronic inflammation. But the reason that happens is, again, in large part, a mismatch between our evolutionary history and modern environment. [Being obese was uncommon in our evolutionary past], because that would be unheard of under normal, natural conditions where you have to walk for 10 miles to find something to eat every day. 

In the modern environment, obesity is common. But that's not what our genes evolved to deal with and they misinterpret it, induce inflammation and then obesity-associated inflammation then becomes a problem. 

And the second example of that is aging-associated inflammation. Most of our ancestors throughout history would be dead by 30 years of age. Therefore the body is not, sort of, designed to deal with changes that happen at an advanced age. Many age-related deteriorations in body functions can be interpreted by inflammation as, "oh, something is off, I'm supposed to get in action when something gets off a normal homeostatic [self-regulating] range." And what happens then? It creates this vicious cycle where, [in response to] these deviations that are age-related or obesity-related or [related to] other evolutionarily-new and modern aspects of our lifestyle, inflammation is induced. [The body is] thinking "I will try to fix it." But there's nothing to fix. And that's what is, really, mostly bad inflammation. 

Related: DNA-damaging gut bacteria may fuel colon cancer in patients with inflammatory bowel disease

EC: Is it possible to modulate "bad" inflammation with lifestyle changes, for example with anti-inflammatory diets? Is the evidence actually there? 

RM: Yes, it is possible to modulate it.  But if you look at the common denominator —  so exercise, diet, healthy food, diverse food, avoid processed foods, avoid sedentary lifestyle, have enough sleep, reduce stress — if you think about what is the common denominator, all of them have one thing in common: modify your lifestyle to approximate, slightly better, the way we evolved to be. 

EC: From an immunobiology perspective, what message would you want people to know if they were concerned about inflammation? 

RM: Well, I would say that inflammation in general is something that we all need to protect ourselves. We don't want to completely eliminate it, that would be lethal basically. Without inflammation we cannot survive. That most causes of unwanted or "bad" inflammation in the modern world, in industrialized countries at least, have to do with aspects of our lifestyles that are unnatural and unhealthy. And I think diet and physical activity are probably the major drivers. 

I mean, this is not anything new. 

But having said that, there are also conditions that are truly pathological, like autoimmune diseases, for example, or sepsis, and that's where inflammation is mostly evil and mostly just needs to be knocked down and controlled. 

But for the majority of people this has to do with chronic inflammation that may be even asymptomatic, sub-clinical, but under the hood slowly contributes to various sorts of unhealthy conditions. And that's where the steps of simple interventions of having the right diet and the right physical activity [come in.]

And I would just add one more thing. Nobody knows what the right diet actually is. I think it's a failure, both on the part of the scientists, and the part of communicators of science. Because if the science is not there, what do you communicate? 

And that's that we don't really understand food. We don't understand what a healthy diet is. We don't understand how it affects our bodies. We know some obvious things, trivial things, calories and things like that, vitamins. But beyond that our knowledge is really at the medieval level. 

And that, I think, is going to be the next big frontier in biomedical science. So when I say healthy food, healthy diet, I'm just saying it in sort of, in terms of the obvious aspects of it. Eating processed food, highly processed simple sugars, high calorie, unbalanced, those are things that are obviously bad. But beyond those trivial aspects, there is a lot more to it that we don't really understand. So, I say healthy diet, but with the qualification that we only know very little about what a healthy diet really is. 

Editor's Note: This interview has been condensed and edited for clarity.

Feline obesity is a growing problem, with roughly 60% of cats in the United States classified as being overweight or obese, according to the 2022 State of U.S. Pet Obesity Report.

And, just like in humans, packing on additional pounds can often lead to a host of different health problems in cats, including changes to their digestive system, type 2 diabetes and chronic inflammation, according to a study published Sept. 29 in the Journal of Animal Science.

"It is a huge problem," study co-author Kelly Swanson, a professor of human nutrition and the interim director of the Division of Nutritional Sciences at the University of Illinois Urbana-Champaign, told Live Science in an email. "Similar to other species, feline obesity is associated with numerous health problems. If we can avoid obesity, many other health issues may be prevented or delayed."

Related: Cats have nearly 300 facial expressions, including a 'play face' they share with humans

To find out what happens when our feline friends habitually overindulge, scientists corralled 11 adult spayed female cats and let them gobble up as much standard dry cat food as they wanted, according to a statement. The study also included several cats that were fed a controlled diet to compare the effects of their food intake.

The overeating cats' average body condition score (BCS) — a measurement system similar to body mass index (BMI) in humans — was 5.41 on a 9-point scale at the beginning of the study, but after 18 weeks of overindulging, that number shot up to 8.27, which corresponded to being 30% overweight, according to the study.

As the felines tipped the scales, researchers observed not only a surge in poop production but also a rise in gastrointestinal transit time, which is the amount of time between eating and bowel movements. (To measure this, cats were fed a bright-green, non-digestible dye that turned their poop green.)

"That led to a reduced amount of time for the body to digest the food consumed, resulting in a reduced digestive efficiency (nutrient digestibility)," Swanson said. "That also affected the fecal microbiota of the cats, likely due to the reduced digestion (more nutrients passing through)."

Because the cats were not getting all of their proper nutrients, the researchers noticed "significant changes" in the gut microbial compositions in the fat cats. For instance, they recorded an increase in Bifidobacterium, bacteria that inhibit pathogens and stimulate the immune system, and a decrease in Collinsella, bacteria that break down fiber and can protect against inflammatory diseases, according to the statement.

Interestingly, this is the opposite of what happens in overweight humans. However, more research is needed to understand why.

The cats' poop also became more acidic due to a decrease in fecal pH, indicating poor absorption of carbohydrates and fat — which is related to "higher food intake and reduced digestibility," according to the statement.

Swanson said that because the study was relatively short and lasted only 18 weeks, none of the cats developed any long-term health conditions, and that once the study commenced, researchers "placed [them] on a weight-loss study so they are all back at a healthy body weight again."

When Ötzi the Iceman was ambushed and killed about 5,300 years ago in the Alps, he may have been balding and getting fat, a new study suggests. 

Ötzi has been famous ever since German tourists discovered his mummified body in 1991 in an Alpine pass in northern Italy. The latest study is one of many to investigate the prehistoric man, including the tools and weapons he carried, his clothes, his last meal, what the climate was like during his lifetime, and the route of his final journey before his high-altitude murder.

In the new study, researchers studied DNA preserved in Ötzi's left ilium — part of his pelvis, which also underwent a genetic analysis in 2012 — and determined that Ötzi, who died in his mid-40s, had a predisposition to male-pattern baldness, diabetes and obesity.

The findings also reveal that Ötzi largely descended from the latest wave of immigrants to Europe from Anatolia — modern Turkey — who brought early farming techniques to the continent about 8,000 years ago. 

The DNA analysis also indicates that Ötzi had darker skin than previously thought and would have had dark hair — before he started going bald, at least.

Related: Ötzi the Iceman had just sharpened his tools days before his murder

Iceman genome

The new study, published Wednesday (Aug. 16) in the journal Cell Genomics, is a revision of the 2012 study by a different group of scientists; genetic tests were complex and costly at that time, and the latest researchers have determined that the earlier samples were significantly contaminated with modern DNA.

The team sampled the same iliac bone, but they used updated genetic techniques to generate a more thorough sequence of Ötzi's genome. They then applied what has been learned about genetics over the past 10 years.

The results show that Ötzi probably looked different than many people thought.

"Ötzi might have had relatively dark skin and a risk of male-pattern baldness," study lead author Ke Wang, an archaeogeneticist at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, told Live Science.

The findings are contrary to previous assumptions about Ötzi's appearance; he is often portrayed as looking like a light-skinned European with long fair hair. But "the new findings fit better with the actual appearance of the mummy," Wang said in an email.

Study co-author Albert Zink, a palaeoanthropologist and the director of Italy's Institute for Mummy Studies, noted some of the portrayals should be updated. "It's not urgent, because these are always just an interpretation," he told Live Science. "But in the future they should consider making his skin and hair darker."

Ötzi's genetics also reveal surprising details about his ancestry. Earlier research suggested he may have been related to modern Sardinians, but the new analysis shows he had an unusually high level of ancestry from early Anatolian farmers.

These results suggest that Ötzi came from an isolated Alpine population that seldom interbred with other hunter-gatherer groups, Zink said.

Ötzi reconsidered

The latest study is not the first to reassess who Ötzi was and how he died; an archaeological study last year determined that he probably died somewhere away from the gully where he was found and that his body had been carried there by the subsequent movements of the ice.

Lars Pilø, an archaeologist with the Secrets of the Ice project who led that research but was not involved in the latest study, told Live Science that the latest study resolved the lingering question about whether the skin of Ötzi's mummy was his natural hue. (It was.)

However, Pilø didn't completely agree about Ötzi's baldness. Although Ötzi may have been genetically predisposed to going bald, the hairlessness of his mummy was probably the result of the preservation process, he said.

"Ötzi the Iceman keeps having new surprises in store for us, which is remarkable as he must be the most investigated archaeological find ever," Pilø said.

Over the past year, there has been an explosion in the popularity of GLP-1 receptor agonist drugs — namely Ozempic and Wegovy, which are respectively used to treat diabetes and obesity.   

However, recent reports, heralded by a CNN story published on July 25, have highlighted several cases of persistent vomiting and "stomach paralysis" in people who take the drugs. The U.S. Food and Drug Administration (FDA) also told CNN that they'd received reports of people experiencing such symptoms after taking semaglutide — the active ingredient in Ozempic and Wegovy — but have not yet determined whether the problems arose from the drug itself or from underlying medical issues. 

And in the first case of its kind, a woman in Louisiana has now sued the makers of Ozempic and another GLP-1 agonist, Mounjaro, over claims that the drugs caused her severe gastrointestinal injuries. 

So should consumers be worried? And if so, how might these drugs be causing these side effects? 

Related: Could Ozempic be used to treat addiction? Studies hint yes, but questions remain

How do GLP-1 agonists work?

To make sense of these anecdotal reports, let's go back to the basics of how these drugs work. GLP-1 receptor agonists mimic the action of a hormone — glucagon-like peptide 1 — that the gut secretes after eating. 

GLP-1 has two major roles, Dr. David Levinthal, director of the University of Pittsburgh Medical Center Neurogastroenterology & Motility Center, told Live Science. "One is glucose control, so promoting insulin release and helping reduce blood sugar, and the other is actually programming some of the body's response to a meal, which includes both what the stomach does and what the intestine may do as well."

In the stomach, GLP-1 works almost like a "brake system," essentially slowing down the rate at which the stomach would normally empty food into the small intestine, he said. 

Could GLP-1 agonists cause "stomach paralysis"?

According to Levinthal, stomach problems are a known and common side effect of GLP-1 receptor agonists like Ozempic and Wegovy. Most commonly, these stomach issues include nausea and diarrhea. 

"Probably a lot of the weight loss [caused by these drugs] is because it actually does impact the stomach's function in a way that probably influences people's appetite, because the stomach isn't emptying very well," Levinthal said. Plus, they interact with parts of the brain that regulate appetite.  

Dr. Robert Kushner, a professor of medicine in endocrinology at Northwestern University Feinburg School of Medicine, told Live Science that the way these drugs slow down stomach emptying has been known from "the very beginning of time when these hormones were identified." He explained that patients can expect to experience reduced stomach emptying as their treatment dose is raised to the optimum level, at which point it is crucial that they eat slowly, monitor fat intake and spread meals throughout the day. 

Some users may be more likely to experience a greater reduction in stomach emptying as they are already predisposed to this side effect. For example, if they have type 1 diabetes, where high amounts of blood sugar can cause damage to the vagus nerve that normally instructs the stomach to empty food, Kushner said. Patients with type 2 diabetes may also experience similar symptoms, but their risk is lower than that of those with type 1. In a late-stage trial of Ozempic, which included people with type 2 diabetes, most patients who reported gastrointestinal side effects had mild to moderate symptoms which reduced over time. 

Typically, patients with severely reduced stomach emptying experience symptoms of vomiting, abdominal pain and feeling full after eating only a small amount of food. Kushner warned, however, that referring to this slow stomach emptying as "paralysis" may cause alarm. 

"The medical term [for this condition] is actually gastroparesis, which means slowing of the stomach," he said. The condition is also called gastric stasis, where "statis" refers to a state of inactivity. "Paralysis sounds scary to me, so I can understand why some people would be worried about that." 

"In the vast majority of people, this [drug-induced gastroparesis] is readily reversible with decreasing dose or stopping the medication," Dr. Siddharth Singh, a gastroenterologist at UC San Diego Health, told Live Science in an email.

Related: Watch out for Ozempic copycats containing unauthorized active ingredients, FDA warns

What about "cyclic vomiting"?

According to the CNN report, one Ozempic user who'd experienced gastroparesis was also diagnosed with "cyclic vomiting syndrome" (CVS), and reported having to "throw up multiple times a day" even after she stopped taking the drug.

"Cyclic vomiting syndrome is a distinct disorder that looks a lot different than gastroparesis," Levinthal said. "It's an episodic disorder where people are fine almost all the time, and then have an episode of intense nausea and repetitive vomiting." By comparison, the vomiting associated with gastroparesis tends to occur towards the end of meals or just after someone has finished eating a meal. 

He emphasized that he'd need to know more about the woman to make a diagnosis but implied the need to be cautious in distinguishing between the two disorders and determining the influence of GLP-1 receptor agonists in both contexts. "It would be very unusual, I think, to link these drugs to that disorder [CVS]," he concluded. 

Singh also urged caution about interpreting the reports of vomiting and about being aware of the distinction between typical gastroparesis and CVS. 

"There have been rare reports of this [drug-induced gastroparesis] persisting after stopping the medication," he said. "I would not equate this with 'cyclic vomiting' — cyclic by nature implies intermittent or periodic, and I'm not sure if this drug would cause cyclic vomiting."

Related: Woman who spontaneously vomited up to 30 times a day likely had rogue antibodies

So, what should consumers know?

First and foremost, Kushner warned that when starting one of these drugs, patients should ensure that they're under a clinician's supervision. 

"It is important that anyone who goes on these medications works closely with the prescriber," he said. People should not attempt to take the drugs by other means, for instance, through being "prescribed by the internet without any guidance or supervision."

Patients should also know the potential side effects, and understand what measures can be taken to mitigate them. This may include reducing dietary fat, not skipping meals and staying hydrated, Kushner said. He added that anyone who experiences any side effects should let their prescriber know as soon as possible.

Levinthal also felt that the fear of potential side effects should not put people off taking the drugs if they could benefit from them. 

"It's becoming kind of a cornerstone of treatment for people with gastrointestinal problems — diabetes, and obviously more recently, weight loss, with astounding effect sizes," Levinthal said. "I wouldn't want people to be scared off from even trying the medication in the first place."

The diabetes drug Ozempic has dramatically reshaped weight-loss treatment. Combined with dieting and exercise, weekly injections of the drug can help people drop 15% of their weight. However, Ozempic doesn't directly change the body's ability to burn fat. Rather, it works in part by altering the brain's response to food.

So how does the brain regulate body weight?

Each of us has a given weight — known as a set point — that our brain wants to maintain, much in the same way it keeps body temperature within certain limits, Dr. Michael Schwartz, a professor of medicine at the University of Washington, told Live Science. Over the course of human evolution, those that maintained their body fat at a constant level were more likely to survive periods of food scarcity, as well as avoid health problems that come with being overweight, he said.

Set point theory explains why diets so often fail: The brain "wants" to keep people at a higher weight than average, and sends out chemical signals that spur hunger and other cues that make it hard to shed pounds. People who do manage to lose that weight struggle to keep it off over the long term for the same reason.

It's the "single biggest obstacle to long-term weight loss," Schwartz said.

Related: Invisible nerve-cell superhighway allows fat cells to 'talk' to the brain — and it may promote obesity

When we eat, the gut secretes hormones and small peptides — tiny fragments of proteins — into the bloodstream, including glucagon-like peptide 1 (GLP-1), which Ozempic messes with, and ghrelin, which helps regulate hunger. These chemicals reach the brainstem via the gut-brain axis, a communication highway between the gut and brain.

The brainstem then sends signals to the hypothalamus, an almond-shaped structure deep inside the brain, that makes people feel full. The hypothalamus — the brain region that defends the set point — keeps tabs on both how much people are eating and their stored body fat. It detects the hormone leptin, which is released in direct proportion to the percentage of fat tissue.

If leptin levels fall below the range dictated by the set point, the hypothalamus sends out a flurry of signals to the rest of the brain, Schwartz said. The resultant brain changes make people feel hungrier, make food more rewarding and reduce sensitivity to pain — or anything that might distract people from eating.

Neurons within the hypothalamus also switch on motor neurons that plug into the jaw, resulting in chewing movements. This chain of events relies on a simple circuit in the brain, consisting of three types of neurons. If that circuit is activated, an animal will start chewing regardless of whether there is any food around, according to a 2024 study published in the journal Nature. Researchers found this simple brain circuit in mice and they expect something similar is in people.

If the brain is hardwired to maintain a certain body weight, how do people become obese?

There are conflicting hypotheses among obesity researchers, but one theory involves so-called AgRP neurons, a cluster of brain cells in the hypothalamus. These cells play a powerful role in appetite: Inhibiting the neurons in adult mice causes the animals to ignore food, even to the point of starvation, while stimulating them triggers uncontrollable eating.

Under normal conditions, AgRP neurons are kept quiet by hormones and nutrients that signal energy surplus — including leptin, insulin and glucose. Interestingly, even the sight of food is enough to dampen the cells' activity.

Related: Doctors identify never-before-seen genetic mutations that led to 2 children's insatiable hunger

But when mice are fed a high-fat diet, support cells called glia, which surround the AgRP neurons, become activated and increase in number. This response, called gliosis — which is typically seen when neurons are damaged — has also been detected in brain scans of people with obesity.

Some scientists propose that gliosis may prevent AgRP neurons from detecting the body's inhibitory, "keep quiet" signals, Schwartz said. When researchers show obese mice food, their AgRP neurons are 50% to 70% less inhibited than when their lean littermates are presented with food.

And this reduced sensitivity to inhibitory signals could lead to dramatic weight changes. If the hypothalamus detects only half of the body's total leptin levels, it will miscalculate stored fat levels as much lower than its set point, triggering brain signals that increase cravings and promote weight gain, Schwartz explained.

So how does semaglutide, the active ingredient in Ozempic and the related weight-loss drug Wegovy, trick the brain into losing weight?

The drug mimics GLP-1. By binding to GLP-1 receptors in the brainstem, it stimulates the neural circuits that make people feel full. This is thought to counteract the appetite-inducing signal from AgRP neurons, thereby reining in cues from the hypothalamus that would trigger more eating.

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

Editor's note: This article was updated on Nov. 4, 2024 to include information about the brain circuit in mice. The original article was published on July 27, 2023.

The global fitness industry will generate over US$80 billion in revenue in 2023, estimates suggest. And why not, given the many excellent reasons to exercise? Better cardiovascular health, lower risk of Type 2 diabetes, stronger immune system – the list goes on.

One of the biggest reasons many people choose to exercise is to lose weight. As a biobehavioral scientist, I study links between behavior and health, and I heed the time-honored advice that eating less and exercising more are necessary to lose weight. But a recent debate in the scientific community highlights the growing suspicion that the "exercising more" part of this advice may be erroneous.

At the center of the debate is the constrained total energy expenditure hypothesis, which asserts that exercise won't help you burn more calories overall because your body will compensate by burning fewer calories after your workout. Thus, exercise won't help you lose weight even if it will benefit your health in countless other ways.

Obesity researchers take issue with this hypothesis, because it's based on observational research rather than randomized controlled trials, or RCTs, the gold standard of scientific evidence. In RCTs, participants are randomly assigned to either a treatment or a control group, which allows researchers to determine whether the treatment causes an effect. Randomized controlled trials have shown that exercise causes weight loss.

The verdict is actually more mixed when considering all the gold-standard evidence available.

What the evidence says

Spectators of this hypothesis have emphasized the importance of systematically reviewing the evidence from all gold-standard trials. They pointed to a 2021 review of more than 100 exercise studies that examined the effect on weight loss in adults of aerobic, resistance or high-intensity interval training in combination or alone. The review concluded that supervised exercise regimens do cause weight loss, even if only a modest amount.

So that settles the debate, yes? If you eat too much dessert, then you can just go on an extra run to burn off those extra calories, right?

Well, not exactly.

If extra physical exertion burns extra calories overall, then exercise should also keep the weight from coming back after low-calorie dieting. But keeping those lost pounds off after dieting is a common challenge. The same 2021 review includes the few randomized controlled trials that address the question of whether exercise facilitates weight maintenance. However, the results weren't as good as they were for weight loss. The researchers found that six to 12 months of aerobic exercise, resistance training or both after dieting did not prevent weight regain in adults.

Exercise adherence

But what about compliance? Did all the people in those studies actually exercise regularly?

The 2021 review found only one randomized controlled trial on weight maintenance that reported an objective compliance rate, meaning each exercise session was supervised by a trainer. This tells us the percentage of time that participants in the study actually exercised as prescribed.

In that trial, the compliance rate was only 64% for 25 post-menopausal women who completed a resistance training program after diet-induced weight loss. This was for a regimen in which participants had to come in and exercise two to three times per week for an entire year. From the perspective of keeping up with a program for that long, doing so 64% of the time doesn't seem so bad.

But they still gained back as much weight as the 29 women in the control group who were not enrolled in the exercise program.

Energy balance

Many people would say that it's all about balancing energy in from food and energy out from exercise. If exercise didn't keep the weight off, then maybe a bigger dose of exercise was needed.

The American College of Sports Medicine highlighted this issue of exercise dose in its 2009 position statement on physical activity for weight maintenance, stating that the amount of physical activity needed for weight maintenance after weight loss is uncertain. Moreover, it stated that there is a lack of randomized controlled trials in this area that use state-of-the-art techniques to monitor the energy balance of participants.

Fortunately, some of the authors of the position statement went on to use state-of-the-art techniques to monitor energy balance in their own randomized controlled trial. In 2015, they enrolled overweight adults into a 10-month aerobic exercise program and compared the energy intake of those who lost weight with the energy intake of those who didn't lose weight while on the program. They found that those who didn't lose weight were indeed taking in more calories.

Mystery of the disappearing calories

But there's something else in that 2015 study's energy measurements that is quite interesting. By the end of the study, the number of total daily calories the exercisers burned was not significantly different from what the nonexercisers burned. And this was in spite of the fact that trainers verified the exercisers burned an extra 400 to 600 calories per session at their nearly daily exercise sessions. Why didn't those extra exercise calories show up in the total daily calories burned?

The answer to that question may help explain why exercise doesn't always help you keep the weight off: Your metabolism responds to regular exercise by decreasing the number of calories you burn when you're not exercising. That's according to the constrained total energy expenditure hypothesis that spurred the current debate.

Researchers recently tested the hypothesis by measuring the nonexercise calorie burn of 29 obese adults over a nearly 24-hour period, both before and after a six-month exercise program. They found that the calories they burned when they weren't working out did decrease after months of regular exercise – but only in those who were prescribed the higher of two different exercise doses.

Those who exercised at the lower dose for general health, meaning they burned an extra 800 to 1,000 calories per week, saw no change in their metabolic rate. But those who exercised at the higher dose to lose weight or maintain weight loss, meaning they burned an extra 2,000 to 2,500 calories per week, had a decrease in their metabolic rate by the study's end.

Exercise for health

Perhaps both sides of the debate are right. If you want to lose a modest amount of weight, then a new exercise routine might make a modest contribution toward meeting that goal.

However, as others have said, don't fool yourself into thinking you can "outrun a bad diet" by simply exercising more. There is a diminishing marginal return to exercise – you eventually take less weight off for the additional exercise you put in.

But even if extra exercise might not help you lose weight and keep it off, there are still the other great health dividends that regular exercise pays out.

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

Body mass index (BMI) is an "imperfect" measure of body fat with a "problematic history," so the metric should be used in conjunction with other measures of health risk, such as a patient's genetics, blood pressure, cholesterol and other metabolic factors, according to new guidelines from the American Medical Association (AMA).

In a new report presented at the 2023 AMA Annual Meeting in Chicago this month, AMA council members noted that BMI, which roughly estimates a person's body fat based on their weight and height, doesn't distinguish between body fat and lean body mass. Moreover, BMI doesn't capture where on the body people carry excess fat. This is important because upper body fat increases the risk of type 2 diabetes and coronary artery disease more than does lower body fat. 

Moreover, although cheap and easy to calculate, BMI is "inaccurate in measuring body fat in multiple groups" because it doesn't account for differences in the relative body shape and composition of people of different sexes, ages, races and ethnicities, the AMA said in a statement released June 14. 

This is partly because the BMI scale is "primarily on data collected from previous generations of non-Hispanic white populations," according to the statement. In outlining the history of the BMI's advent and use, the association's new report notes that "BMI cutoffs are based on the imagined ideal Caucasian."

Related: Childhood obesity should be treated early and aggressively, new guidelines say. Is that safe?

Crucially, this means that the same BMI thresholds don't indicate the same level of disease risk in all patients — for example, evidence suggests that, at the same BMI, Black and Hispanic women have a slightly higher risk of developing type 2 diabetes than white women and Asian women have about double the risk of white women.

In general, the widespread use of BMI in medical research skews scientists' and doctors' understanding of the risk of disease and death linked to obesity.

Frequently, the report states, in studies that find a correlation between high BMI and disease or death, the researchers fail to account for other key factors that may affect people's risk, like a history of smoking, alcohol use, medication use or a family history of disease. In addition, such studies often don't account for the expected fluctuation of weight with age and lack nuance regarding the amount of time participants spend in a given BMI category, and therefore don't capture how those factors shape later disease risk.

Based on the new report, the AMA has adopted a new policy on the use of BMI: The association now recommends that, due to the limitations of the metric, BMI should be used in conjunction with "other valid measures of risk," including but not limited to measures of visceral fat (the fat that surrounds the internal organs), relative fat mass (a body fat estimate that uses a height-to-waist ratio) and waist circumference. Genetic factors, including family history of diabetes and heart disease, and metabolic factors, such as high blood pressure and fasting blood sugar levels, are additional metrics to consider. 

Furthermore, the AMA emphasized that overreliance on BMI can lead to the underdiagnosis and undertreatment of eating disorders because doctors may not flag affected patients with "normal" or "above normal" BMIs. Insurance companies also use BMI to determine whether people's inpatient eating-disorder treatments will be covered, and this can lead to substandard treatment for patients who don't meet the weight cutoffs, the AMA noted.

"There are numerous concerns with the way BMI has been used to measure body fat and diagnose obesity, yet some physicians find it to be a helpful measure in certain scenarios," Dr. Jack Resneck Jr., immediate past president of the AMA, said in the statement. "It is important for physicians to understand the benefits and limitations of using BMI in clinical settings to determine the best care for their patients."

Two children who experienced intense, insatiable hunger that drove them to overeat have rare, never-before-seen genetic mutations that interfere with leptin, a key hormone that helps tell the body when it is full, a new case report says.

After white fat cells make leptin, it plugs into the brainstem and hypothalamus, brain regions that help control appetite. While the "hunger hormone" ghrelin constantly fluctuates, rising with fasts and falling after food intake, leptin levels remain relatively steady and are related to the body's total amount of white fat. Thus, leptin tells the body how much energy it has stored in fat and shifts the body into "starvation mode" when those stores fall too low. 

Rarely, people can carry genetic mutations that interfere with the production or secretion of leptin, or effectively block its effects in the brain. Prior to the new case report, published Wednesday (June 14) in The New England Journal of Medicine, scientists had found 21 genetic variants that messed with leptin production, release or sensitivity, resulting in insatiable hunger, known as hyperphagia.

In the new case report, the authors describe two unrelated children, a 14-year-old boy and a 2-year-old girl, who carried slightly different leptin-disrupting genetic mutations.

Related: Why does hunger sometimes cause nausea? 

Both children had high levels of leptin in their blood, which coincided with their high body fat percentages. After ruling out the Prader–Willi and Bardet–Biedl syndromes — two other rare genetic conditions that can lead to high appetite and weight gain in childhood — doctors checked each child's leptin gene, called LEP. They found that each child carried a distinct version, or variant, of the LEP gene; they named the boy's P64S and the girl's G59S. These genes coded for slightly modified versions of leptin.

Through studies with human cells in lab dishes, the team tested how well the children's leptin bound to the receptor it would normally plug into in the brain. Both versions of leptin bound to the receptor, but they triggered "marginal, if any, signaling." In the presence of normal leptin, the variant versions blocked the receptor and didn't allow normal leptin to plug in.

So while the children made high quantities of modified leptin, the hormone couldn't signal to the brain that their bodies contained ample amounts of stored energy. Without this signal, the kids' appetites couldn't be sated — their brains were attempting to compensate for an energy deficit that didn't exist.  

To treat the children, the doctors provided metreleptin, a synthetic form of leptin. At first, both kids required "higher-than-usual doses" of the treatment to overcome the effects of their leptin variants in the brain. Both children also participated in fasting and exercise programs, to help reduce their white fat and therefore their leptin production. This "eventually evoked a therapeutic response, with a normalization of food intake and satiety and weight loss," the authors wrote in the case report.

Both children developed antibodies against the metreleptin, which their doctors expected, but this didn't appear to affect the drug's effectiveness. There were no serious side effects and "both patients eventually attained near-normal weight."

A common weight-loss surgery for teens and young adults with obesity is weakening patients' bones, a new study finds. 

Sleeve gastrectomies permanently remove roughly 75% of a patient's stomach to curb their appetite and promote weight loss; this is the most common type of weight-loss surgery performed in teens and adults, worldwide. Weight-loss surgeries like this have also become increasingly common for teens in the U.S. in the past five years. 

While evidence suggests these surgeries can help reduce the cardiometabolic risks associated with obesity, such as high blood pressure and type 2 diabetes, they can also reduce bone strength, according to the new study, published Tuesday (June 13) in the journal Radiology. 

"We should not forget the bone," said study co-author Dr. Miriam Bredella, a radiologist and professor of radiology at Harvard Medical School. "It's really important that [physicians] are aware of bone health after weight-loss surgery," she told Live Science. 

The study followed 54 participants between the ages of 13 and 24 with moderate to severe obesity, as measured by their body mass index (BMI), a rough estimation of body fat made using a person's weight and height. The participants were split into two groups: 25 participants underwent a sleeve gastrectomy and 29 received only dietary and exercise counseling. 

Related: How body fat is calculated

Before each participant's treatment and then two years later, the scientists tested the patient's bone health through physical exams, blood tests and scans, including quantitative CT scans of their spine, used to measure changes in bone mineral density. The researchers then modeled how these changes would affect bones' strength using finite element analysis, a "method that's typically used when you design airplanes or bridges or cars to test the strength of material," said Bredella. This model can help researchers predict what force is required for a bone to break.  

"This is novel information in young people, which is important," said Dr. Thomas Link, a radiologist and professor at the University of California, San Francisco, who was not involved in the study. "It also includes information on bone strength and bone marrow fat which are newer technologies characterizing the bone quality," he wrote Live Science in an email. 

The sleeve gastrectomy patients had significantly lower BMIs two years out, while the counseled patients' BMIs slightly increased, on average. However, the surgery group had lost bone density in their lower spine and had significantly more fat in their bone marrow, which can weaken overall skeletal strength. 

Previous studies have suggested that adults also lose bone density after sleeve gastrectomies, the study authors wrote, but bone loss in adolescence is of particular concern. "Adolescence is the time where you really have the most bone accrual," Bredella said. "It's really the critical time because once we are 20 or 25, we have our peak bone mass and from then on, it goes downhill, so these pubertal years are so critical." 

So why would getting surgery on your stomach affect your bones? Decreasing the size of the stomach can also limit the nutrients your body absorbs from food, including vitamin D and calcium, which are critical for bone growth. Sleeve gastrectomies could also affect hormones normally released by the stomach that help support bone strength, Bredella said. And again, having less weight to carry can affect bone strength. But people can help counter this through weight-bearing exercises. 

Weakening bones in adolescence could increase the risk of fractures later in life. However, obesity also carries various long-term health risks, and recently released guidelines from the American Academy of Pediatrics urge doctors to treat adolescent obesity early and aggressively. 

While promoting bone health is crucial, "heart trumps the bone," said Bredella. Rather than avoiding weight-loss surgeries altogether, she recommends that individuals adopt a healthy diet before being treated to help reinforce their bone strength, and take vitamin D and calcium supplements after their surgery, and likely for the rest of their lives.

"I hope that for our paper, we raised the awareness of bone loss because people just don't think about it," said Bredella. 

Space is as vast as it is mysterious, so perhaps it’s not surprising that we’ve overlooked alien star system debris floating around in our planet’s orbit, but what about a "quasi-moon" that has been circling Earth since 100 B.C.? How did that slip through the net? Perhaps we were too busy looking for aliens saying hello.

Back on terra firma, archaeologists in South Africa found 153,000-year-old footprints that are the oldest Homo sapiens tracks on record — a discovery that left the team who found them "pleasantly astonished." Another pleasantly astonishing find was the collection of 2,700-year-old petroglyphs depicting people, ships and animals discovered in Sweden.

Sadly, researchers made a far more chilling discovery when they unearthed a "horror bunker" near the city of Anda in northeast China holding secrets that are too barbaric to contemplate. This bunker is believed to be the largest test site of imperial Japan's infamous Unit 731, which conducted horrifying human experiments during the 1940s. The researchers said the bunker "highlights the ongoing legacy of Unit 731's atrocities and their impact on global efforts to prevent biological warfare."

On the other side of the North Pacific, a man in Arizona was stung over 250 times by "killer" bees. They stung his eyes, mouth, ears, legs and back in a swarm attack. He survived and is now recovering at home — but how many bee stings does it take to kill? 

Also in the U.S., more teens with obesity are now getting weight-loss surgery to manage the condition. Researchers found the rate of surgery increased 19% between 2020 and 2021, with study authors saying they are cautiously optimistic that barriers to metabolic and bariatric surgeries are decreasing. 

Finally, spare a thought for the suspected Russian spy whale known as Hvaldimir, who was recently spotted in waters off the coast of Sweden. Given his age and behavior, he was probably looking for a mate. Sadly for him, beluga whales only live in the high Arctic in areas such as Norway's Svalbard archipelago, Greenland, Canada and Russia. 

 Picture of the week 

When Finnish photographer Mikko Peussa captured this beautiful image of rainbow-colored rings surrounding the sun, he could hardly have imagined the surprising source of this stunning effect — tree pollen. 

The effect is created by sunlight scattering, or separating into its individual wavelengths, when it hits the pollen's surface. Pollen coronas only appear when pollen concentrations are very high and can only be clearly seen when the sun or the full moon is partially obscured.

 Weekend reading 

• Crabs are so awesome that animals keep evolving into them — but why?
• Here’s everything you need to know about  the "Strawberry Moon," which you can see in the sky tonight.
• If you’re looking for something a little more evergreen, these are the world’s oldest trees.
• Which civilization lasted the longest? It turns out, that's not a straightforward question.
• Scientists keep resurrecting ancient viruses trapped in permafrost and frozen remains.
• The Tunguska event was the biggest asteroid impact in recorded history. So how did it vanish without a trace?

 And finally… 

Once upon a time — at least according to the ancient Greek writer Plutarch — the hero Theseus sailed from Athens, Greece, to the island of Crete, where he slayed the half-man, half-bull Minotaur before sailing back to rule Athens. 

The wooden ship that Theseus sailed on, Plutarch imagined, must have become a national treasure, and he posed a thought experiment that has fascinated philosophers ever since: If you repaired Theseus' ship plank by plank so that no original planks remained, is it still the same ship? 

More teens with obesity are getting weight-loss surgeries year over year in the U.S., a new analysis suggests.

The study, published Tuesday (May 30) in the journal JAMA Pediatrics, focused on a time period before and after the American Academy of Pediatrics (AAP) issued a 2019 policy statement saying that teens with severe obesity needed better access to weight-loss surgeries because lifestyle interventions aren't very successful in helping this group lose and keep weight off in the long-term. 

Just this year, the AAP released more detailed guidelines for treating children and teens with obesity. These new guidelines also emphasized surgeries as a treatment option to consider for teens with severe obesity, meaning those with a body mass index (BMI) equal to or greater than 120% of the 95th percentile for their age and sex. (BMI is a rough estimate of body fat calculated using a person's weight and height.) 

The guidelines issued this year framed weight-loss surgeries and weight-loss drugs (a treatment option for children ages 12 and up) as adjunct therapies to "intensive health behavior and lifestyle treatment," programs focused on introducing sustainable weight-loss-promoting lifestyle changes.

Related: Invisible nerve-cell superhighway allows fat cells to 'talk' to the brain — and it may promote obesity 

Despite barriers to accessing weight-loss surgery — "including low referral rates, limited access, and poor insurance coverage" — the number of young people undergoing the procedures has still increased in recent years, the authors of the JAMA Pediatrics analysis wrote.

The analysis pulled data from patients ages 10 and up from the national accreditation program for bariatric surgery centers, called the Metabolic and Bariatric Surgery Accreditation and Quality Improvement Program. The analysis included data collected between 2015 and 2021 from more than 1.3 million patients, in total. 

In each year assessed, far more adults than youth got weight-loss surgery — the annual rate of metabolic and bariatric surgeries in adults ranged from roughly 160,000 to just over 200,000, while the rate in youth ranged from about 700 to 1,400.

However, the data revealed an interesting trend among U.S. youth: After dipping between 2015 and 2016, the rate of weight-loss surgeries increased steadily between 2016 and 2021, both overall and in each racial and ethnic subgroup analyzed. This upward trend even continued through 2020 and 2021, the first years of the COVID-19 pandemic, when the rate of adult surgeries briefly declined. Among young patients, surgery rates increased about 19% between 2020 and 2021.

"This data shows us that adolescents and their families are indeed interested in pursuing surgery as a treatment option if they are given access and a good candidate," study co-author Sarah Messiah, a professor and pediatric obesity researcher at UTHealth Houston School of Public Health, told CNN. 

Evidence suggests that weight-loss surgeries help teens with obesity lose and keep off weight and counter conditions linked to obesity, such as diabetes and high blood pressure, according to the AAP. However, patients must follow a restrictive diet plan following surgery, and eating disorder experts have raised concerns about how this might impact teens' long-term relationship with food. Other medical experts worry that, now that surgeries are being emphasized in official recommendations, doctors might push the procedures without first exhausting other weight-loss options. 

The American Academy of Pediatrics (AAP) released new guidelines for treating children and teens with obesity. 

The 73-page guidelines outline a proactive approach, where children and their families receive counseling about weight-loss treatments sooner, rather than later. Treatments include time-intensive programs that address children's nutrition and physical activity, as well as weight-loss drugs for children as young as age 12 and metabolic and bariatric surgeries for teens 13 and older.

The guidelines aim to curb the negative health outcomes linked to untreated childhood obesity. In both the short-term and long-term, kids and teens with obesity face an elevated risk of heart disease, high blood pressure, insulin resistance, prediabetes and type 2 diabetes. Studies suggest that a child's weight is highly predictive of weight in adolescence and adulthood, and the links between obesity and increased health risks in adults are established, the report states. So by having doctors treat obesity early, the AAP is aiming to head off a lifetime of health problems, the authors wrote. 

The new guidance received a mixed response, with some experts hailing it as an "overdue and crucial" shift in how American doctors approach childhood obesity. Others argued that it perpetuates anti-fat bias and may prompt physicians to reach for the aggressive interventions as first-line treatments, rather than last resorts.

Live Science asked experts what they think of the guidelines, and they generally agreed that the AAP presented an evidence-based review of childhood obesity and the best available treatments. However, for now, most children likely won't receive the gold standard of care recommended by the guidelines. Thus, there's a risk that harried pediatricians will recommend that children lose weight but lack the time to guide them safely through the process, potentially leaving kids vulnerable to disordered eating, one expert suggested. In addition, scientists are still learning about the long-term consequences of weight-loss drugs, they added. 

Related: How body fat is calculated

"I think the challenge is that many patients do not have access, resources, or time to participate in structured and professionally run pediatric obesity treatment," Dr. Jason Nagata, a pediatrician and adolescent eating disorder specialist at the University of California, San Francisco, told Live Science in an email. Outside of these programs, kids recommended weight loss treatment may not be adequately monitored, Nagata said.

"As an eating disorder specialist, I have received many referrals for teens who were previously told they were obese and needed to lose weight, and they took the weight loss to the extreme," he said. Research led by Nagata suggests that, compared with their leaner peers, older teens and young adults with overweight or obesity are more likely to engage in disordered eating behaviors, like fasting, but less likely to be diagnosed with eating disorders than underweight peers. That's dangerous because teens with disorders like anorexia can still be dangerously ill, even if they are not underweight. 

Doctors should discourage patients from using dangerous weight control strategies, explain the risks, and monitor the rate and degree of patients' weight loss, Nagata said, and AAP gives similar, if brief, guidance in its report. But many doctors have limited training in eating disorders and limited time to interact with their patients, Nagata said, so ensuring that kids receive this type of care could be tough.

The AAP also provides examples of neutral language to use in conversations about a child's weight, and broadly, the guidelines frame obesity as a complex, chronic disease influenced by myriad factors, from genetics to socioeconomics, rather than a "reversible consequence of personal choices," as it's been considered in the past, the guidelines authors wrote.    

The guidelines emphasize "treating the whole child," rather than fixating on a number on a scale, Dr. Sheethal Reddy, a clinical psychologist who specializes in obesity medicine at the Emory Bariatric Center, told Live Science. "The goal here is not to get kids skinny — it's not to have them fit into a certain size pair of pants," said Reddy, who until recently worked with children and teens at a pediatric obesity clinic.

In practice, that means taking a child's and their family's medical history, vital signs and labs, nutrition and physical activity habits, mental health and social circumstances into account, rather than checking only their body mass index (BMI) — an estimate of body fat calculated using weight and height. 

That said, BMI still factors into a child's evaluation, although the measure has been widely criticized as an imprecise measure of fat and poor indicator of overall health. More-precise methods of measuring body fat are more cost- and time-intensive, and thus not regularly used in clinics or in research. 

"Even though it's flawed, it's still a useful tool," Reddy said. "I sort of think of BMI as kind of the yellow traffic light" — a signal to slow down and see what else is going on with a child's health.

"The higher the percentile, the more likely it is that a child is carrying excess adiposity," meaning fat, said Dr. Sarah Hampl, chair of the AAP's Clinical Practice Guideline Subcommittee on Obesity and a lead author of the guidelines. "Overweight" is defined as a BMI at or above the 85th percentile and below the 95th percentile for children of the same age and sex, and "obesity" is defined as a BMI at or above the 95th percentile. These categories are reflected in the Centers for Disease Control and Prevention's new extended BMI growth charts for kids and teens.  

"And yet it's still only one of several measures we look at in terms of determining the child's health," and whether or not their weight is negatively affecting them, Hampl said. 

Related: High-sugar diet disrupts the gut microbiome, leading to obesity (in mice) 

If a child is recommended for weight-loss treatment, what are their options?

One is a motivational interviewing, a type of counseling where doctors help kids and their families work towards adjusting their nutrition and physical activity. A similar but more extensive intervention, called intensive health behavior and lifestyle treatment (IHBLT), focuses on introducing similar lifestyle changes and making them sustainable in the long-term.

"IHBLT is most often effective when it occurs face-to-face, engages the whole family, and delivers at least 26 hours of nutrition, physical activity, and behavior change lessons over 3 to 12 months," the guidelines state. Although backed by research, these types of programs aren't readily accessible to many kids, as few institutes host them and they're rarely covered by insurance, Reddy said.    

As an adjunct to IHBLT, doctors may offer children with obesity weight-loss drugs, provided they are age 12 and older. These treatments include Wegovy (generic name semaglutide), a once-weekly injection that affects how the brain and gut communicate and reduces the user's appetite.

Weight-loss drugs approved for children have been tested in roughly year-long trials, but we don't yet have data on what happens after five or 10 years of use, for example, Hampl said. And there aren't set recommendations as to how long children should use the medications.

Teens ages 13 and older with severe obesity — meaning their BMI is equal to or greater than 120% of the 95th percentile for age and sex — may also be referred to a specialist to be evaluated for metabolic and bariatric surgery.

Evidence suggests that these surgeries can reduce teens' weight and counter health conditions linked to obesity, such as diabetes and high blood pressure. However, eating disorder experts have raised concerns that the procedures alter how and what patients can eat, which can damage their relationship to food, NPR reported; other experts worry that doctors will turn to surgery too quickly, without exhausting other options, according to STAT. 

Others argue that surgery is just another option for patients and should be considered, if needed. 

"There is too much hype or over emphasis on the mention that [pharmacotherapy] and surgery 'MAY or CAN' be offered," said Dr. Stephen Cook, an internist and associate professor who researches childhood and adolescent obesity at the University of Rochester Medical Center, told Live Science in an email. "There are a number of steps before those could be considered, and they are only to be considered for those with more severe levels of obesity," he said. 

The brains of older adults with obesity show patterns of gray matter loss that are strikingly similar to those seen in people with early Alzheimer's disease, a new study suggests. These patterns overlap in the location of the tissue loss but not in the severity; in other words, Alzheimer's patients exhibit a far greater degree of brain atrophy than cognitively healthy, obese adults of the same age do.

"The degree of the changes is much lower in obesity," confirmed Filip Morys, first author of the new study and a postdoctoral fellow at McGill University's Montreal Neurological Institute. However, the spatial distribution of the tissue loss may help to explain why obesity is a major risk factor for Alzheimer's, Morys told Live Science; past studies have specifically linked midlife obesity to an increased risk of Alzheimer's and other types of dementia down the line. 

"It's further evidence that this major cardiovascular risk factor of obesity is linked with evidence of neurodegeneration," or the progressive loss of brain cells, said Dr. Jeffrey Burns, co-director of the Alzheimer's Disease Research Center at the University of Kansas Medical Center, who was not involved in the study. 

However, the new research, published Tuesday (Jan. 31) in the Journal of Alzheimer's Disease, cannot reveal the exact cause of this tissue loss, nor can it pinpoint which of the cognitively healthy, obese participants might go on to develop dementia, Burns told Live Science. That's partly because the analyses captured only one point in time, in each participant's early to mid-70s.

Related: New Alzheimer's drug slightly slows cognitive decline. Experts say it's not a silver bullet.

"We need long-term, longitudinal studies where we're measuring these things over time," Burns said. "For these individuals without cognitive issues, how strongly is this linked to poor outcomes in the future?" We don't know yet.

Prior to their new study, Morys and his colleagues found evidence that, in people in their 60s, obesity seems linked to distinct patterns of thinning in the brain's gray matter. Named for its color, gray matter is made up of the bodies of brain cells, or neurons, and the uninsulated wiring that extends from those cells; gray matter is found primarily in the cerebral cortex, the brain's wrinkled outer surface.

"We saw that the patterns there are very similar to the ones we see in Alzheimer's disease," Morys said of that previous work, published in 2021 in The Journal of Clinical Endocrinology and Metabolism. To further investigate these similarities, the team tapped two huge databases of brain scans: the Alzheimer's Disease Neuroimaging Initiative (ADNI) database and the UK Biobank.  

From the ADNI database, which was compiled in the U.S., the team pulled brain scans from people diagnosed with mild Alzheimer's and from healthy individuals without any cognitive impairment. From the UK Biobank, they compiled brain scans from cognitively healthy individuals and grouped them by body mass index (BMI), a measure used to estimate excess body fat. 

In all, the team used brain scans from more than 1,300 individuals to generate maps of cortical thickness for people of different BMIs and people with and without Alzheimer's. By comparing the maps, they pinpointed regions of the cortex that appeared thin in people with obesity and those with Alzheimer's, but not in lean, cognitively healthy individuals. These overlapping regions showed up even when people with both obesity and Alzheimer's were excluded from the analysis.

"This study demonstrates that areas of cortical thinning seen in lean persons with AD [Alzheimer's disease] are the same areas that are thin in those with obesity," Dr. Heather Ferris, an assistant professor of endocrinology and metabolism and neuroscience at the University of Virginia (UVA) Health who was not involved in the study, told Live Science in an email.

These thinned-out regions included the right temporo-parietal cortex and left prefrontal cortex, which are involved in high-level cognitive functions, such as long-term memory, language, attention and executive functioning, or the ability to plan and execute tasks, Morys said. "If you look at patients with AD, [problems with these functions] are often the first signs of the disease," he added. 

But again, as this study offered only a snapshot in time, the researchers cannot predict if any of the cognitively healthy, obese participants will go on to develop dementia, Morys said. And the team cannot conclusively say what caused these individuals' gray matter to thin in the first place. 

Conditions that often occur in obesity — such as systemic inflammation, high blood pressure and type 2 diabetes — can potentially injure brain cells and have been linked to Alzheimer's-related brain changes, the researchers wrote in their report. That said, there may be brain-thinning mechanisms at play in obesity that are totally independent of those seen in Alzheimer's, the team wrote.

In the future, Morys and his colleagues aim to conduct a large clinical trial to see if weight loss treatments can guard against later cortical thinning and cognitive decline. On that front, there's a huge question as to when such interventions should be started, Ferris said. 

"While many of the effects of obesity are reversed with weight loss, once a neuron has died it is gone and [is] not going to be replaced," Ferris said. "That means that if weight loss will lower the risk of AD, it likely needs to occur before significant brain loss occurs. When that is can't be answered by this study." 

Editor's note: This article first ran on Dec. 9, 2021, after an earlier version of the study was posted to the preprint database bioRxiv. The article was updated on Sept. 23, 2022 to reflect the new information contained in the peer-reviewed journal.

The coronavirus SARS-CoV-2 directly infects fat cells and specific immune cells found in fat tissue, sparking inflammation that can then spread to uninfected "bystander" cells nearby. 

In a study, published Sept. 22 in the journal Science Translational Medicine, scientists experimented with fat tissue obtained from patients undergoing bariatric, heart and chest surgeries, to see if the tissue could be infected by the coronavirus. They found that the virus could infect and replicate within mature fat cells, known as adipocytes, and these infected cells became inflamed. They also found that specific subsets of immune cells housed within the fat tissue, called macrophages, also became infected and kicked off a much more intense inflammatory response.

Notably, the virus could not make new copies of itself inside the macrophages — the pathogen could break into the immune cells, but the buck stopped there. However, even this short-lived invasion triggered a significant change in the macrophages, causing them to spew inflammatory substances into the surrounding tissue. There, immature fat cells, called pre-adipocytes, reacted to the onslaught of chemical signals by becoming inflamed themselves. 

These pre-adipocytes cannot be directly infected by SARS-CoV-2, the team found, but through this chain reaction, they were indirectly affected by the virus.   

Related: COVID-19 can infiltrate insulin-producing cells in the pancreas, study suggests

In addition to these experiments, the team examined fat tissue from patients who died from COVID-19 infections and found coronavirus genetic material in the fat that surrounded various organs. Viruses like HIV and influenza can squirrel themselves away in fat tissue, as a way of hiding from the immune system. Similarly, "adipose tissue could serve as a potential reservoir for SARS-CoV-2," and in theory, this hidden reservoir could contribute to the enduring symptoms seen in people with long COVID, the team wrote in their report.

What's more, in two patients who died of COVID-19, the team found inflammatory immune cells had assembled around infected adipocytes in the fat tissue surrounding the heart. "This was of great concern to us, as epicardial fat lies right next to the heart muscle, with no physical barrier separating them," co-senior author Dr. Tracey McLaughlin, professor of endocrinology at Stanford University School of Medicine, said in a statement. "So, any inflammation there may directly affect the heart muscle or coronary arteries."

Since the early days of the pandemic, people with obesity have faced a higher risk of developing severe symptoms, requiring hospitalization and dying from COVID-19, Live Science previously reported. A number of theories arose to explain why fat increased the risk of bad COVID-19 outcomes.  

For starters, excess fat in the abdomen can push on the diaphragm and thus restrict airflow in the lungs; if people are already struggling to get enough oxygen into their lungs on a good day, they may fare worse against COVID-19, Science reported. In addition, obese people's blood tends to clot more easily than those with lower fat levels — another major problem in the context of COVID-19, which can trigger extensive blood clotting. 

In addition, as fat builds up in the body, fat cells infiltrate the spleen, bone marrow and thymus, where many immune cells are produced. This can weaken the immune system by both reducing the number and undermining the efficacy of immune cells produced. Excess fat can also spur chronic, low-grade inflammation throughout the body, as fat cells release inflammatory substances called cytokines and macrophages do the same, in an effort to clear dead fat cells from the body, Science reported.

While all these factors may worsen COVID-19 outcomes for people with obesity, now there's this evidence that the virus infects fat cells directly. 

"Infected fat tissue pumps out precisely the inflammatory chemicals you see in the blood of severe COVID patients," co-senior author Dr. Catherine Blish, a professor of infectious diseases at the Stanford University School of Medicine, said in the statement. "It's reasonable to infer that having a lot of infected fat could contribute to the overall inflammatory profile of severely ill COVID-19 patients."

It's still not clear how the virus infiltrates fat and fat tissue-borne immune cells. That's because the study authors found negligible amounts of ACE2 — the main "doorway" that the virus uses to enter cells — in their tissue samples. "It’s highly unlikely the virus is entering through ACE2, because we couldn’t detect the functional protein in adipose tissue," Blish said.

Originally published on Live Science.

Sugar may disrupt the community of bacteria living in the gut, thereby depleting crucial immune cells and causing obesity down the line, a new mouse study suggests. 

So far, the results have been shown only in mice. But if follow-up studies show similar trends in humans, that could eventually lead to treatments for metabolic disease and obesity, said senior author Ivaylo Ivanov, an associate professor of microbiology and immunology at Columbia University Vagelos College of Physicians and Surgeons. 

In the recent study, published online Aug. 29 in the journal Cell, scientists found that feeding mice a high-sugar diet containing sucrose and maltodextrin caused specific bacteria, called segmented filamentous bacteria (SFB), in the mice's intestines to die due to an overgrowth of different gut bugs. The sudden loss of SFB triggered a chain reaction in the mouse gut that ultimately changed how the animals absorbed dietary fat. 

This, in turn, caused the mice to become obese and develop features of "metabolic syndrome," a cluster of conditions — such as high blood pressure, high blood sugar and insulin resistance — that collectively raise the risk of heart disease, stroke and type 2 diabetes. 

Related: Gut bacteria may 'talk' to the brain, mouse study suggests 

The results suggest that SFB somehow protect against metabolic syndrome and excess weight gain, but how do the gut bugs do it? It turns out that SFB "talk" to the immune system, encouraging the production of a specific type of immune cell called Th17. These immune cells release proteins that affect the lining of the intestine, preventing excess fat from being absorbed through the tissue and into the bloodstream. 

Broadly, SFB can be found in many animals — including rodents, fish and birds — but they haven't been found in humans, Ivanov noted. However, humans do carry a different set of gut bacteria that can induce Th17 cells just like SFB do, and early research hints that these bacteria may be similarly depleted by high-sugar diets, he said. In other words, although humans may not carry SFB, sugar may still exert similar effects on the mouse and human gut microbiomes and immune systems.

"Really what's providing the effect is the T cells — so the bacteria are inducing the T cells, and T cells are providing the effect," Ivanov told Live Science. "We hypothesize that, in humans, inducing these T cells will also be beneficial."

In their recent mouse study, the researchers placed mice on a high-sugar, high-fat diet for a month to see how their gut bugs might change. They found that the diet spurred the growth of a bacterium called Faecalibaculum rodentium, which essentially crowded out the SFB growing in the mouse gut, depleting its numbers. As the mice steadily lost SFB, their overall number of Th17 cells also fell, and they gained weight and developed insulin resistance and glucose intolerance — all signs of metabolic syndrome. 

These effects weren't observed in mice that were fed a low-sugar, low-fat diet, or in mice fed a sugar-free, high-fat diet, but mice fed a high-sugar, low-fat diet also swiftly lost their SFB. This suggests that it was specifically the sugar that was driving the harmful loss of the bacteria and the Th17 cells. 

Basically, the Th17 cells provided an "armor" that protected the mice from developing metabolic disease, and sugar indirectly destroyed that armor by messing with the microbiome, Ivanov explained.

In a different experiment, the team eliminated SFB from a group of mice and then fed them a sugar-free, high-fat diet. They found that these mice also gained weight and developed metabolic disease, despite not having eaten sugar. So what gives? In essence, without the right gut bugs, the mice didn't make enough Th17 cells and they thus lacked that aforementioned armor. The team found that they could provide that armor in two ways: by feeding the mice a probiotic imbued with SFB or by directly injecting Th17 cells into their bodies.

This suggests that, if a mouse's gut has already been depleted of SFB, cutting down on sugar won't help the rodent avoid metabolic disease. If this finding carries over to humans, that suggests that consuming less sugar wouldn't necessarily be helpful if one's gut microbiome is already disrupted. Therefore, an additional intervention might be needed to restore the gut bugs or Th17 cells of those people, Ivanov said.  

Again, more research is needed to know if similar forces are at work in the human gut. Ivanov and his team are also trying to understand how gut bacteria help Th17 cells grow in the mouse gut and whether that mechanism also applies in humans.

"Even after 10 years of studying this, we don't understand completely this process, this mechanism, how exactly the bacteria is inducing these T cells," Ivanov said. "We know a lot, but still there are a lot of questions."

Originally published on Live Science.

The most common form of diabetes, type 2 diabetes is a chronic disease whose defining factor is high blood sugar, or glucose. 

Glucose is a critical source of energy for the body's cells. When someone eats food, any of the sugars in that food ultimately enters the blood; then, the pancreas releases the hormone insulin, which guides the blood glucose into cells. That step is essential to keeping the body’s cells fueled and also maintaining a healthy level of glucose in the blood.. However, in people with type 2 diabetes, the pancreas doesn't produce enough insulin and/or the body doesn't use that insulin efficiently. 

The result is an elevated level of glucose in the blood, which, over time, can lead to a host of serious complications, including heart disease, kidney disease and eye disease. 

More than 37 million people in the U.S., or roughly 1 in 10, have diabetes, according to the Centers for Disease Control and Prevention (CDC); of those, about 90% to 95% have type 2 diabetes. 

In addition, about 96 million people in the U.S., or about 1 in 3, have prediabetes, in which blood sugar levels are high but not high enough for a person to be diagnosed with type 2 diabetes, per the CDC. This condition puts them at risk for diabetes, heart disease and stroke, but most are unaware they have it.

• Related: Which vegetables are good for diabetics?
• Related: Which fruits are good for diabetics?

Causes

Type 2 diabetes is linked to both genetic and lifestyle factors. Risk factors include having prediabetes, being overweight, engaging in less than 150 minutes of exercise a week and being older than 45, the CDC says. The disease also tends to run in families and occurs more often in African American, Hispanic/Latino American Indian and Alaska Native populations. 

Why these factors raise the risk of the chronic disease is unclear. One possible link, according to the National Institute of Diabetes and Digestive and Kidney Diseases, involves extra weight, particularly around the waist. Extra fat has been linked to insulin resistance, in which the body does not use insulin efficiently to regulate blood sugar. Though researchers aren’t certain the mechanism behind this link, according to the American Diabetes Association, that extra fat could lead to inflammation, physiological stress or other changes in the body’s cells that ultimately cause insulin resistance. Notably, however, type 2 diabetes can also develop in people who are not overweight or obese, mostly in older adults.

Symptoms & complications

Early symptoms of type 2 diabetes include increased thirst, urination and hunger; fatigue; blurred vision; tingling extremities; and slowly healing sores or skin infections, according to the National Library of Medicine. But these symptoms often appear gradually over the course of years and can be so mild that they are missed. Sometimes, there are no symptoms at all. 

Unexplained weight loss can also be a symptom of type 2 diabetes, said Dr. Minisha Sood, an endocrinologist at Northwell Health in New York. This symptom can sometimes be confusing to patients, because diabetes is associated with obesity and too much weight gain. And although this is true, type 2 diabetes can lead to weight loss, mostly through a decrease in "water weight," she said.

"When blood sugar exceeds a certain level … the body has to eliminate that sugar somehow," Sood said. This is done mostly through the kidneys, and the body also gets rid of water along with the sugar. "Patients end up losing a lot of water," she said.

The long-term complications of type 2 diabetes include heart attack, nerve and kidney damage, blindness, erectile dysfunction and dementia, according to the Cleveland Clinic. For instance, having too much glucose in your blood can lead to eye diseases such as diabetic retinopathy, which affects blood vessels in the retina and is the leading cause of blindness in the U.S.; glaucoma, which in the case of diabetes can result from damage to blood vessels in the front of the eye that ultimately causes fluid build-up and damage to the optic nerve; cataracts, which tends to develop more readily in someone with diabetes, possibly due to deposits of glucose in the eyes' lenses, according to Medline Plus.

Although these complications may seem varied, there is a common link. "Glucose can be toxic to blood vessels," Sood said, and damage to blood vessels over time causes some of these serious conditions.

COVID-19, the disease caused by the coronavirus SARS-CoV-2, can also be more serious in individuals with diabetes compared with people who don’t have diabetes. For instance, research published April 23, 2020 in the Journal of Infection, suggested people with diabetes were 3.7 times more likely to have a severe case of COVID-19 or to die from it as compared with individuals with no underlying health conditions. That research was based on a review of 13 relevant studies.  

There is also preliminary research suggesting that COVID-19 can cause both type 1 diabetes and type 2 diabetes. In a study based on information from two health databases, researchers found that individuals younger than 18 were more likely to be diagnosed with diabetes more than 30 days after a COVID-19 infection compared with individuals not infected with the disease, researchers reported online Jan. 14, 2022 in the CDC journal Morbidity and Mortality Weekly Report. Diabetes diagnoses in these COVID-19 patients were 166% and 31% greater compared with non-COVID-19 individuals, respectively for the two databases.

Diagnosis

Some people learn they have type 2 diabetes through routine blood testing — for example, when a doctor checks blood glucose levels during an annual exam, or for diabetes screening, Sood said.

The American Diabetes Association recommends screening for all adults age 45 and older, as well as in the following groups, the Mayo Clinic reported:

• Individuals who are under 45 and who are overweight or have obesity, plus have one or more risk factors tied to diabetes.
• Women who have been diagnosed with gestational diabetes.
• Individuals with a prediabetes diagnosis.
• Kids who are overweight or have obesity, plus have a family history of type 2 diabetes or one or more other risk factors.

Though normal blood sugar levels can vary among individuals, there are certain ranges that are considered "normal." For instance, fasting blood sugar (the amount of glucose in the blood at least eight hours after a meal) is between 70 and 100 milligrams per deciliter (mg/dL), according to the World Health Organization (WHO). Most people's blood glucose levels rise after they eat. According to the American Diabetes Association (ADA), the normal blood sugar range two hours after someone eats is generally less than 140 mg/dL.

According to the ADA, a person can be diagnosed with diabetes if they meet one of these criteria:

• They have a fasting blood glucose level greater than or equal to 126 mg/dL.
• They have a blood glucose level greater than or equal to 200 mg/dL two hours after they drink a special sugar solution.
• They get a result of greater than or equal to 6.5% on an A1C test, which measures average blood sugar for the past three months, roughly.

Given that a family history of type 2 diabetes raises the risk of developing the condition, people who fall into that category should talk to their doctor about being screened, Sood said.

"If it's screened for, and identified early, changes can be implemented that could prevent progression of the disease, and complications," Sood told Live Science.

Treatment

To manage type 2 diabetes, doctors recommend changes to your diet. Eating a healthy including smaller portion sizes; increased intake of high-fiber foods, such as fruits, non-starchy vegetables and whole grains; and fewer calories — and getting regular exercise, the Mayo Clinic says. A keto diet may also be a potential way for diabetics to manage their condition.

Doctors also may prescribe insulin, other injectable medications, or oral diabetes medicines, such as metformin, to address the high blood sugar. Metformin works by both reducing the amount of glucose produced by the liver and increasing the body’s sensitivity to insulin (to become less insulin resistant), according to the diaTribe Foundation. Patients are typically given blood sugar targets and are advised to check their glucose levels periodically.

For people who have obesity and type 2 diabetes and who also have trouble controlling their blood sugars with these treatments, weight loss surgery, also called bariatric surgery, can be a last resort option, according to the National Institute of Diabetes and Digestive and Kidney Diseases. However, the long-term results of this surgery are still being studied.

In 2016, the U.S. Food and Drug Administration approved the use of an "artificial pancreas" that automatically tests blood glucose levels periodically and releases insulin accordingly, Live Science previously reported.  

For people who are diagnosed with type 2 diabetes and have weight issues, Sood recommends they lose at least 5% to 10% of their current body weight. If lifestyle changes don't work well enough to get a person's blood sugar levels under control, then doctors generally prescribe medications to complement those changes, she said.

Is there a cure for type 2 diabetes?

Type 2 diabetes is a progressive disease. New research now suggests that in some cases patients can go into remission, in which their blood sugar levels fall into normal range. Sustained weight loss has proved to be especially successful. 

For instance, in the Diabetes Remission Clinical Trial in the U.K., researchers placed individuals with type 2 diabetes on a calorie-restrictive diet for a year, they reported Oct. 2, 2018 in the journal Cell Metabolism. Out of the 58 patients that stuck with the trial, 69% reached blood glucose levels (measured with the A1C test) that were in the non-diabetic range, meaning they would be classified as “in remission,” after they had lost weight; at the end of the 12 months, 64% showed non-diabetic blood glucose levels, the researchers reported. On average, those who responded to the treatment lost 35.7 pounds (16.2 kilograms). 

• Related: Keto diet vs low carb: what's the difference?
• Related: Type 3 diabetes: Symptoms, causes and treatments

In another study, detailed in 2019 in the journal The Lancet Diabetes & Endocrinology, researchers looked at 300 people in the U.K. with type 2 diabetes. The study is still ongoing, but so far, it's shown encouraging results. In the study, half of the participants stopped taking their diabetes medications and started on a diet replacement formula, after which food was gradually reintroduced; the other half of the participants received standard diabetes care. Two years later, more than a third (36%) of the people with type 2 diabetes who took part in the weight management program were in remission.

However, remission does not mean the diabetes is "cured." That's because blood glucose levels constantly change and if a person were to regain lost weight or revert back to lifestyles that were impacting those levels, their sugars could go back up again to diabetic levels, according to the National Institute of Diabetes and Digestive and Kidney Diseases.

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

This article was updated on April 11, 2022, by Live Science Contributor Natalie Grover.

Additional resources

• Learn about how having diabetes can affect pregnancy in this explainer from the National Institute of Diabetes and Digestive and Kidney Diseases.
• Check out the latest data on the rising incidence of type 2 diabetes in children and teens in this report by the CDC.
• Learn how blood sugar works and how to achieve blood sugar health in the book "Blood Sugar 101: What They Don't Tell You about Diabetes".

Bibliography

"Type 2 Diabetes," National Institute of Diabetes and Digestive and Kidney Diseases
https://www.niddk.nih.gov/health-information/diabetes/overview/what-is-diabetes/type-2-diabetes#diagnose 

"Mean fasting blood glucose," World Health Organization  https://www.who.int/data/gho/indicator-metadata-registry/imr-details/2380 

"Symptoms & Causes of Diabetes," National Institute of Diabetes and Digestive and Kidney Diseases
https://www.niddk.nih.gov/health-information/diabetes/overview/symptoms-causes#type2

"Type 2 Diabetes" Centers for Disease Control and Prevention
https://www.cdc.gov/diabetes/basics/type2.html

"Prediabetes – Your Chance to Prevent Type 2 Diabetes," Centers for Disease Control and Prevention
https://www.cdc.gov/diabetes/basics/prediabetes.html 

"Understanding A1C," American Diabetes Association
https://www.diabetes.org/a1c/diagnosis

"Diabetes: An Overview," Cleveland Clinic
https://my.clevelandclinic.org/health/diseases/7104-diabetes-mellitus-an-overview

"Type 2 diabetes," The Mayo Clinic
https://www.mayoclinic.org/diseases-conditions/type-2-diabetes/diagnosis-treatment/drc-20351199 

"Insulin, Medicines, & Other Diabetes Treatments," National Institute of Diabetes and Digestive and Kidney Disease
https://www.niddk.nih.gov/health-information/diabetes/overview/insulin-medicines-treatments

"Achieving Type 2 Diabetes Remission through Weight Loss," National Institute of Diabetes and Digestive and Kidney Disease
https://www.niddk.nih.gov/health-information/professionals/diabetes-discoveries-practice/achieving-type-2-diabetes-remission-through-weight-loss

"Durability of a primary care-led weight-management intervention for remission of type 2 diabetes: 2-year results of the DiRECT open-label, cluster-randomised trial," 2019 The Lancet
https://www.thelancet.com/journals/landia/article/PIIS2213-8587(19)30068-3/fulltext 

A diabetes drug may also be a promising treatment for obesity — in a new study, people taking the drug lost a stunning 15% of their body weight, which is more than has been seen with any other obesity drug on the market.

The drug, known as semaglutide, is an injectable medication that's already approved to help control blood sugar levels in people with Type 2 diabetes. But the drug also suppresses appetite.

Related: The best way to lose weight safely

In the new study, published Wednesday (Feb. 10) in The New England Journal of Medicine, researchers randomly assigned 1,961 adults who were obese or overweight to receive semaglutide or a placebo as an injection once a week for 68 weeks. Participants also received counseling sessions once a month to help them adhere to a reduced-calorie diet, and they were encouraged to increase their physical activity.

By the end of the study, those who received semaglutide lost 14.9% of their body weight, on average, compared with just 2.4% of body weight in the placebo group.

Five other drugs are approved to treat obesity, but even the most effective of these drugs results in about 7.5% weight loss, according to The New York Times. And these drugs can typically be used for only short periods of time, the Times reported. For example, the weight loss drug phentermine is typically taken for 3 to 6 weeks, according to the National Institutes of Health, a much shorter amount of time than the 68-week treatment with semaglutide used in the study.

"This is the start of a new era of effective treatments for obesity," Dr. Robert F. Kushner, an obesity researcher at Northwestern University Feinberg School of Medicine, who led the study, told the Times.

People who took semaglutide were more likely to experience gastrointestinal side effects, including nausea, diarrhea, vomiting and constipation, compared with the placebo group. But these side effects tended to be temporary.

The study also did not look at the drug's effects beyond 68 weeks, and people would likely need to stay on the drug for life to prevent their weight from coming back, the Times reported. 

And weight loss drugs that appear to do well in trials may not be as effective in real-world settings, according to CNN. What's more, several weight loss drugs that achieved approval from the Food and Drug Administration were later recalled because of side effects, CNN reported.

The study was funded by the maker of semaglutide, Novo Nordisk. The Danish pharmaceutical company has already submitted an application with the FDA for approval of semaglutide for chronic weight management, according to CNN.

Originally published on Live Science. 

The COVID-19 pandemic has thrust the obesity epidemic once again into the spotlight, revealing that obesity is no longer a disease that harms just in the long run but one that can have acutely devastating effects. New studies and information confirm doctors’ suspicion that this virus takes advantage of a disease that our current U.S. health care system is unable to get under control.

In most recent news, the Centers for Disease Control and Prevention reports that 73% of nurses who have been hospitalized from COVID-19 had obesity. In addition, a recent study found that obesity could interfere with the effectiveness of a COVID-19 vaccine.

I am an obesity specialist and clinical physician working on the front lines of obesity in primary care at the University of Virginia Health System. In the past, I often found myself warning my patients that obesity could take years off their life. Now, more than ever, this warning has become verifiable.

More damage than believed

Initially physicians believed that having obesity increased only your risk of getting sicker from COVID-19, not your chance of being infected in the first place. Now, newer analysis shows that not only does obesity increase your risk of being sicker and dying from COVID-19; obesity increases your risk of getting infected in the first place.

In March 2020, observational studies noted hypertension, diabetes and coronary artery disease as the most common other conditions – or co-morbidities – in patients with more severe COVID-19 disease. But it was the editors of Obesity journal who first raised the alarm on April 1, 2020 that obesity would likely prove to be an independent risk factor for more severe effects of COVID-19 infection.

Additionally, two studies including nearly 10,000 patients have shown that patients who have both COVID-19 and obesity have a higher risk of death at days 21 and 45 compared to patients with a normal body mass index, or BMI.

And a study published in September, 2020 reported higher rates of obesity in COVID-19 patients who are critically ill and require intubation.

It is becoming overwhelmingly evident from these studies and others that those with obesity are facing a clear and present danger.

Stigma and lack of understanding

Obesity is an interesting disease. It is one that many physicians talk about, often in frustration that their patients cannot prevent or reverse it with the oversimplified treatment plan that we have been taught in our initial training; “Eat less and exercise more.”

It is also a disease that causes problems physically, such as sleep apnea and joint pain. It also affects one’s mind and spirit due to societal and medical professionals’ bias against those with obesity. It can even adversely affect the size of your paycheck. Can you imagine the outcry if the headline read “Patients with high blood pressure earn less”?

We doctors and researchers have understood for quite some time the long-term consequences of excess weight and obesity. We currently recognize that obesity is associated with at least 236 medical diagnoses, including 13 types of cancer. Obesity can decrease one’s lifespan by up to eight years.

Despite knowing this, U.S. physicians are not prepared to prevent and reverse obesity. In a recently published survey, only 10% of medical school deans and curriculum experts feel that their students were “very prepared” in regards to obesity management. Half of the medical schools responded that expanding obesity education was a low priority or not a priority. An average of 10 hours total was reported as dedicated to obesity education during their entire training in medical school.

And doctors sometimes don’t know how or when to prescribe medications for patients with obesity. For example, eight FDA-approved weight loss medications are on the market, but only 2% of eligible patients receive prescriptions for them from their physicians.

What goes on in the body

So, here we are, with a collision of the obesity epidemic and the COVID-19 pandemic. And a question I find patients asking me more and more: How does obesity create more severe disease and complication from COVID-19 infection?

There are many answers; lets start with structure.

Excess adipose tissue, which stores fat, creates a mechanical compression in patients with obesity. This limits their ability to take in and completely release a full breath of air.

Breathing takes more work in a patient with obesity. It creates restrictive lung disease, and in the more serious cases, lead to hypoventilation syndrome, which can cause a person to have too little oxygen in their blood.

And then there is function. Obesity results in an excess of adipose tissue, or what we colloquially call “fat.” Over the years, scientists have learned that adipose tissue is harmful in and of itself. One may say that adipose tissue acts as an endocrine organ all its own. It releases multiple hormones and molecules that lead to a chronic state of inflammation in patients with obesity.

When the body is in a constant state of low-grade inflammation, it releases cytokines, proteins that fight inflammation. They keep the body on guard, simmering and ready to fight disease. That’s all well and good when they are kept in check by other systems and cells. When they are chronically released, however, an imbalance can occur that causes injury to the body. Think of it like a small but contained wildfire. It’s dangerous, but it’s not burning the entire forest.

COVID-19 causes the body to create another cytokine wildfire. When a person who is obese has COVID-19, two small cytokine wildfires come together, leading to the raging fire of inflammation that damages the lungs even more so than patients with normal BMI.

Additionally, this chronic state of inflammation can lead to something called endothelial dysfunction. In this condition, instead of opening up, blood vessels close down and constrict, further decreasing oxygen to the tissues.

In addition, increased adipose tissue may have more ACE-2, the enzyme that allows the coronavirus to invade cells and begin to damage them. A recent study has shown an association of increased ACE-2 in adipose tissue rather than lung tissue. This finding further strengthens the hypothesis that obesity plays a major role in more serious COVID-19 infections. So in theory, if you have more adipose tissue, the virus can bind to and invade more cells, causing higher viral loads that stay around longer, which can make the infection more severe and prolong recovery.

ACE-2 can be helpful in counteracting inflammation, but if it otherwise bound to COVID-19, it cannot assist with this.

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The novel SARS COVID-19 virus has forced the medical profession to face the reality that many U.S. physicians inherently know. When it comes to prevention of chronic diseases such as obesity, the U.S. health care system is not performing well. Many insurers reward physicians by meeting metrics of treating the effects of obesity rather than preventing it or treating the disease itself. Physicians are reimbursed, for example, for helping patients with Type 2 diabetes to attain a certain A1C level, or a set blood pressure goal.

I believe is time to educate physicians and provide them with resources to combat obesity. Physicians can no longer deny that obesity, one of the strongest predictors for COVID-19 and at least 236 other medical conditions, must become public enemy number one.

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

Follow all of the Expert Voices issues and debates — and become part of the discussion — on Facebook and Twitter. The views expressed are those of the author and do not necessarily reflect the views of the publisher. This version of the article was originally published on Live Science.

It's one of life's great injustices: Some people must carefully pay attention to everything they put in their mouths in order to maintain their weight, while others can eat doughnuts to their heart's content and achieve the same result. So what's the secret? How do some people manage to never gain weight?

There isn't one simple answer to this question, said Kathleen Melanson, a professor of nutrition and food sciences at the University of Rhode Island. "There's genetic, nutritional, and even behavioral factors involved," Melanson told Live Science, "and the extent to which each of those factors come into play in any given individual is going to vary."

One of the most important factors has nothing to do with body type, metabolism, or performing a spell during the full moon: It's perception. Many people who appear to eat whatever they like without gaining weight aren't actually eating more than the rest of us, Melanson said. For example, your friend who eats ice cream on a daily basis might naturally compensate for those extra calories by eating less at another meal, or snacking less throughout the rest of the day. Or perhaps, when they eat pizza, they're eating slowly, getting full, then stopping after just a few slices. 

Related: Can you turn fat into muscle?

"If you measured these people's calories, they may not eat as much as you think," said Dr. Frank Greenway, the Chief Medical Officer at Pennington Biomedical Research Center. "They're just eating calorically dense foods when they do eat; things other people might have a difficult time not overeating."

Physical activity can also make a difference, but it doesn't have to be a gym workout. "Some people just move more, even if they're not necessarily athletes," Melanson said. For instance, they might fidget or pace, have an active job, or spend all day chasing their kids around. There’s even evidence that some people are genetically predisposed to want to move their body, Melanson said. That extra movement can also rev up the body's metabolism, or how much energy your body spends throughout the day, not including exercise. The more you move, the more  "the mitochondria within the cells of the muscle will increase in number and in their activity. And those are the power plants that are creating energy, using energy for movement," Melanson said. More mitochondria, means more calories burned. 

There's little evidence to suggest that — without exercise — some people are born burning significantly more calories than others, said Dr. Ines Barroso, a researcher at the University of Cambridge in England who studies the genetics of obesity. But there may be physiological differences that allow some people to naturally moderate the number of calories they consume without exercising tremendous self restraint, Melanson said. Cascades of nervous system signals and hormones that circulate in our blood interact to tell us when we're hungry or full. This is called the appetite regulatory system, and it may be more sensitive in some people than others, Melanson said. 

One important hormone involved in this system is leptin. It helps regulate how much food we want to eat over longer periods of time, not just for our next meal. So a person with a more sensitive system might go back for seconds and thirds at a party, then feel full for the next few days and eat less. "They just automatically can kind of recalibrate their energy balance because their appetite signaling system can say, 'Okay, we got enough energy,'" Melanson said. 

Genetics can play a role in a person's tendency to gain or lose weight. Researchers have identified over 250 different regions of DNA that are associated with obesity, according to a 2019 study published in PLOS Genetics. For this study, researchers compared 1,622 healthy people with low body mass index (BMI) against 1,985 people with severe obesity and 10,433 control people of normal weight. They found that the thin participants had fewer genes associated with obesity. But according to Barroso, who was a co-author on the study, genes alone don't determine your weight. "We didn't find genes that were exclusively either protecting from obesity or predisposing someone to obesity. It seemed like a continuum," Barroso said, "You also have people who have the genetic determinants for obesity yet they're not [obese]." Barroso said.

In the end, the answer is complex: our tendency to gain weight or maintain our weight isn't pre-determined, but it's also not entirely under our control. There's no genetic on-off switch that allows some people to eat all they want without gaining weight; at the same time, a tendency to gain weight isn't necessarily due to a lack of self control, Melanson said.

"It's not the same from one person to another."

Originally published on Live Science.

The novel coronavirus causing COVID-19 seems to hit some people harder than others, with some people experiencing only mild symptoms and others being hospitalized and requiring ventilation. Though scientists at first thought age was the dominant factor, with young people avoiding the worst outcomes, new research has revealed a suite of features impacting disease severity. These influences could explain why some perfectly healthy 20-year-old with the disease is in dire straits, while an older 70-year-old dodges the need for critical interventions.

Underlying health conditions are thought to be an important factor influencing disease severity. Indeed, a study of more than 1.3 million COVID-19 cases in the United States, published June 15 in the journal Morbidity and Mortality Weekly Report, found that rates of hospitalizations were six times higher and rates of death were 12 times higher among COVID-19 patients with underlying conditions, compared with patients without underlying conditions. The most commonly reported underlying conditions were heart disease, diabetes and chronic lung disease. 

In general, risk factors for more severe COVID-19 outcomes include:
Age
Diabetes (type 1 and type 2)
Heart disease and hypertension
Smoking
Blood type
Obesity
Genetic factors

Age

About 8 out of 10 deaths associated with COVID-19 in the U.S. have occurred in adults ages 65 and older, according to the U.S. Centers for Disease Control and Prevention (CDC). The risk of dying from the infection, and the likelihood of requiring hospitalization or intensive medical care, increases significantly with age. For instance, adults ages 65-84 make up an estimated 4-11% of COVID-19 deaths in the U.S, while adults ages 85 and above make up 10-27%. 

The trend may be due, in part, to the fact that many elderly people have chronic medical conditions, such as heart disease and diabetes, that can exacerbate the symptoms of COVID-19, according to the CDC. The ability of the immune system to fight off pathogens also declines with age, leaving elderly people vulnerable to severe viral infections, Stat News reported.

Related: Coronavirus in the US: Latest COVID-19 news and case counts

Diabetes

Diabetes mellitus — a group of diseases that result in harmful high blood sugar levels — also seems to be linked to risk of more severe COVID-19 infections. 

The most common form in the U.S. is type 2 diabetes, which occurs when the body's cells don't respond to the hormone insulin. As a result, the sugar that would otherwise move from the bloodstream into cells to be used as energy just builds up in the bloodstream. (When the pancreas makes little to no insulin in the first place, the condition is called type 1 diabetes.)

In a review of 13 relevant studies, scientists found that people with diabetes were nearly 3.7 times more likely to have a critical case of COVID-19 or to die from the disease compared with COVID-19 patients without any underlying health conditions (including diabetes, hypertension, heart disease or respiratory disease), they reported online April 23 in the Journal of Infection.

Even so, scientists don't know whether diabetes is directly increasing severity or whether other health conditions that seem to tag along with diabetes, including cardiovascular and kidney conditions, are to blame. 

That fits with what researchers have seen with other infections and diabetes. For instance, flu and pneumonia are more common and more serious in older individuals with type 2 diabetes, scientists reported online April 9 in the journal Diabetes Research and Clinical Practice. In a literature search of relevant studies looking at the link between COVID-19 and diabetes, the authors of that paper found a few possible mechanisms to explain why a person with diabetes might fare worse when infected with COVID-19. These mechanisms include: "Chronic inflammation, increased coagulation activity, immune response impairment and potential direct pancreatic damage by SARS-CoV-2."

Related: 13 coronavirus myths busted by science 

Mounting research has shown the progression of type 2 diabetes is tied to changes in the body's immune system. This link could also play a role in poorer outcomes in a person with diabetes exposed to SARS-CoV-2, the virus that causes COVID-19. 

No research has looked at this particular virus and immune response in patients with diabetes; however, in a study published in 2018 in the Journal of Diabetes Research, scientists found through a review of past research that patients with obesity or diabetes showed immune systems that were out of whack, with an impairment of white blood cells called Natural Killer (NK) cells and B cells, both of which help the body fight off infections. The research also showed that these patients had an increase in the production of inflammatory molecules called cytokines. When the immune system secretes too many cytokines,a so-called "cytokine storm" can erupt and damage the body's organs. Some research has suggested that cytokine storms may be responsible for causing serious complications in people with COVID-19, Live Science previously reported. Overall, type 2 diabetes has been linked with impairment of the very system in the body that helps to fight off infections like COVID-19 and could explain why a person with diabetes is at high risk for a severe infection.

Not all people with type 2 diabetes are at the same risk, though: A study published May 1 in the journal Cell Metabolism found that people with diabetes who keep their blood sugar levels in a tighter range were much less likely to have a severe disease course than those with more fluctuations in their blood sugar levels. 

People with type 1 diabetes (T1D) are also at elevated risk of adverse outcomes, a small study published in Diabetes Care suggests. The study, coordinated by  T1D Exchange — a nonprofit research organization focused on therapies for those with type 1 diabetes — found that of 64 people with either COVID-19 or COVID-19-like symptoms, two died. Nearly 4 in 10 people had to be treated in a hospital. And nearly a third experienced diabetic ketoacidosis — a potentially deadly condition in which the body experiences a shortage of insulin and blood sugar levels rise dangerously high.  The average patient was about 21 years old, suggesting that risks could be potentially higher for older age groups.

Heart disease and hypertension

People with conditions that affect the cardiovascular system, such as heart disease and hypertension, generally suffer worse complications from COVID-19 than those with no preexisting conditions, according to the American Heart Association. That said, historically healthy people can also suffer heart damage from the viral infection. 

The first reported coronavirus death in the U.S., for instance, occurred when the virus somehow damaged a woman's heart muscle, eventually causing it to burst, Live Science reported. The 57-year-old maintained good health and exercised regularly before becoming infected, and she reportedly had a healthy heart of "normal size and weight." A study of COVID-19 patients in Wuhan, China, found that more than 1 in 5 patients developed heart damage — some of the sampled patients had existing heart conditions, and some did not. 

In seeing these patterns emerge, scientists developed several theories as to why COVID-19 might hurt both damaged hearts and healthy ones, according to a Live Science report. 

In one scenario, by attacking the lungs directly, the virus might deplete the body's supply of oxygen to the point that the heart must work harder to pump oxygenated blood through the body. The virus might also attack the heart directly, as cardiac tissue contains angiotensin-converting enzyme 2 (ACE2) — a molecule that the virus plugs into to infect cells. In some individuals, COVID-19 can also kickstart an overblown immune response known as a cytokine storm, wherein the body becomes severely inflamed and the heart could suffer damage as a result.

Smoking

People who smoke cigarettes may be prone to severe COVID-19 infections, meaning they face a heightened risk of developing pneumonia, suffering organ damage and requiring breathing support. A study of more than 1,000 patients in China, published in the New England Journal of Medicine, illustrates this trend: 12.3% of current smokers included in the study were admitted to an ICU, were placed on a ventilator or died, as compared with 4.7% of nonsmokers. 

Cigarette smoke might render the body vulnerable to the coronavirus in several ways, according to a recent Live Science report. At baseline, smokers may be vulnerable to catching viral infections because smoke exposure dampens the immune system over time, damages tissues of the respiratory tract and triggers chronic inflammation. Smoking is also associated with a multitude of medical conditions, such as emphysema and atherosclerosis, which could exacerbate the symptoms of COVID-19.

A recent study, posted March 31 to the preprint database bioRxiv, proposed a more speculative explanation as to why COVID-19 hits smokers harder. The preliminary research has not yet been peer-reviewed, but early interpretations of the data suggest that smoke exposure increases the number of ACE2 receptors in the lungs — the receptor that SARS-CoV-2 plugs into to infect cells. 

Many of the receptors appear on so-called goblet and club cells, which secrete a mucus-like fluid to protect respiratory tissues from pathogens, debris and toxins. It's well-established that these cells grow in number the longer a person smokes, but scientists don't know whether the subsequent boost in ACE2 receptors directly translates to worse COVID-19 symptoms. What's more, it's unknown whether high ACE2 levels are relatively unique to smokers, or common among people with chronic lung conditions.

Obesity

Several early studies have suggested a link between obesity and more severe COVID-19 disease in people. One study, which analyzed a group of COVID-19 patients who were younger than the age of 60 in New York City, found that those who were obese were twice as likely as non-obese individuals to be hospitalized and were 1.8 times as likely to be admitted into critical care. 

"This has important and practical implications" in a country like the U.S. where nearly 40% of adults are obese, the authors wrote in the study, which was accepted into the journal Clinical Infectious Diseases but not yet peer-reviewed or published. Similarly, another preliminary study that hasn't yet been peer-reviewed found that the two biggest risk factors for being hospitalized from the coronavirus are age and obesity. This study, published in medRxiv looked at data from thousands of COVID-19 patients in New York City, but studies from other cities around the world found similar results, as reported by The New York Times.

A preliminary study from Shenzhen, China, which also hasn't been peer-reviewed, found that obese COVID-19 patients were more than twice as likely to develop severe pneumonia as compared with patients who were normal weight, according to the report published as a preprint online in the journal The Lancet Infectious Diseases. Those who were overweight, but not obese, had an 86% higher risk of developing severe pneumonia than did people of "normal" weight, the authors reported. Another study, accepted into the journal Obesity and peer-reviewed, found that nearly half of 124 COVID-19 patients admitted to an intensive care unit in Lille, France, were obese.

It's not clear why obesity is linked to more hospitalizations and more severe COVID-19 disease, but there are several possibilities, the authors wrote in the study. Obesity is generally thought of as a risk factor for severe infection. For example, those who are obese had longer and more severe disease during the swine flu epidemic, the authors wrote. Obese patients might also have reduced lung capacity or increased inflammation in the body. A greater number of inflammatory molecules circulating in the body might cause harmful immune responses and lead to severe disease.

Blood type

Blood type seems to be a predictor of how susceptible a person is to contracting SARS-CoV-2, though scientists haven't found a link between blood type per se and severity of disease.

Jiao Zhao, of The Southern University of Science and Technology, Shenzhen, and colleagues looked at blood types of 2,173 patients with COVID-19 in three hospitals in Wuhan, China, as well as blood types of more than 23,000 non-COVID-19 individuals in Wuhan and Shenzhen. They found that individuals with blood types in the A group (A-positive, A-negative and AB-positive, AB-negative) were at a higher risk of contracting the disease compared with non-A-group types. People with O blood types (O-negative and O-positive) had a lower risk of getting the infection compared with non-O blood types, the scientists wrote in the preprint database medRxiv on March 27; the study has yet to be reviewed by peers in the field.

In a more recent study of blood type and COVID-19, published online April 11 to medRxiv, scientists looked at 1,559 people tested for SARS-CoV-2 at New York Presbyterian hospital; of those, 682 tested positive. Individuals with A blood types (A-positive and A-negative) were 33% more likely to test positive than other blood types and both O-negative and O-positive blood types were less likely to test positive than other blood groups. (There's a 95% chance that the increase in risk ranges from 7% to 67% more likely.) Though only 68 individuals with an AB blood type were included, the results showed this group was also less likely than others to test positive for COVID-19. 

The researchers considered associations between blood type and risk factors for COVID-19, including age, sex, whether a person was overweight, other underlying health conditions such as diabetes mellitus, hypertension, pulmonary diseases and cardiovascular diseases. Some of these factors are linked to blood type, they found, with a link between diabetes and B and A-negative blood types, between overweight status and O-positive blood groups, for instance, among others. When they accounted for these links, the researchers still found an association between blood type and COVID-19 susceptibility. When the researchers pooled their data with the research by Zhao and colleagues out of China, they found similar results as well as a significant drop in positive COVID-19 cases among blood type B individuals.

Why blood type might increase or decrease a person's risk of getting SARS-CoV-2 is not known. A person's blood type indicates what kind of certain antigens cover the surfaces of their blood cells; These antigens produce certain antibodies to help fight off a pathogen. Past research has suggested that at least in the SARS coronavirus (SARS-CoV), anti-A antibodies helped to inhibit the virus; that could be the same mechanism with SARS-CoV-2, helping blood group O individuals to keep out the virus, according to Zhao's team.

Genetic factors

Many medical conditions can worsen the symptoms of COVID-19, but why do historically healthy people sometimes fall dangerously ill or die from the virus? Scientists suspect that certain genetic factors may leave some people especially susceptible to the disease, and many research groups aim to pinpoint exactly where those vulnerabilities lie in our genetic code. 

In one scenario, the genes that instruct cells to build ACE2 receptors may differ between people who contract severe infections and those who hardly develop any symptoms at all, Science magazine reported. Alternatively, differences may lie in genes that help rally the immune system against invasive pathogens, according to a recent Live Science report.

For instance, a study published April 17 in the Journal of Virology suggests that specific combinations of human leukocyte antigen (HLA) genes, which train immune cells to recognize germs, may be protective against SARS-CoV-2, while other combinations leave the body open to attack. HLAs represent just one cog in our immune system machinery, though, so their relative influence over COVID-19 infection remains unclear. Additionally, the Journal of Virology study only used computer models to simulate HLA activity against the coronavirus; clinical and genetic data from COVID-19 patients would be needed to flesh out the role of HLAs in real-life immune responses.

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Originally published on Live Science.  

Our ancestors of yore were plagued by recurrent bouts of malaria, deadly tuberculosis infections, constant syphilis outbreaks and bacteria-laced wounds that never healed. But armed with vaccines and antibiotics, modern-day humans can now avoid or be treated for these and many other communicable diseases — illnesses caused by infectious agents that can be transmitted between people or from animals to people. 

Nowadays, most people don't die from communicable diseases but rather those that cannot be passed on to other people. About 41 million people worldwide die each year from cardiovascular disease, cancer, respiratory disease, diabetes or another chronic illness; noncommunicable diseases account for more than 70% of all deaths globally, according to the World Health Organization. 

By definition, noncommunicable diseases are thought to arise from a combination of genetic, environmental and lifestyle factors rather than being transmitted by bacteria, fungi or viruses. In recent years, however, scientists have realized that the collection of microbes crawling in and on the human body — known as the microbiome — has a large influence on our health. Could it be that noncommunicable diseases can actually pass between people via the mighty microbiome?    

Some scientists think the answer is yes.

 Related: Could Humans Live Without Bacteria? 

An interesting hypothesis 

Communities of microbes make their abode in the human body, and research suggests that these bugs help direct the function of various physiological systems, including metabolism, digestion and immune defense. Scientists don't yet fully understand what distinguishes a healthy microbiome from an unhealthy one, but certain diseases do seem to be linked to a bacterial imbalance in the body.

For instance, people with diabetes, inflammatory bowel disease and cardiovascular disease tend to host a different collection of bacteria in their guts than those without the diseases, according to a report published Jan. 16 in the journal Science. The paper suggests that healthy people could potentially "catch" aspects of these ailments through exposure to these mixed-up microbes.  

"It is a radical thought to think that [noncommunicable diseases] might actually be communicable, and [this hypothesis] gives us a whole new way of thinking about these diseases," author B. Brett Finlay, a microbiologist at The University of British Columbia in Vancouver, told Live Science in an email. Several recent studies led Finlay and his colleagues to formulate this hypothesis, but a 2019 study conducted in Fiji really "tipped the scales," he said. 

In that study, researchers collected saliva and stool samples from about 290 people living in close proximity to determine the types of bacteria that appeared in their mouths and guts. The results, published in March 2019 in the journal Nature Microbiology, revealed distinct patterns of bacterial transmission within each community, particularly among people living in the same household. While mothers and their children shared many microbes, the microbiomes of spouses seemed to share the most similarities. The team could even predict which study participants were paired up as a couple based on their microbiomes alone. 

Related: Is It Better to Wash With Antibacterial Soap?

The Fiji study suggests that at least some elements of the microbiome can be passed between people. But could the transmitted bugs actually drive disease? Quite possibly. 

Spouses of people with type 2 diabetes, for example, stand a higher chance of developing the disease themselves within a year of their partner's diagnosis, Finlay noted. In an animal model of the disease, germ-free mice developed diabetic symptoms after receiving a bacteria-laden fecal transplant from a diseased mouse. Similar trends have been uncovered in inflammatory bowel disease, both in human spouses and animal models. 

Even cardiovascular disease may be linked to the presence of particular bacteria in the gut, Finlay noted. Certain microbes produce an enzyme that breaks red meat down into a compound called  trimethylamine N-oxide (TMAO). People with high concentrations of TMAO in their blood have a high chance of developing cardiovascular disease, and their risk rises if these enzyme-producing bacteria appear in their gut. 

Studies show that the bacteria can induce cardiovascular disease if transferred from a human into a mouse, but it's unknown whether the same might occur between people. 

Testing the idea 

Additional studies hint that more noncommunicable diseases may be influenced by bacteria and that those bacteria may travel between people. "Our lab has shown that early-life microbes impact hugely on asthma ... and we have some very exciting preliminary data with Parkinson’s," Finlay said. Microbes also alter immune function, which may prove relevant to cancer patients whose immune systems fail to recognize and attack tumors in the body, he added. 

Obesity, a major risk factor for noncommunicable diseases, also involves potentially transmittable microbes. Lean mice become obese when they receive a fecal transplant from already-obese mice, while humans with obese friends or siblings stand a higher chance of being obese than those who don't have obese friends or siblings. Living in a country with a high obesity rate also raises a person's risk of being obese. 

But all of these studies raise a similar question:How can scientists tell which aspects of a disease might be linked to troublesome microbes, as opposed to diet, exercise, genes or environmental factors?

This is a hard question to answer, Finlay said. "Ideally, one does a fecal transfer from a diseased person into a healthy one and causes disease, but of course this can't be done [for ethical reasons]," he said. To test his hypothesis, Finlay and his colleagues will have to rely on animal models and population studies akin to the one conducted in Fiji. If any noncommunicable diseases can be transmitted through microbes, the bugs will meet three criteria: They will appear distinct in diseased people versus healthy people; they will be able to be isolated from a disease host; and they will induce disease when transferred into healthy animals.

Related: Why Is Poop Brown? 

"As we identify mechanisms further, we can actually test these mechanisms, inhibit them ... and really show microbes are involved," Finlay said. 

Once scientists clarify how and whether noncommunicable diseases hop between people, they can develop treatments to "correct" diseased microbiomes. Some companies have already begun developing so-called second generation probiotics for inflammatory bowel disease, concocted from a mixture of microbes designed to rebalance the gut microbiome, Finlay said. Dietary changes, pharmaceuticals and, in extreme cases, fecal transplants could also serve as potential treatment options. Fecal transplants involve placing poop from a healthy donor into the colon of another person in order to revitalize their collection of gut bacteria.

"'Repopulating' people with lab-grown mixtures of microbes is probably better [than using fecal transplants], as we know exactly what is going in and don't have to worry about some virus that we haven't discovered yet being transplanted," Finlay said. Fecal transfers will be licensed only for fixing "serious diseases," as the procedure would have to be repeated numerous times, he added.

Scientists still have a lot to learn about how our in-house bacteria shape our health. A slew of fungi and viruses also live in the human body and may offer an additional route for "noncommunicable" diseases to pass from person to person. If Finlay's hypothesis garners support over time, it could lead to an entirely new understanding of noncommunicable disease.     

"It has significant public health policy implications," Finlay said, "and further suggests that looking after your own microbes will not only benefit you but also people close to you."

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Originally published on Live Science. 

People with obesity, high blood sugar, high blood pressure or high cholesterol are often advised to eat less and move more, but our new research suggests there is now another simple tool to fight off these diseases: restricting your eating time to a daily 10-hour window.

Studies done in mice and fruit flies suggest that limiting when animals eat to a daily window of 10 hours can prevent, or even reverse, metabolic diseases that affect millions in the U.S.

We are scientists - a cell biologist and a cardiologist - and are exploring the effects of the timing of nutrition on health. Results from flies and mice led us and others to test the idea of time-restricted eating in healthy people. Studies lasting more than a year showed that TRE was safe among healthy individuals. Next, we tested time-restricted eating in patients with conditions known collectively as metabolic syndrome. We were curious to see if this approach, which had a profound impact on obese and diabetic lab rats, can help millions of patients who suffer from early signs of diabetes, high blood pressure and unhealthy blood cholesterol.

A leap from prevention to treatment

It's not easy to count calories or figure out how much fat, carbohydrates and protein are in every meal. That's why using TRE provides a new strategy for fighting obesity and metabolic diseases that affect millions of people worldwide. Several studies had suggested that TRE is a lifestyle choice that healthy people can adopt and that can reduce their risk for future metabolic diseases.

However, TRE is rarely tested on people already diagnosed with metabolic diseases. Furthermore, the vast majority of patients with metabolic diseases are often on medication, and it was not clear whether it was safe for these patients to go through daily fasting of more than 12 hours — as many experiments require — or whether TRE will offer any benefits in addition to those from their medications.

In a unique collaboration between our basic science and clinical science laboratories, we tested whether restricting eating to a 10-hour window improved the health of people with metabolic syndrome who were also taking medications that lower blood pressure and cholesterol to manage their disease.

We recruited patients from UC San Diego clinics who met at least three out of five criteria for metabolic syndrome: obesity, high blood sugar, high blood pressure, high level of bad cholesterol and low level of good cholesterol. The patients used a research app called myCircadianClock, developed in our lab, to log every calorie they consumed for two weeks. This helped us to find patients who were more likely to spread their eating out over the span of 14 hours or more and might benefit from 10-hour TRE.

We monitored their physical activity and sleep using a watch worn on the wrist. As some patients with bad blood glucose control may experience low blood glucose at night, we also placed a continuous glucose monitor on their arm to measure blood glucose every few minutes for two weeks.

Nineteen patients qualified for the study. Most of them had already tried standard lifestyle interventions of reducing calories and doing more physical activity. As part of this study, the only change they had to follow was to self-select a window of 10 hours that best suited their work-family life to eat and drink all of their calories, say from 9 a.m. to 7 p.m. Drinking water and taking medications outside this window were allowed. For the next 12 weeks they used the myCircadianClock app, and for the last two weeks of the study they also had the continuous glucose monitor and activity monitor.

Timing is the medicine

After 12 weeks, the volunteers returned to the clinic for a thorough medical examination and blood tests. We compared their final results with those from their initial visit. The results, which we published in Cell Metabolism, were pleasantly surprising. We found most of them lost a modest amount of body weight, particularly fat from their abdominal region. Those who had high blood glucose levels when fasting also reduced these blood sugar levels. Similarly, most patients further reduced their blood pressure and LDL cholesterol. All of these benefits happened without any change in physical activity.

Reducing the time window of eating also had several inadvertent benefits. On average, patients reduced their daily caloric intake by a modest 8%. However, statistical analyses did not find strong association between calorie reduction and health improvement. Similar benefits of TRE on blood pressure and blood glucose control were also found among healthy adults who did not change caloric intake.

Nearly two-thirds of patients also reported restful sleep at night and less hunger at bedtime — similar to what was reported in other TRE studies on relatively healthier cohorts. While restricting all eating to just a six-hour window was hard for participants and caused several adverse effects, patients reported they could easily adapt to eating within a 10-hour span. Although it was not necessary after completion of the study, nearly 70% of our patients continued with the TRE for at least a year. As their health improved, many of them reported having reduced their medication or stopped some medication.

Despite the success of this study, time-restricted eating is not currently a standard recommendation from doctors to their patients who have metabolic syndrome. This study was a small feasibility study; more rigorous randomized control trials and multiple location trials are necessary next steps. Toward that goal, we have started a larger study on metabolic syndrome patients.

Although we did not see any of our patients go through dangerously low levels of glucose during overnight fasting, it is important that time-restricted eating be practiced under medical supervision. As TRE can improve metabolic regulation, it is also necessary that a physician pays close attention to the health of the patient and adjusts medications accordingly.

We are cautiously hopeful that time-restricted eating can be a simple, yet powerful approach to treating people with metabolic diseases.

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This article was originally published at The Conversation. The publication contributed the article to Live Science's Expert Voices: Op-Ed & Insights.

About 4.5 million American children are severely obese, and pediatricians say more of them should be recommended to get weight-loss surgery.

A new policy statement from the American Academy of Pediatrics (AAP) asserts that the obesity epidemic now places many children and adolescents at risk of living significantly shorter lives than their parents. While pediatricians can help patients lose weight through lifestyle changes, these adjustments often don't result in significant or lasting improvements in children with severe obesity, who may be more than a hundred pounds overweight, according to the paper, published Oct. 27 in the journal Pediatrics. 

"While lifestyle changes remain the mainstay of treatment, medical care is unlikely to significantly change the trajectory for most children with severe obesity," Dr. Sarah Armstrong, a Duke University professor of pediatric medicine and lead author of the policy, said in a statement. Over the last decade, studies have shown that weight-loss surgery is safe and effective for children and teens when performed in high-quality centers, Armstrong said. But the procedure is currently underutilized among children who could benefit from it, she added. 

Related: 7 Biggest Diet Myths

In children, severe obesity is defined as having a body mass index (BMI) of at least 120% of the 95th percentile for one's age and sex, according to the statement. At this weight, children and teens face greater risk of developing chronic diseases than their peers. Health conditions such as high blood pressure, sleep apnea and type 2 diabetes occur more often in severely obese children, along with mental health conditions such as depression.   

Weight-loss surgery may offer a better solution than standard treatment for severe childhood obesity and its accompanying health problems, wrote Armstrong and her co-authors. The group compiled studies of people 18 years old and younger who had undergone the procedure and found that many enjoyed lasting weight loss and a reduction in related health conditions. For example, one study followed adolescents up to 12 years post-surgery and found that patient BMI dropped 29%, on average, and the incidence of diabetes and high blood pressure dropped significantly. In contrast, severely obese children who made only lifestyle changes gained weight in the long term. 

In addition, few patients who had the surgery experienced complications, and when they did, the problems were usually minor, the report said. But despite its safety and effectiveness, weight-loss surgery isn't a "quick fix," Armstrong told the Associated Press. "It's a lifelong decision with implications every single day for the rest of your life," she said. After surgery, patients must stick to "specific nutrition and activity recommendations," according to HealthyChildren.org, the AAP informational website for parents. 

Unfortunately, as of now, most kids with severe obesity don't get weight-loss surgery because it's usually not covered by public or private health insurance, and it can cost up to $20,000, Armstrong told the AP. Some children may live far from surgery centers, which also reduces access to the surgery, she said. In its policy statement, the AAP said that insurance should cover both the surgery and follow-up care in order to enable more children with severe obesity to undergo the procedure.  

Although pediatric obesity surgery rates have tripled in recent decades, American doctors still perform fewer than 2,000 operations each year, the AP reported. Faith Newsome, now a senior at the University of North Carolina in Chapel Hill, underwent the procedure at age 16. At the time, she was 5 feet, 8 inches tall and weighed 273 pounds, meaning her BMI was almost 42. The following year, she dropped about 100 pounds. Today, her weight is within a normal range. 

The AP asked if she ever regrets the surgery.

"Never," Newsome said. "Teens should be able to discuss every option with their doctors, and surgery should be one of those options."

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Originally published on Live Science. 

Add this to the list of insidious places that fat can accumulate: your lungs.

A new study shows, for the first time, that fat can accumulate in the airway walls of the lungs, the authors wrote. The amount of fat accumulation was higher among people who were overweight or obese, compared with those of normal weight. 

What's more, the findings may explain, at least in part, why obesity is a risk factor for asthma, according to the study, published Thursday (Oct. 17) in the European Respiratory Journal.

The link between obesity and asthma has been known for years, but the reason for the link is not completely understood. Some researchers have suggested that excess weight places direct pressure on the lungs, making breathing more difficult. Others have suggested that obesity may increase inflammation throughout the body, which contributes to asthma.

But the new study "suggests that another mechanism is also at play," study co-author Peter Noble, an associate professor at the University of Western Australia in Perth, said in a statement. Fat accumulation may change the structure of people's airways in a way that raises asthma risk, the authors said.

Still, more research is needed to confirm whether fatty tissue in airways really does contribute to asthma, and whether weight loss could reduce asthma risk.

Related: Gasp! 11 Surprising Facts About the Respiratory System

Hidden fat

The researchers had been studying changes in the airways tied to respiratory diseases when they noticed that their lung samples showed that fatty tissue built up in the walls of the airways within the lungs, said study lead author John Elliot, a senior research officer at Sir Charles Gairdner Hospital in Perth. The scientists wondered whether this fat accumulation was tied to body weight.

To figure that out, Noble, Elliot and their colleagues analyzed postmortem samples of airway tissue from 52 people, including 16 who had died of asthma-related causes, 21 people who had asthma but had died of other causes, and 15 people who had no history of asthma prior to their deaths.

When the researchers used special dyes to analyze the tissue samples under a microscope, they saw fatty tissue that had accumulated in the airway walls among people in each of the three groups.

In addition, the amount of fat in the airway walls was linked with each person's body mass index (BMI), meaning that more fat accumulated in individuals  with higher BMIs, compared with those with lower BMIs.

The researchers propose that fat accumulation may lead to a thickening in the airways, which limits airflow. "That could at least partly explain an increase in asthma symptoms," among people with obesity, Noble said.

"This is an important finding on the relationship between body weight and respiratory disease because it shows how being overweight or obese might be making symptoms worse for people with asthma," Thierry Troosters, president of the European Respiratory Society, who was not involved with study, said in a staetment. "This goes beyond the simple observation that patients with obesity need to breathe more with activity … the observation points at true airway changes that are associated with obesity."

Although the findings still need to be confirmed, doctors should support asthma patients to help them achieve or maintain a healthy weight, he said.

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Originally published on Live Science. 

Shorter people may be at higher risk for developing type 2 diabetes compared with taller people, a new study from Europe suggests.

The study researchers analyzed information from thousands of people in Germany who underwent a physical exam and blood tests, and were followed for about seven years.

The researchers found that every 4-inch (10 centimeter) increase in a person's height was linked with a 41% reduced risk of developing type 2 diabetes for men and a 33% reduced risk for women. 

The findings held even after the researchers took into account factors that could affect a person's risk of type 2 diabetes, such as age, waist circumference, physical activity levels, smoking habits and alcohol consumption.

Related: 5 Diets That Fight Diseases

The results add to a growing body of research linking shorter stature with an increased risk of heart and metabolic problems.

The reason for the link isn't fully understood. But the results of the new study also suggested that people with shorter stature tended to have higher levels of fat in their liver, which may in part explain their increased risk of type 2 diabetes, the authors said.

The study only found an association and cannot prove that short stature directly leads to type 2 diabetes. For example, problems with nutrition in childhood, which the study couldn't take into account, might lead to both short stature and an increased risk of type 2 diabetes.

Still, "shorter individuals should be more closely monitored for diabetes and CVD [cardiovascular disease] risk factors," the authors wrote in their study, published today (Sept. 9) in the journal Diabetologia.

The researchers, from the German Institute of Human Nutrition Potsdam-Rehbruecke, pulled data from more than 27,000 people ages 35 to 65 who took part in an earlier study investigating ties between diet, lifestyle behaviors and the risk of cancer and other chronic diseases. Of these participants, the researchers randomly selected about 2,500 participants who were representative of the whole group. (Having a smaller group made it easier for the researchers to study levels of biomarkers in participants blood.) About 800 of these participants developed type 2 diabetes over the study period. 

The link between height and type 2 diabetes risk was strongest for participants with a healthy weight (BMI between 18 and 25), as opposed to those who were overweight or obese.It may be that for taller people, a larger waist circumference somewhat counteract the reduced risk o type 2 diabetes that is associated with their height, the authors said.

The researchers also found that having longer legs (as opposed to a longer torsos) was linked with a lower risk of type 2 diabetes, particularly for men.

When the researchers took into account measures of fat in the liver and in the blood, the link between height and diabetes risk was weakened. This suggests that levels of liver fat and fat in the blood could in part explain the link.

It may be that biological pathways that affect a person's height also influence the risk of type 2 diabetes through an effect on fat metabolism, the authors said.

"Our findings suggest that short people might present with higher cardiometabolic risk factor levels and have higher diabetes risk compared with tall people," the authors wrote. The findings also suggest that a person's height might be used to help predict their risk of developing diabetes, along with other traditional risk factors, such as obesity.

A 2016 study published in the New England Journal of Medicine suggested that certain genes may play a role in the link between short stature and an increased risk of heart disease. That study found that people who had more genetic markers tied to taller height were at lower risk for coronary artery disease, compared with those who had fewer of these markers, Live Science previously reported.

But genes aren't destiny when it comes to your risk of heart disease or type 2 diabetes. "The goal is to take the genes you have been given and put them in the best possible environment," with habits such as healthy eating and regular exercise, Dr. Andrew Freeman, director of clinical cardiology at National Jewish Health in Denver, who wasn't involved with either study, told Live Science in a 2016 interview. 

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 Originally published on Live Science. 

People who are genetically prone to obesity may gain weight more easily than others. But having so-called "obesity genes" does not make a person destined to pack on the pounds.

Case in point: A new study suggests that certain types of exercise may help ward off obesity, even for those who are genetically predisposed to the condition.

The study researchers analyzed information from more than 18,000 people in Taiwan ages 30 to 70 who provided blood samples and had their genomes sequenced. Participants reported whether they exercised regularly, and if so, what type of exercise they typically did. [The Best Way to Lose Weight Safely]

The researchers then scanned participants' genomes, looking for genes that were tied to an increased risk of obesity. Next, the investigators examined whether certain exercises seemed to counteract this risk. (The researchers used several measures of obesity, including body mass index, or BMI; body fat percentage; and waist and hip circumference.)

Overall, people who reported engaging in any type of regular exercise tended to have a lower BMI than those who didn't engage in regular exercise. This was true even among people who were genetically prone to obesity.

But one tried-and-true exercise stood out as the one with the strongest anti-obesity effect: jogging.

Participants with obesity genes who jogged tended to have a lower BMI, lower body fat percentage and a smaller hip circumference than people with similar genetic risk who did not jog.

But for those who loathe jogging, fear not: Five other types of exercise were also tied to a lower BMI among individuals at risk for obesity. These included mountain climbing, walking, power walking, certain types of dancing (such as ballroom dancing) and lengthy yoga sessions.

The benefits of these exercises were biggest among those with the greatest genetic risk of obesity.

These findings indicate that "although hereditary factors are critical to obesity, performing different kinds of exercise can modify this relationship," the authors wrote in their paper, which was published Aug. 1 in the journal PLOS Genetics. In other words, your genes aren't your destiny.

Interestingly, several other types of exercise failed to counteract the genetic risk of obesity. These included cycling, stretching exercises and swimming, as well as the video game "Dance Dance Revolution" — to the disappointment of "DDR" fans everywhere.

The findings don't mean that these latter exercises can't help with weight control. It's just that they didn't seem to offset the genetic propensity to gain weight.

There could be several reasons for this. The researchers noted that, for the average Joe or Jane, cycling and stretching exercises tend to require less energy expenditure than the six exercises that were tied to a lower obesity risk. In addition, exercising in relatively cold water, as happens with swimming, may stimulate appetite and increase food consumption, the authors said. And "DDR" is not a formal exercise that requires consistent training, as is the case with ballroom dancing, the researchers noted.

Because few participants in this study reported engaging in weight training, badminton, tennis or basketball, the study could not determine whether these exercises offset the risk of obesity genes.

It's important to note that most of the participants in the study were of Han Chinese descent, so it's not clear that the results would apply to other populations.

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Originally published on Live Science.

Exposure to light at night — from the glare of a bedroom TV or a street light through a window — may do more than disrupt sleep; it may increase the risk of weight gain and obesity in women, a new study suggests.

The study researchers found that women who reported exposure to light at night while sleeping were more likely to gain weight and become obese over nearly six years, compared with women who were not exposed to light at night.

The findings add to a growing body of evidence suggesting that light at night may be bad for health. Previous studies in animals have suggested that exposure to light at night may disrupt sleep and circadian rhythms, alter eating behaviors, and promote weight gain, the authors said.

The new findings, published today (June 10) in the journal JAMA Internal Medicine, suggest that "reducing exposure to artificial light at night while sleeping might be a useful strategy to prevent obesity," study lead author Dr. Yong-Moon Park, a postdoctoral fellow at the National Institute of Environmental Health Sciences (NIEHS), and senior author Dale Sandler, chief of the NIEHS's Epidemiology Branch, told Live Science in an email.

However, the researchers found only an association, and they can't prove that exposure to light at night directly causes weight gain or obesity. The study's authors could not fully account for factors that could affect the link, such as unhealthy eating behaviors and low levels of physical activity — factors that might be tied to poor sleep and exposure to light at night. [11 Surprising Things That Can Make Us Gain Weight]

In other words, exposure to light at night might represent a "constellation" of factors, including those related to unhealthy behaviors, "all of which could contribute to weight gain and obesity," the authors said.

More research is needed to better understand the link and determine whether reducing light at night may prevent obesity, the authors concluded.

Although the new findings aren't conclusive, reducing your exposure to light and night may not be a bad idea. "It seems reasonable to advise people not to sleep with lights on," Park and Sandler said.

Harmful light?

Previous studies have found a link between exposure to light at night and obesity in humans. However, most of this research was conducted in night-shift workers who are exposed to high levels of light at night; these results may not apply to the general population. The few studies that have been conducted in the general population have typically collected data at a single point in time, so researchers haven't been able to determine whether light at night is tied to weight gain over time.

In the new study, the researchers analyzed information from nearly 44,000 women ages 35 to 74 from all 50 U.S. states. Participants' weight was recorded at the start of the study, and they were followed for an average of 5.7 years. The women also answered questions about their level of exposure to light at night while sleeping, such as light from other rooms, light from outside, light from a TV, or light in the bedroom.

Among women who weren't obese at the study's, those who reported exposure to any light at night were about 20% more likely to become obese during the study, compared with those who didn't report exposure to light at night.

Women who slept with a TV or light on in the room were 17% more likely to gain at least 11 pounds (5 kilograms) during the study, compared with the no-night-light group.

The findings held even after the researchers took into account factors such as where participants lived (in an urban, suburban or rural area), their household income, their level of caffeine and alcohol consumption, and any experiences of depression or high stress.

Behind the link

It may be that exposure to light at night indirectly affects obesity risk by decreasing sleep duration, which can disrupt appetite hormones and, in turn, increase food consumption; less sleep can also lead to reduced physical activity, the authors said.

Or light at night might have a more direct effect on obesity — exposure to light at night may disrupt levels of sleep or stress hormones, or directly affect metabolism, in ways that contribute to weight gain, they said.

The study authors didn't specifically assess exposure to light from smartphones, computer screens or tablets, but previous research has also linked exposure to light from these devices (which emit "blue light") to poor sleep and daytime sleepiness, the authors said. It's likely that exposure to blue light at night is also linked with weight gain and obesity, but future studies will be needed to examine this, Park and Sandler said.

Future research should also include objective measures of light intensity and duration of light exposure, which weren't assessed in the current study, the authors said.

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Originally published on Live Science.

Filling your plate with ultraprocessed foods really does appear to lead people to eat more and gain weight, according to a new study.

Ultraprocessed foods refers to products that tend to go through a number of manufacturing steps to be produced, and contain ingredients that result from industrial-food manufacturing, such as hydrogenated oils, high-fructose corn syrup, flavoring agents and emulsifiers, according to the study.

For example, an ultraprocessed breakfast meal could consist of a bagel with cream cheese and turkey bacon, while an unprocessed breakfast could contain oatmeal with bananas, walnuts and skim milk.

The study, published May 16 in the journal Cell Metabolism, involved 20 healthy volunteers who spent about a month in a laboratory at the National Institutes of Health's (NIH) Clinical Center in Bethesda, Maryland, where all of their meals were prepared for them. Participants were randomly assigned to a diet of either ultraprocessed or minimally processed foods for two weeks, after which they were switched to the opposite diet for another two weeks. Importantly, meals for both groups had about the same amount of calories, sugars, fiber, fat and carbohydrates; participants could eat as much as they wanted.

The researchers found that, when people were given the ultraprocessed diet, they ate about 500 calories more per day than they did when they were on the unprocessed diet. What's more, participants gained about 2 pounds (0.9 kilograms) while they were on the ultraprocessed diet; they lost about 2 pounds while on the unprocessed diet. [7 Tips for Moving Toward a More Plant-Based Diet]

Previous studies that involved large groups of people have linked diets high in ultraprocessed foods with health problems, and even a higher risk of early death. But these studies observed people over time, rather than assigning them specific diets, and so could not prove that ultraprocessed foods actually cause people to eat more or gain weight. For example, it might be the case that people who eat ultraprocessed foods develop health problems for other reasons, such as a lack of access to fresh foods.

Although the new study was small, "results from this tightly controlled experiment showed a clear and consistent difference between the two diets," study lead author Kevin Hall, a senior investigator at NIH's National Institute of Diabetes and Digestive and Kidney Diseases, said in a statement. "This is the first study to demonstrate causality — that ultraprocessed foods cause people to eat too many calories and gain weight."

"Limiting consumption of ultraprocessed food may be an effective strategy for obesity prevention and treatment," the researchers concluded.

The study was not designed to determine why people ate more and gained more weight while on the ultraprocessed diet, so future research should investigate this, the authors said.

Still, the study did find that people tended to eat their meals faster when they were on the ultraprocessed diet, compared with the unprocessed diet. Some previous studies have suggested that faster-eating rates can result in increased overall food intake, the researchers said. The researchers noted that ultraprocessed foods tend to be softer and easier to swallow, which may have led to the faster-eating rate and delayed feelings of fullness, which could have contributed to increased food intake.

"We need to figure out what specific aspect of the ultraprocessed foods affected people's eating behavior and led them to gain weight," Hall said.

Future studies could try using different formulations of ultraprocessed foods to see what effect this has on people's overall consumption and weight gain.

The researchers noted that ultraprocessed foods can be difficult to cut back on, given their convenience and low cost. "We have to be mindful that it takes more time and more money to prepare less-processed foods," Hall said. "Just telling people to eat healthier may not be effective for some people without improved access to healthy foods."

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Originally published on Live Science.

Sometimes, the only thing holding our sanity together on a stressful day is a string of fatty and sugary snacks, aka comfort food.

But a new study, conducted in mice, provides more evidence that stress eating — especially of high-calorie meals — leads to more weight gain than eating while, well, not stressed. Chronic stress turns on a key mechanism in the brain that prompts mice to keep eating, a group of researchers reported today (April 25) in the journal Cell Metabolism.

The team analyzed the behavior and weight gain of a group of mice. Researchers chronically stressed some of the mice by isolating them from other mice and replacing their bedding with a thin layer of water. The other mice were placed in typical, nonstressful living conditions. The researchers fed some of the mice in each group chow and others a high-fat diet. [11 Surprising Things That Can Make Us Gain Weight]

After two weeks, the investigators found that the stressed mice that ate the healthy chow showed no difference in body weight compared with unstressed mice. However, the stressed mice that ate high-calorie food gained more weight than the nonstressed mice that ate the same, high-calorie food. Researchers found that this difference was, in part, because the stressed mice ate a lot more than their chill counterparts.

The investigators then peered into the mice brains to try to figure out the reasons for these differences.

The hypothalamus, a tiny area in the center of the brain (in both mice and humans), controls appetite and hunger, whereas the nearby amygdala controls emotional responses, such as anxiety and stress, according to a statement.

Both the amygdala and the hypothalamus produce a molecule called neuropeptide Y (NPY) in response to stress. In the hypothalamus, this molecule is known to stimulate food intake.

Following a hunch that this molecule could be driving the additional weight gain linked to stress, the researchers turned off the process that produces NPY in mice. When they blocked the ability of the amygdala to make this molecule in mice, the researchers found that the stressed and nonstressed mice on a high-calorie diet gained about the same amount of weight. This suggests that NPY does, in fact, drive the increased weight gain associated with stress eating.

That effect of NPY may involve an interaction with insulin. It turns out that these NPY molecules have docking stations for that hormone, which the body uses to control how much food mice (and humans) eat.

Insulin levels increase slightly right after a meal in order to help the body absorb glucose from the blood and signal to the hypothalamus to stop eating, according to the statement. The study showed that chronic stress resulted in slightly elevated insulin levels in the mice. But in stressed mice that were on a high-calorie diet, insulin levels were 10 times higher than in stress-free mice that ate the chow.

This high level of insulin circulating around the amygdala caused brain cells to become desensitized to the hormone. This, in turn increased the production of NPY and promoted eating, while decreasing the body's ability to burn energy, according to the statement.

It's unclear why the brain has such a mechanism, but a "lack of food and starving is stressful, so eating higher amounts under these conditions can be a survival advantage," said senior author Herbert Herzog, the head of the Eating Disorders laboratory at the Garvan Institute of Medical Research.

Even though this study was conducted in mice, since mice and humans use the same NPY system to regulate these processes, the situation is "very likely the same in humans," Herzog told Live Science. The researchers now hope to look at this pathway in more detail and search for any steps or molecules along the way that could be targeted for obesity intervention.

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Originally published on Live Science.

Obesity is tied to a slew of harmful effects in the body, and now, a new study suggests it may also affect brain structure.

The researchers analyzed brain scans and found that higher levels of body fat were tied to lower brain volumes in certain areas. Specifically, too much body fat was linked to reduced amounts of gray matter — the brain tissue that contains nerve cells — in structures in the center of the brain, the researchers said.

The link between body fat and brain volume was stronger among men compared with women, according to the study, published today (April 23) in the journal Radiology.

The researchers, from Leiden University Medical Center in the Netherlands, also saw changes in the brain's white matter — long nerve fibers that allow areas of the brain to communicate — tied to body fat. [10 Things You Didn't Know About the Brain]

The study adds to a growing body of research linking obesity with changes in the brain, including lower brain volumes, or brain shrinkage. Previous studies have also found a link between obesity and brain diseases such as dementia.

Still, the new study showed only an association between body fat and lower brain volume and can’t prove that too much body fat actually causes brain shrinkage, or vice versa.

More studies are needed to investigate that link and to determine whether weight loss could benefit the brain, the authors said.

Obesity and the brain

Some previous studies have found a link between obesity and lower brain volumes as well as changes in white matter. But those studies tended to be small, and they used indirect measures of body fat, such as body mass index (BMI), which is a ratio of weight to height.

In a study published in January, researchers also found a link between belly fat and lower brain volumes, but this study used waist-to-hip ratio, another indirect measure of obesity.

In the new study, the researchers analyzed information from 12,087 people living in the United Kingdom, with an average age of 62. Participants underwent an MRI to assess their brain's gray- and white-matter structure. Researchers also measured participants' body fat levels using a method called bioelectrical impedance, which sends small electric currents through the body to estimate a person's percentage of body fat.

The researchers found that, in men, high levels of body fat were linked with a lower gray matter volume overall and lower volumes in certain gray matter areas in the center of the brain. Those include the thalamus, caudate nucleus, hippocampus, globus pallidus, putamen and nucleus accumbens. Some of these areas are involved in the brain's reward circuit, and others help to regulate body movements.

Among women, the researchers found a link only between body fat and reduced volume in the globus pallidus.

But among both men and women, high body fat levels were linked with differences in the microscopic structure of the white matter, as compared with people who had lower levels of body fat.

Behind the link

It's not clear why body fat levels are linked with reduced brain volume or differences in white matter. One idea is that high levels of body fat may produce inflammation that harms brain tissue. The smaller brain volumes seen in the study could indicate a loss of neurons in those areas, the researchers said.

Still, because the study was conducted at one point in time, it's unclear if obesity changes the brain or if people with lower volumes of gray matter in certain areas are at a higher risk of obesity.

Future studies should follow people forward in time to examine whether changes in body fat indeed result in changes in brain structure, the researchers said.

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Originally published on Live Science.

An experimental obesity treatment that involves injecting tiny beads into the arteries of the stomach may help some people lose weight and keep it off for at least a year, according to a new study.

In the study, people who received the treatment, called "bariatric embolization," lost about 11 percent of their excess weight, or 17 lbs. (7.6 kilograms), on average, after one year.

However, the study was small, involving only 20 participants, and much more research is needed to confirm the procedure's safety and effectiveness, the authors said. [The Best Way to Lose Weight Safely]

Still, "this is a great step forward for this procedure," which has been under development for the past decade, study lead author Dr. Clifford Weiss, an associate professor of radiology at Johns Hopkins University School of Medicine in Baltimore, said in a statement.

The study was published today (April 2) in the journal Radiology.

Microscopic beads

For the procedure, doctors first use a thin tube called a catheter and thread it through an artery in the wrist or groin to the stomach. Then, they inject the microscopic beads into the catheter, which travel along the tube and partially block the arteries that supply blood to the stomach. This, in turn, is thought to suppress the production of hunger-stimulating hormones, thereby reducing appetite, the researchers said.

The procedure aims to change people's metabolism in a way that's similar to what's seen in people who undergo weight-loss surgery, also known as bariatric surgery. But bariatric embolization is less invasive than bariatric surgery, and it takes patients less time to recover, the researchers said.

In the study, the 20 participants were considered "severly obese," with an average weight of more than 300 lbs. (139 kg) and a body mass index (BMI) of 45. On average, participants were more than 150 lbs. overweight.

During the first month after the procedure, the participants lost, on average, about 8 percent of their excess weight (the amount of weight above their ideal weight) and reported a reduction in feelings of hunger. After the first month, their reports of hunger increased but were still less than they were before the procedure.

After 12 months, participants had lost, on average, 11.5 percent of their excess weight and reported improvements in their quality of life.

There were no serious complications tied to the procedure. Eight patients developed stomach ulcers that didn't cause any symptoms and healed after three months.

Obesity treatment?

Dr. David Cummings, an endocrinologist and professor of medicine at the University of Washington School of Medicine, said it's unclear whether the weight loss in the participants was due to the placebo effect — one that results from a person's belief that the treatment is working, rather than any physiological effect of the treatment.

"Anyone enrolled in a [weight loss] trial typically loses a little weight," regardless of whether they receive the real treatment or a placebo, said Cummings, who wasn't involved with the study. (The new study can't determine how much weight loss was due to the placebo effect because it didn't have a placebo group.)

Cummings noted that although the study participants lost about 11 percent of their excess weight, their overall weight loss was only around 5 percent, which is "right at the level you'd expect from the placebo effect."

This research needs to move to "a more definitive trial where they compare it against a placebo group," Cummings told Live Science.

Dr. Scott Cunneen, director of Bariatric Surgery at Cedars-Sinai Medical Center in Los Angeles, said the method seemed promising, "but you need a lot more people [in a study] before you'd really know that it's safe."

One potential safety concern is that the procedure reduces blood flow too much, which could lead to stomach perforation and leaking, Cunneen said, although this wasn't reported in the current study.

It's important to note that bariatric embolization doesn't lead to as much weight loss as does bariatric surgery, which is tied to weight losses of more than 30 percent.

But the weight loss seen in the study is "well within the range that people generally can achieve with [weight loss] medications," Cunneen said.

The researchers stress that bariatric embolization isn't meant to replace bariatric surgery. Instead, it could be used as a supplement to diet and lifestyle changes to help treat obesity, they said.

Cunneen agreed. "Less than 1 percent of the people that qualify for surgery to help them with their weight are [actually getting] surgery … they're looking for something that's less invasive and less severe," Cunneen told Live Science. "This could fill that category."

Cummings added that it would be interesting to see if the procedure does reduce levels of ghrelin, a hormone that stimulates appetite, and if so, how long the effect lasts. (Levels of ghrelin drop significantly after bariatric surgery.) The researchers plan to report hormonal changes in a separate study.

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Originally published on Live Science.

Soda and other sugary beverages aren't exactly known for being healthy. But now, a new study finds that sugar-sweetened beverages are tied to an increased risk of early death.

In the study, published today (March 18) in the journal Circulation, researchers analyzed information from more than 80,000 women and 37,000 men in the health profession who were followed for about three decades. Participants filled out surveys about their diet every four years, and also answered questions about their lifestyle and overall health every two years.

The more sugary beverages people drank — including soft drinks, fruit drinks, energy drinks and sports drinks — the greater their risk of death was during the study period.

For example, those who drank two to six sugar-sweetened beverages (SSBs) per week were 6 percent more likely to die during the study period, compared with those who drank less than one SSB per month. Those who drank one to two SSBs per day were 14 percent more likely to die during the study period compared with those who drank less than one SSB per month. [11 Ways Processed Food Is Different from Real Food]

The findings held even after the researchers took into account factors that could affect people's risk of premature death and disease, such as smoking, alcohol use, physical activity, and consumption of fruits, vegetables and red meat.

"Our results provide further support to limit intake of SSBs and to replace them with other beverages, preferably water, to improve overall health and longevity," study lead author Vasanti Malik, a research scientist at the Harvard T.H. Chan School of Public Health's Department of Nutrition, said in a statement.

It's important to note that the study found only an association and cannot prove that drinking soda or other sugary drinks causes early death.

Added sugar

Sugar-sweetened beverages are the largest source of added sugar in the U.S. diet. While SSB consumption had been dropping in the U.S. over the past decade, in recent years, there's been an increase in consumption among U.S. adults. Consumption of SSBs is also rising in developing countries.

Previous studies have linked SSB intake with weight gain and an increased risk of type 2 diabetes, heart disease and stroke. However, few studies have examined the link between SSB consumption and early death, the researchers said.

In the new study, SSB consumption was particularly strongly linked with an increased risk of death from heart disease. Those who consumed two or more SSBs per day had a 31-percent higher risk of early death from heart disease, compared with those who consumed SSBs infrequently.

"These findings are consistent with the known adverse effects of high sugar intake on metabolic risk factors; and the strong evidence that drinking sugar-sweetened beverages increases the risk of type 2 diabetes, itself a major risk factor for premature death," said study co-author Dr. Walter Willett, professor of epidemiology and nutrition at the same institution.

But what about diet drinks? For the most part, diet drinks — which are sweetened with sugar substitutes — were not linked with an increased risk of death during the study period. Indeed, the study found that replacing one SSB per day with a diet drink was actually tied to a reduced risk of early death.

However, consuming very high levels of diet drinks — four or more servings per day — was linked with an increased risk of early death among women. This finding may have been due to so-called "reverse causation," that is, when people with known heart disease risks (such as high blood pressure and obesity) switch from SSBs to diet drinks. In other words, the people may have switched to diet drinks because of their existing health conditions. But further studies are needed to better examine the link between diet beverage consumption — particularly at high levels — and heart disease, the researchers said.

In a statement regarding the study, the American Beverage Association (ABA) said that it considers soft drinks "safe to consume as part of a balanced diet," and that the sugar used in the beverages is the same as sugar used in other food products. "We don't think anyone should overconsume sugar, that's why we're working to reduce the sugar people consume from beverages across the country," the statement said.

Editor's note: This article was updated on March 19 to include a statement from the ABA.

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Originally published on Live Science.

The obesity epidemic may be contributing to an increase in certain cancers among millennials in the U.S., a new study suggests.

The study found that rates of certain cancers linked to obesity — including colorectal, kidney and pancreatic cancer — increased among adults ages 25 to 49 from 1995 and 2014; with steeper rises seen in the youngest age groups. Rates of some of these same cancers also increased among older adults, but the increases were much smaller, the researchers said.

What's more, millennials had about double the risk of developing certain obesity-related cancers than baby boomers had at the same age. [10 Do's and Don'ts to Reduce Your Risk of Cancer]

The researchers noted that young adults still have an overall lower risk of developing these cancers, compared with older adults.

The findings could serve as a warning sign of a future rise in cancer rates as millennials get older, and could "potentially [halt] or [reverse] the progress achieved in reducing cancer mortality over the past several decades," study senior author Dr. Ahmedin Jemal, scientific vice president of surveillance and health services research at the American Cancer Society, said in a statement. "Cancer trends in young adults often serve as a sentinel for the future disease burden in older adults, among whom most cancer occurs."

The study was published today (Feb. 4) in the journal The Lancet Public Health, to coincide with World Cancer Day.

Obesity-related cancers

Excess body fat is known to increase the risk of certain cancers. In 2016, the International Agency for Research on Cancer (a branch of the World Health Organization) published a report linking obesity to a higher risk of 12 cancers: Colorectal, esophageal, gallbladder, gastric cardia (a type of stomach cancer), kidney, liver and bile duct, multiple myeloma (a type of bone marrow cancer), pancreatic and thyroid cancer; and, in women, endometrial, breast and ovarian cancer.

In the new study, the researchers analyzed information on cancer rates from 25 U.S. state cancer registries (covering about two-thirds of the U.S. population) diagnosed from 1995 to 2014. They looked at the rates of 30 different cancers, including the 12 obesity-related cancers, and 18 other cancers that have not been tied to obesity, such as lung and skin cancer.

The researchers found that rates of six obesity-related cancers — colorectal, endometrial, gallbladder, kidney, pancreatic, and thyroid — increased among adults ages 25 to 49 during the study period. Although rates of most of these cancers also rose in older adults, the increases were much smaller.

For example, pancreatic cancer rates increased, on average, by less than 1 percent per year among people ages 40 to 84; but rates increased 2.5 percent among people ages 30 to 34 years old; and 4.3 percent per year among those ages 25 to 29. [5 Things Women Should Know About Ovarian Cancer]

In contrast to obesity-related cancers, rates of most of the 18 non-obesity related cancers did not increase among young adults during the study period.

"Younger generations are experiencing earlier and longer-lasting exposure to excess fat and to obesity-related health conditions that can increase cancer risk," Jemal said.

Caution needed

It's important to keep in mind that, although young adults experienced greater rises in the rates of some obesity-related cancers, the overall rate of these cancers is lower in young adults compared with older adults. For example, the rate of pancreatic cancer from 2010 to 2014 was about 2 cases per 100,000 people per year among those ages 25 to 49, compared with about 37 cases per 100,000 people per year among those ages 50 to 84.

In addition, the researchers noted that their study found only an association between obesity and cancer, and cannot prove that obesity causes these cancers. Nor can it prove that the obesity epidemic is responsible for the increases in cancer rates in young adults.

Although the researchers speculated that increases in obesity in recent decades may have played a role in the rise of obesity-related cancers seen in the study, future studies are needed to tease out the exact reason why these cancers are increasing among young adults, they said.

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Originally published on Live Science.

Amphetamines are central nervous system (CNS) stimulants, also called psycho-stimulants, that are often used to treat attention deficit hyperactivity disorder (ADD and ADHD), narcolepsy, Parkinson's disease and obesity, according to the Center for Substance Abuse Research (CESAR) at the University of Maryland. Because of their high potential for abuse, the substances are also classified as Schedule II drugs by the U.S. Drug Enforcement Administration (DEA).

Amphetamines are derived from ephedra (Ephedra sinica), a plant native to China and Mongolia. For centuries, many cultures have used ephedra as a stimulant and for treating congestion and asthma, according to the National Center for Complementary and Integrative Health (NCCIH). The plant contains ephedrine and pseudoephedrine, which are natural alkaloids, or nitrogenous organic compounds that cause a physiological response in humans. These chemicals are the basis on which amphetamines (including methamphetamine) were created.

The history of amphetamine

Nagai Nagayoshi, a Japanese chemist and pharmacologist, first isolated ephedrine in 1885. Only two years later, in 1887, Lazar Edeleanu, a Romanian chemist, synthesized amphetamine from ephedrine, according to the University of Arizona's Methamphetamine and Other Illicit Drug Education (MethOIDE) program.

In 1929, Gordon Alles, a U.S. biochemist, discovered that amphetamine had physiological effects. Soon after Alles' discovery, pharmaceutical companies developed amphetamine medications for treating congestion and asthma, according to a review published in the American Journal of Public Health in 2008. From 1933 to 1948, amphetamine was included in an over-the-counter nasal-congestion inhaler called Benzedrine.

Additional clinical trials found that amphetamine had positive effects on weight loss, narcolepsy and depression. It's popularity then grew during World War II as active service members from the U.S., Japan, Germany and England were administered the drug to treat mild depression and to enhance alertness and endurance.

Amphetamines have been used since then in the development of a variety of drugs, most notably Adderall and Ritalin, which treat ADD and ADHD. Addiction to amphetamines has been an issue since the 1940s, but it escalated in the 1980s with increased illicit production of methamphetamine, a very addictive stimulant known for its euphoric effects.

How amphetamines work

Amphetamines are used in treatments for ADD and ADHD, obesity, narcolepsy, and Parkinson's disease, according to CESAR.

"People with ADHD [are hypothesized to] have too little dopamine in the prefrontal cortex — the rational thinking, cognitive, planning part of your brain — the part of your brain that tells the rest of your brain to calm down," said Catherine Franssen, assistant professor of biopsychology and director of neurostudies at Longwood University in Virginia.

An amphetamine-based medication, such as Adderall or Ritalin, increases dopamine production in the connections between the prefrontal cortex and other locations in the brain, Franssen explained. This allows the prefrontal cortex to regain control.

Certain formulations of amphetamine, typically pseudoephedrine, are used in medications that treat cold symptoms, such as Sudafed, Franssen said. The amphetamine stimulants reduce the swelling of the blood vessels in the nose; this helps open up the airways, allowing for easier breathing. The medications are available without a prescription but are stored behind the pharmacy counter because they can be illegally used to brew methamphetamine, according to the American Council on Science and Health.

There's some evidence that amphetamines may treat obesity by acting as appetite suppressants. A 2015 clinical trial published in the journal Frontiers in Endocrinology reported that patients who took amphetamine medications experienced increased weight loss and motivation. The mechanism was unclear, and more research is needed to determine if amphetamines can be used for long-term weight loss and maintenance.

Amphetamine side effects

When taken properly, amphetamine-based medications can be safe and effective. But as with any prescribed medication, there are potential side effects.

Amphetamines can have a powerful effect on the body and brain, even when taken only once. According to MedlinePlus, side effects of taking amphetamines include:

• Enhanced mood
• Increased wakefulness and physical activity
• Increased respiration
• Insomnia
• Increased heart rate and blood pressure
• Irregular or rapid heartbeat
• Cardiovascular collapse
• Reduced appetite
• Changes in sex drive
• Hyperthermia
• Permanent brain damage
• Memory loss, confusion, paranoia and hallucinations
• Convulsions or Parkinson's-like tremors
• Cardiovascular collapse or stroke

Side effects such as enhanced mood are linked to the increase production and release of dopamine, a neurotransmitter associated with pleasure.

Amphetamines also cause an increase in norepinephrine, the hormone involved with the activation of the sympathetic nervous system, which is what controls our "fight-or-flight" mechanism, Franssen said. Norepinephrine causes the physical side effects, such as increased respiration, heart rate and blood pressure.

Together, those two chemicals can also have other mental effects.

"The increase of dopamine, as well as the activation of the sympathetic nervous system, [can lead to] hallucinations and psychosis, similar to schizophrenia," Franssen said.

Addiction and abuse

Amphetamines, particularly methamphetamine, can be highly addictive.

Amphetamine can cause the brain to produce such high amounts of dopamine that the brain compensates by getting rid of dopamine receptors, Franssen said, similar to how we cover our ears to decrease the volume when someone is shouting at us. 

Removing these receptors decreases the person's ability to feel pleasure and can increase depression or suicidal thoughts when the person's not using the drug, according to American Addiction Centers. Those depressing feelings may drive people to continue using the drug so that the dopamine and the positive feelings it produces return.

In 1971, the Bureau of Narcotics and Dangerous Drugs — now the U.S. DEA — classified all forms of amphetamine, including the highly addictive methamphetamine, as Schedule II drugs. The classification means the drugs have an accepted medical use but also a high potential for abuse.

Beginning in the 1980s, abuse of amphetamine skyrocketed as illegal methamphetamine production took off. This period also saw a surge in prescriptions of amphetamine drugs for treating attention deficit disorders. Abuse and medical use of amphetamines has continued to increase over the past decade.

It wasn't until 2004, according to the NCCIH, that the U.S Food and Drug Administration banned the sale of any supplement containing ephedrine, which had become a common supplement for athletes. The ban stemmed from a rise in the number of health issues related to the drug and several deaths of people looking to increase endurance and lose weight with ephedrine supplements, according to Harvard Health Publishing.

In the U.S., an estimated 4.8 million people ages 12 and up abused their amphetamine-based prescriptions and about 1.7 million used methamphetamine in 2015, according to a National Survey on Drug Use and Health. However, it's difficult to accurately track methamphetamine use, because the drug is manufactured and distributed illegally. Additionally, the majority of methamphetamines come from outside the U.S., where they are produced cheaply and illegally with little consequence.

In early 2018, The New York Times reported that methamphetamine use in the U.S. had greatly increased over the past decade. In Portland, Oregon, more than 200 people died from methamphetamine use in 2016; that was three times more than just 10 years earlier, the Times reported. Portland was just one such example of a location that inundated by methamphetamine use.

While the physical changes amphetamines cause in the brain are permanent, several therapeutic treatment programs that can help people overcome their addiction. The most-successful treatments include addiction education, family counseling, cognitive behavior therapy and peer-support groups.

Further reading:

• More about methamphetamine from the National Institute on Drug Abuse.
• Amphetamine, past and present.
• Fact sheet on amphetamine from the U.S. DEA.

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

CHICAGO — Late-night meals may take a toll on heart health, a new study suggests.

The research, presented here today (Nov. 10) at the American Heart Association's Scientific Sessions annual meeting, found that eating more later in the evening was associated with an increased risk of heart disease.

People in the U.S. now have a "delayed lifestyle" — they go to sleep later at night and get fewer hours of sleep, said lead study author Nour Makarem, a postdoctoral fellow in cardiology at Columbia University Vagelos College of Physicians and Surgeons. And with that delayed lifestyle, you also see higher rates of late-night eating, she said. [9 New Ways to Keep Your Heart Healthy]

Makarem and her colleagues thought that this meal timing may play a role in the rise in rates of obesity, high blood pressure and diabetes seen in recent years.

So, they set out to see if that's the case. In the study, the researchers used a database called the Hispanic Community Health Study/Study of Latinos to look at information on more than 12,700 Hispanic and Latino adults ages 18 to 76.

(Though the study looked at just one specific population in the U.S., the Hispanic and Latino population, "we do expect to see similar associations in other populations in the U.S.," Makarem told Live Science. Indeed, several studies conducted abroad have shown that meal timing may be associated with developing risk factors for heart disease, she added.)

In the study, the team looked at data from two separate days in which participants reported their eating habits, and compared this information with measurements such as blood pressure and blood sugar.

They found that over half of the people in the study consumed 30 percent or more of their daily calories after 6 p.m. Those participants had higher levels of fasting blood sugar (a measure of the amount of sugar in the blood when someone hasn't eaten in hours), higher levels of insulin (the hormone that regulates the amount of sugar in the blood), higher levels of HOMA-IR (a marker of resistance to insulin) and higher blood pressure than participants who reported eating less than 30 percent of their daily calories after 6 p.m.

A high fasting blood sugar level can be considered a sign of prediabetes, according to the Mayo Clinic. (Prediabetes means that a person's blood sugar levels are abnormally high, but not high enough to be considered diabetes.) Indeed, the researchers found that those who consumed 30 percent or more of their daily calories after 6 p.m. were 19 percent more likely to develop prediabetes than those who ate more earlier in the day. Seventy percent of people with prediabetes go on to develop type 2 diabetes, which is a risk factor for heart disease, Makarem noted. [Where Is Heart Disease Risk Highest and Lowest? (Maps)]

Those same participants were also 23 percent more likely to develop hypertension, compared with people who ate more earlier the day. These associations were especially common in women, Makarem added.

The late-night link

The study only found an association between meal timing and a person's risk of certain medical problems; it didn't prove a cause-and-effect link.

However, Makarem said that one possible explanation for the link is that problems can arise when our body clocks aren't synced to our environment. Almost every cell in the body can tell time, following a roughly 24-hour cycle. A small part of the brain called the suprachiasmatic nucleus serves as the body's master clock, receiving external light cues (ideally from the sun) and sets the rest of the clocks in the body's cells accordingly, telling people when to wake up, sleep and eat, Makarem said.

"These clocks are regulated by bright-light exposure, but also by behaviors, particularly food signals," Makarem said. So, when we eat at unconventional times — for example, by consuming more calories in the evening — the body's clocks can become misaligned with the master clock, leading to problems in metabolism and increasing the risk for chronic diseases such as diabetes, hypertension and heart disease, she said.

"The evidence is fairly consistent that eating more, later in the day, seems to be worse metabolically," said Kristen Knutson, an associate professor of neurology and preventative medicine at Northwestern Univeristy Feinberg School of Medicine who was not involved with the research, but attended Makarem's talk. These problems arise because "you're not eating at the time that's optimal for your circadian system," she told Live Science.

The findings have not yet been published in a peer-reviewed journal. 

Originally published on Live Science.