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The ‘breakthrough’ obesity drugs that have stunned researchers

McKenzie Prillaman The hotel ballroom was packed to near capacity with scientists when Susan Yanovski arrived. Despite being 10 minutes early, she had to manoeuvre her way to one of the few empty seats near the back. The audience at the ObesityWeek conference in San Diego, California, in November 2022, was waiting to hear the results of a hotly anticipated drug trial. The presenters — researchers affiliated with pharmaceutical company Novo Nordisk, based in Bagsværd, Denmark — did not disappoint. They described the details of an investigation of a promising anti-obesity medication in teenagers, a group that is notoriously resistant to such treatment. The results astonished researchers: a weekly injection for almost 16 months, along with some lifestyle changes, reduced body weight by at least 20% in more than one-third of the participants1. Previous studies2,3 had shown that the drug, semaglutide, was just as impressive in adults. The presentation concluded like no other at the conference, says Yanovski, co-director of the Office of Obesity Research at the US National Institute of Diabetes and Digestive and Kidney Diseases in Bethesda, Maryland. Sustained applause echoed through the room “like you were at a Broadway show”, she says. This energy has pervaded the field of obesity medicine for the past few years. After decades of work, researchers are finally seeing signs of success: a new generation of anti-obesity medications that drastically diminish weight without the serious side effects that have plagued previous efforts. These drugs are arriving in an era in which obesity is growing exponentially. Worldwide obesity has tripled since 1975; in 2016, about 40% of adults were considered overweight and 13% had obesity, according to the World Health Organization (WHO). With extra weight often comes heightened risk of health conditions such as type 2 diabetes, heart disease and certain cancers. The WHO recommends healthier diets and physical activity to reduce obesity, but medication might help when lifestyle changes aren’t enough. The new drugs mimic hormones known as incretins, which lower blood sugar and curb appetite. Some have already been approved for treating type 2 diabetes, and they are starting to win approval for inducing weight loss. © 2023 Springer Nature Limited

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 28621 - Posted: 01.04.2023

Weight-loss drugs are a milestone for the obese but expose health inequity

By Laurie McGinley and Lenny Bernstein Rachel Graham has battled excess weight for years, cycling through trendy diets, various drugs, even bariatric surgery. Nothing worked for long. But last summer, she started a new medication, and today is 40 pounds lighter — and still shedding weight. “It used to be that if I saw food, I would want to eat it,” said the 54-year-old Graham, who is 5-foot-7 and 190 pounds. “Now, if I have three or four bites of food, I don’t want to eat more.” The drug she’s taking, Mounjaro by Eli Lilly, is part of a new crop of therapies that experts are hailing as a medical milestone — a long-sought way to transform the treatment of obesity, one of the nation’s most serious health threats. Designed for diabetes but used for obesity at higher doses, the medications induce loss of 15 to 22 percent of body weight on average — more than enough to significantly reduce cardiovascular and other health risks. That makes them far superior to old-style diet pills that delivered smaller benefits along with nasty side effects such as high blood pressure and loose stools. But during the past year, soaring demand for the drugs has ignited a mad scramble, exposing some of the most persistent problems in the nation’s health-care system, including supply shortages, high costs and health-care inequities. Tensions are surging as patients with diabetes and those with weight problems sometimes compete for the same medications, which are self-administered in weekly injections. Some doctors worry that the drugs, which might have to be taken for life, will overshadow the need for lifestyle changes involving diet and exercise.

Gut microbes make mice exercise more. Might they do the same in humans?

ByElizabeth Pennisi Willpower might be key to getting off the couch to exercise, but bacteria may lend a helping hand. Studies in mice reported today in Nature suggest microbes in the gut may be behind differences in the desire to work out. A research team has homed in on specific microbial molecules that stimulate a rodent’s desire to run—and keep running. By revealing exactly how these molecules talk to the brain, this group has set the stage for finding out whether similar signals help keep humans active. The work “establishes just how critical the microbiome is for exercise and goes incredibly deep in providing a new gut-brain [connection],” says Aleksandar Kostic, a microbiologist at Harvard Medical School who is co-founder of FitBiomics, a company developing probiotics to improve fitness. Kostic, who wasn’t involved in the research, and others speculate that exercise-inducing commands from the microbes might one day be packaged into pills people could take. To explore why some people like to exercise and others don’t, University of Pennsylvania microbiologist Christoph Thaiss studied mice bred to have a lot of genetic and behavioral variation. His team found more than a fivefold difference in how far the mice ran on wheels in their cages—some covered more than 30 kilometers in 48 hours, whereas others rarely moved in their wheels. The active and lazy mice didn’t show any significant differences in their genetics or biochemistry. But the researchers did notice one clue: When treated with antibiotics, mice that were normally highly energetic tended to exercise less. Follow-up studies showed the antibiotic treatment affected the brains of the formerly active mice. The activity of certain brain genes declined, along with levels of dopamine, a neurotransmitter that has been linked to “runner’s high”—that sense of wellbeing that comes with prolonged exercise.

How much water should you drink a day? It depends on several factors.

By Allison Gasparini Are you drinking enough water? The question seems like it should have a straightforward answer — a specific amount of water you need to drink daily to combat dehydration. But the rate and way in which the human body takes in and excretes water is not as universal as you might expect. By studying more than 5,000 people living in 23 countries and ranging in age from 8 days to 96 years, researchers have found that the turnover of water in a person’s body varies widely depending on the individual’s physical and environmental factors. The results, published in the Nov. 24 Science, suggest that the idea that a person should ideally consume eight 8-ounce glasses of water a day is not a one-size-fits-all solution to peak hydration. Even within the calculations, “individual variabilities could be huge,” says biomedical engineer Kong Chen, director of the metabolic research program at the National Institutes of Health’s Clinical Center. Yosuke Yamada, a physiologist at the National Institute of Biomedical Innovation, Health and Nutrition in Japan, and colleagues used a stable isotope of hydrogen known as deuterium to track the movement of water through people’s bodies. Drinking water accounts for only half of the total water intake by humans, with the rest coming from food. Simply measuring the amount of water that a person drinks in a day is not enough to accurately gauge water turnover or the amount of water used by the body daily. © Society for Science & the Public 2000–2022.

How Brains Send a Signal That It’s Time to Vomit

By Veronique Greenwood Anyone who’s had a shady oyster or a mushroom soup that didn’t sit well remembers the ominous queasiness heralding impending bad times. Bacteria release toxins that start the body’s process of speedily evacuating the contents of the stomach. It’s a protective mechanism of sorts — getting rid of the invaders en masse is probably helpful in the long term, even if it’s unpleasant in the short. But it has remained something of a mystery how the brain gets the alarm signal, then sends another one to tell the stomach to initiate a technicolor yawn. Your next bout of food poisoning isn’t the only reason to understand this particular neural pathway. Figuring out how to counter it could be helpful for people who develop nausea caused by chemotherapy medication and other drugs. As if fighting cancer isn’t painful and scary enough, patients are often so turned off by food that keeping their weight up becomes a major struggle. In a new study, researchers report that both bacteria and chemotherapy drugs appear to trigger the same molecular pathways in the gut. The findings, which were based on experiments with mice and published Tuesday in the journal Cell, showed that a bacterial toxin and a chemo medication both set in motion a cascade of similar neural messages that cause queasiness. Choosing mice for the study was unusual. Mice, it turns out, can’t puke — a little foible that typically makes it difficult to use them to study nausea. Researchers have used cats and dogs in the past, but the biology of mice in general is so much better understood, with much better tools available to scientists to do so. Cao Peng, a professor at Tsinghua University in Beijing, and his colleagues wondered whether mice might still be capable of feeling ill in the way people do after ingesting a chemo drug or a bad salad — or close enough, anyway, that researchers could use the creatures to understand the origins of the sensation. © 2022 The New York Times Company

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 11: Emotions, Aggression, and Stress
Link ID: 28537 - Posted: 11.02.2022

She saw the obesity epidemic coming. Then an unexpected finding mired her in controversy.

By Alice Callahan Katherine Flegal wanted to be an archaeologist. But it was the 1960s, and Flegal, an anthropology major at the University of California, Berkeley, couldn’t see a clear path to this profession at a time when nearly all the summer archaeology field schools admitted only men. “The accepted wisdom among female archaeology students was that there was just one sure way for a woman to become an archaeologist: marry one,” Flegal wrote in a career retrospective published in the 2022 Annual Review of Nutrition. And so Flegal set her archaeology aspirations aside and paved her own path, ultimately serving nearly 30 years as an epidemiologist at the National Center for Health Statistics (NCHS), part of the US Centers for Disease Control and Prevention. There, she spent decades crunching numbers to describe the health of the nation’s people, especially as it related to body size, until she retired from the agency in 2016. At the time of her retirement, her work had been cited in 143,000 books and articles. In the 1990s, Flegal and her CDC colleagues published some of the first reports of a national increase in the proportion of people categorized as overweight based on body mass index (BMI), a ratio of weight and height. The upward trend in BMI alarmed public health officials and eventually came to be called the “obesity epidemic.” But when Flegal, along with other senior government scientists, published estimates on how BMI related to mortality — reporting that being overweight was associated with a lower death rate than having a “normal” BMI — she became the subject of intense criticism and attacks. Flegal and her coauthors were not the first to publish this seemingly counterintuitive observation, but they were among the most prominent. Some researchers in the field, particularly from the Harvard School of Public Health, argued that the findings would detract from the public health message that excess body fat was hazardous, and they took issue with some of the study’s methods. Flegal’s group responded with several subsequent publications reporting that the suggested methodological adjustments didn’t change their findings. © 2022 Annual Reviews

How Fat Signals Us to Eat More of It

Short ribs glazed in a sweet sticky sauce and slow-cooked to perfection, potato chips hand-fried and tossed with a generous coating of sour cream, chicken wings battered and double-fried so that they stay crispy for hours. What is it about these, and other, mouth-watering — but incredibly fatty — foods that makes us reach out, and keep coming back for more? How they taste on the tongue is one part of the story, but to really understand what drives “our insatiable appetite for fat,” we have to examine what happens after fat is consumed, says Columbia University’s Charles Zuker, a neuroscientist and molecular geneticist who has been a Howard Hughes Medical Institute (HHMI) Investigator since 1989. Two years ago, Zuker and his team reported how sugar, upon reaching the gut, triggers signals that are sent to the brain, thus fueling cravings for sweet treats. Now, in an article published in Nature on September 7, 2022, they describe a similar gut-to-brain circuit that underlies a preference for fat. “The gut is the source of our great desire for fat and sugar,” says Zuker. The topic in question is an incredibly timely one, given the current global obesity epidemic. An estimated 13 percent of adults worldwide are obese — thrice that in 1975. In the US, that figure is even higher — at a staggering 42 percent. “It’s a very significant and important health problem,” says Zuker. Having a high body-mass index is a risk factor for stroke, diabetes, and several other diseases. “It’s clear that if we want to help make a difference here, we need to understand the biological basis for our strong appetite for fat and sugar,” he says. Doing so will help us design interventions in the future to “suppress this strong drive to consume” and combat obesity.

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 8: Hormones and Sex
Link ID: 28468 - Posted: 09.10.2022

Brain scran: pictures of food appear to trigger specific neurons

Sascha Pare Homer Simpson may not be the only one with a region of the brain dedicated to doughnuts: researchers have found that images of food appear to trigger a specific set of neurons. Previous research found that similar regions of the brain are highly specialised to identify and remember faces, places, bodies and words. The team, based at the Massachusetts Institute of Technology (MIT), say they stumbled upon the food-sensitive neurons by accident – and they could have evolved due to the evolutionary and cultural importance of food for humans. “Our most novel result is the discovery of a new neural response that has not been reported previously for the ventral visual pathway and that is highly selective for images of food,” the scientists wrote in the journal Current Biology. The researchers examined brain scans of eight participants taken as they viewed 10,000 images. Pictures of food appeared to trigger a population of neurons in the ventral visual cortex, which processes visual information. “We were quite puzzled by this because food is not a visually homogenous category,” said Meenakshi Khosla, one of the lead authors of the study. “Things like apples and corn and pasta all look so unlike each other, yet we found a single population that responds similarly to all these diverse food items.” Cooked meals such as a cheesy slice of pizza provoked a slightly stronger reactions than raw fruit and vegetables, the researchers noted. To test whether this was due to warmer colours in prepared food, they compared participants’ reactions with cool-toned images of food and richly coloured non-food objects. They found food caused a sharper signal. © 2022 Guardian News & Media Limited

Doctor Prescribed an Obesity Drug. Her Insurer Called It ‘Vanity.’

By Gina Kolata Maya Cohen’s entree into the world of obesity medicine came as a shock. In despair over her weight, she saw Dr. Caroline Apovian, an obesity specialist at Brigham and Women’s Hospital, who prescribed Saxenda, a recently approved weight-loss drug. Ms. Cohen, who is 55 and lives in Cape Elizabeth, Maine, hastened to get it filled. Then she saw the price her pharmacy was charging: $1,500 a month. Her insurer classified it as a “vanity drug” and would not cover it. “I’m being treated for obesity,” she complained to her insurer, but to no avail. While Ms. Cohen was stunned by her insurer’s denial, Dr. Apovian was not. She says it is an all too common response from insurers when she prescribes weight-loss drugs and the universal response from Medicare drug plans. Obesity specialists despair but hope that with the advent of highly effective drugs, the situation will change. Novo-Nordisk, the maker of the medicine Dr. Apovian prescribed, and patient advocacy groups have been aggressively lobbying insurers to pay for weight-loss drugs. They also have been lobbying Congress to pass a bill that has languished through three administrations that would require Medicare to pay for the drugs. But for now, the status quo has not budged. No one disputes the problem — more than 40 percent of Americans have obesity, and most have tried repeatedly to lose weight and keep it off, only to fail. Many suffer from medical conditions that are linked to obesity, including diabetes, joint and back pain and heart disease, and those conditions often improve with weight loss. © 2022 The New York Times Company

Patients Taking Experimental Obesity Drug Lost More Than 50 Pounds, Maker Claims

By Gina Kolata An experimental drug has enabled people with obesity or who are overweight to lose about 22.5 percent of their body weight, about 52 pounds on average, in a large trial, the drug’s maker announced on Thursday. The company, Eli Lilly, has not yet submitted the data for publication in a peer-reviewed medical journal or presented them in a public setting. But the claims nonetheless amazed medical experts. “Wow (and a double Wow!)” Dr. Sekar Kathiresan, chief executive of Verve Therapeutics, a company focusing on heart disease drugs, wrote in a tweet. Drugs like Eli Lilly’s, he added, are “truly going to revolutionize the treatment of obesity!!!” Dr. Kathiresan has no ties to Eli Lilly or to the drug. Dr. Lee Kaplan, an obesity expert at the Massachusetts General Hospital, said that the drug’s effect “appears to be significantly better than any other anti-obesity medication that is currently available in the U.S.” The results, he added, are “very impressive.” Dr. Kaplan who consults for a dozen pharmaceutical companies, including Eli Lilly, said he was not involved in the new trial or in the development of this drug. On average, participants in the study weighed 231 pounds at the outset and had a body mass index, or B.M.I. — a commonly used measure of obesity — of 38. (Obesity is defined as a B.M.I. of 30 and higher. At the end of the study, those taking the higher doses of the Eli Lilly drug, called tirzepatide, weighed about 180 pounds and had a B.M.I. just below 30, on average. The results far exceed those usually seen in trials of weight-loss medications and are usually seen only in surgical patients. Some trial participants lost enough weight to fall into the normal range, said Dr. Louis J. Aronne, director of the comprehensive weight control program at Weill Cornell Medical Center, who worked with Eli Lilly as the study’s principal investigator. Most of the people in the trial did not qualify for bariatric surgery, which is reserved for people with a B.M.I. over 40, or those with a B.M.I. from 35 to 40 with sleep apnea or Type 2 diabetes. The risk of developing diabetes is many times higher for people with obesity than for people without it. © 2022 The New York Times Company

Could gut microbes regulate appetite and body temperature?

pmByElizabeth Pennisi With more microbes than cells in our body, it’s not surprising that bacteria and other invisible “guests” influence our metabolism, immune system, and even our behavior. Now, researchers studying mice have worked out how bacteria in the mammalian gut can ping the brain to regulate an animal’s appetite and body temperature—and it involves the same molecular pathway the immune system uses to detect bacterial pathogens. “It’s quite an important finding,” says Antoine Adamantidis, a neuroscientist at the University of Bern who was not involved with the work. “Our life depends on food intake, and this is one more [thing] that bacteria can [influence].” Over the past 20 years, researchers have uncovered connections between the human gut and the rest of the body. They have linked certain intestinal microbes to conditions such as depression, multiple sclerosis, and immune system disorders; they have also documented nervous system connections between the gut and the brain. But researchers have been hard pressed to understand exactly how gut microbes—or the molecules they make—influence the brain. When certain gut bacteria infiltrate the rest of the body, our immune system picks up on them by sensing fragments of their cell walls, known as muropeptides. Our molecular detectors for these muropeptides, proteins called Nod2, coat the surfaces of cells involved in the body’s first line of defense. Ilana Gabanyi, a neuroimmunologist at the Pasteur Institute, wanted to know whether these molecular detectors also exist in the brain’s nerve cells. © 2022 American Association for the Advancement of Science.

Weight-loss techniques can halve meat consumption, Oxford trial finds

Linda Geddes Setting daily meat reduction goals and keeping an online diary of intake helped frequent meat eaters to halve their consumption in just over nine weeks, a trial has found. The trial, by researchers at the University of Oxford’s Livestock, Environment and People (Leap) programme, also found the routine was popular with participants, who felt it supported them to change their diet. Many people wish to reduce their meat consumption, whether for health or environmental reasons, or animal welfare concerns. Leap researchers wondered whether tapping into psychological principles employed by weight-loss apps, such as Noom, could help boost participants’ resolve. They developed an online platform called the Optimise meat tracker (standing for online programme to tackle individuals’ meat intake through self-regulation). Users log on and pick one meat reduction strategy from a list to focus on for that day, such as “try a new vegetarian recipe”, or “eat no processed meat”. The next morning they report whether they achieved this and record how much fish, poultry, red and processed meat they consumed. They receive weekly feedback on how they have done. The approach is based on self-regulation theory: the idea that people monitor and contextualise their own behaviour, reflect on it in relation to their goals, and try to modify it in response to feedback. “We know that people tend to underestimate the amount of meat they eat, the health and environmental impacts of their meat consumption; we also know that our meat-eating habits are strongly engrained. This process of self-regulation tries to tap into all of that,” said Dr Cristina Stewart at the University of Oxford, who led the research. © 2022 Guardian News & Media Limited

How the Brain Curbs Overeating

By Diana Kwon People with a rare genetic disorder known as Prader-Willi syndrome never feel full, and this insatiable hunger can lead to life-threatening obesity. Scientists studying the problem have now found that the fist-shaped structure known as the cerebellum—which had not previously been linked to hunger—is key to regulating satiation in those with this condition. This finding is the latest in a series of discoveries revealing that the cerebellum, long thought to be primarily involved in motor coordination, also plays a broad role in cognition, emotion and behavior. “We’ve opened up a whole field of cerebellar control of food intake,” says Albert Chen, a neuroscientist at the Scintillon Institute in California. The project began with a serendipitous observation: Chen and his team noticed they could make mice stop eating by activating small pockets of neurons in regions known as the anterior deep cerebellar nuclei (aDCN), within the cerebellum. Intrigued, the researchers contacted collaborators at Harvard Medical School. Scientists there had gathered data using functional MRI to compare brain activity in 14 people who had Prader-Willi syndrome with activity in 14 unaffected people while each subject viewed images of food—either immediately following a meal or after fasting for at least four hours. New analysis of these scans revealed that activity in the same regions Chen’s group had pinpointed in mice, the aDCN, appeared to be significantly disrupted in humans with Prader-Willi syndrome. In healthy individuals, the aDCN were more active in response to food images while fasting than just after a meal, but no such difference was identifiable in participants with the disorder. The result suggested that the aDCN were involved in controlling hunger. Further experiments on mice, conducted by researchers from several different institutions, demonstrated that activating the animals’ aDCN neurons dramatically reduced food intake by blunting how the brain’s pleasure center responds to food. The findings were recently detailed in Nature. © 2022 Scientific American,

Your Body’s Thirst Messenger Is in an Unexpected Place

By Veronique Greenwood Few pleasures compare to a long cool drink on a hot day. As a glass of water or other tasty drink makes its way to your digestive tract, your brain is tracking it — but how? Scientists have known for some time that thirst is controlled by neurons that send an alert to put down the glass when the right amount has been guzzled. What precisely tells them that it is time, though, is still a bit mysterious. In an earlier study, a team of researchers found that the act of gulping a liquid — really anything from water to oil — is enough to trigger a temporary shutdown of thirst. But they knew that gulping was not the only source of satisfaction. There were signals that shut down thirst coming from deeper within the body. In a paper published Wednesday in Nature, scientists from the same lab report that they’ve followed the signals down the neck, through one of the body’s most important nerves, into the gut, and finally to an unexpected place for this trigger: a set of small veins in the liver. The motion of gulping might provide a quick way for the body to monitor fluid intake. But whatever you swallowed will swiftly arrive in the stomach and gut, and then its identity will become clear to your body as something that can fulfill the body’s need for hydration, or not. Water changes the concentration of nutrients in your blood, and researchers believe that this is the trigger for real satiation. “There is a mechanism to ensure that what you’re drinking is water, not anything else,” said Yuki Oka, a professor at Caltech and an author of both studies. To find out where the body senses changes to your blood’s concentration, Dr. Oka and his colleagues first ran water into the intestines of mice and watched the behavior of nerves that connect the brain to the gut area, which are believed to work similarly in humans. One major nerve, the vagus nerve, fired the closest in time with the water’s arrival in the intestines, suggesting that this is the route the information takes on the way to the brain. © 2022 The New York Times Company

Gut microbes help hibernating ground squirrels emerge strong and healthy in spring

Hannah V. Carey Matthew Regan Ground squirrels spend the end of summer gorging on food, preparing for hibernation. They need to store a lot of energy as fat, which becomes their primary fuel source underground in their hibernation burrows all winter long. While hibernating, ground squirrels enter a state called torpor. Their metabolism drops to as low as just 1% of summer levels and their body temperature can plummet to close to freezing. Torpor greatly reduces how much energy the animal needs to stay alive until springtime. That long fast comes with a downside: no new input of protein, which is crucial to maintain the body’s tissues and organs. This is a particular problem for muscles. In people, long periods of inactivity, like prolonged bed rest, lead to muscle wasting. But muscle wasting is minimal in hibernating animals. Despite as much as six to nine months of inactivity and no protein intake, they preserve muscle mass and performance remarkably well – a very handy adaptation that helps ensure a successful breeding season come spring. How do hibernators pull this off? It’s been a real head-scratcher for hibernation biologists for decades. Our research team tackled this question by investigating how hibernating animals might be getting a major assist from the microbes that live in their guts. We knew from previous research that a hibernator’s gastrointestinal system undergoes dramatic changes in its structure and function from summer feeding to winter fasting. And it’s not only the animals who are fasting all winter long – their gut microbes are, too. Along with our microbiology collaborators, we figured out that winter fasting changes the gut microbiome quite a bit. © 2010–2022, The Conversation US, Inc.

The coronavirus may cause fat cells to miscommunicate, leading to diabetes

By Tina Hesman Saey Nola Sullivan recently marked an inauspicious anniversary. A little more than a year ago, on November 16, 2020, the 57-year-old pharmacy technician from Kellogg, Idaho, came down with COVID-19. “I lost my taste and smell, with a very bad head cold, body aches, muscle spasm, fatigue, nausea, vomiting, diarrhea,” she says. It took a month for her muscle spasms and a lingering headache to go away. She missed nearly three months of work. Her senses of smell and taste still haven’t fully returned. And “I still have the fatigue. It’s horrible. I’m nauseous all the time.” Sullivan has another lasting reminder of her battle with the coronavirus, too: diabetes. When she finally returned to work at the pharmacy, “I noticed that I was so thirsty all the time. And I just thought that was part of the COVID,” she says. “I was drinking gallons of water.” As a pharmacy technician, though, she knew that excessive thirst can be sign of diabetes. So she decided to check her blood sugar. A person is considered diabetic when levels of glucose in their blood reach 200 milligrams of glucose per deciliter of blood. Sullivan’s was over 500. Sullivan is not alone. In a study of more than 3,800 COVID-19 patients, just under half developed high blood sugar levels, including many, like Sullivan, who were not previously diabetic, cardiologist James Lo and colleagues reported November 2 in Cell Metabolism. About 91 percent of the intubated COVID-19 patients had high blood sugar, as did almost 73 percent of people who died of the disease, the researchers reported. © Society for Science & the Public 2000–2022

How Exercise Affects Metabolism and Weight Loss

By Gretchen Reynolds Many of us remember “The Biggest Loser,” the somewhat notorious reality television show that ran for more than a decade starting in 2004, in which contestants competed feverishly to drop massive amounts of weight over a short period of time. One of the biggest lessons of the show appeared to be that extreme exercise, along with draconian calorie restriction, would lead to enormous weight loss. Media coverage of the contestants years later, though, seemed to tell a different story, of weight regain and slowed metabolisms and the futility of attempting long-term weight loss. Now a new scientific analysis of the show and its aftermath, published last month in the journal Obesity, suggests many beliefs about “The Biggest Loser” may be misconceptions. The analysis tries to untangle what really happened to the contestants’ metabolisms and why some of them kept off weight better than others. It also looks into the complex role of exercise and whether staying physically active helped the contestants keep their weight under control for years, or not. For those who may have forgotten, or tried to, “The Biggest Loser” ran on NBC to generally high ratings for more than a dozen seasons. Contestants competed to drop the most pounds using extreme calorie restriction and hours of daily strenuous exercise. “Winners” typically shed hundreds of pounds in a few months. Such rapid and extreme weight loss caught the attention of Kevin Hall, a senior investigator at the National Institute of Diabetes and Digestive and Kidney Diseases, which is part of the National Institutes of Health. An expert on metabolism, Dr. Hall knew that when people drop lots of weight in a short period of time, they typically send their resting metabolic rates — the baseline calories we burn every day just by being alive — into free-fall. A lower resting metabolic rate can mean we burn fewer calories over all. © 2021 The New York Times Company

How Exercise Affects Your Appetite

By Gretchen Reynolds Does being active make us ravenous afterward and prone to eating more than we perhaps should? Or does it blunt our appetites and make it easier for us to skip that last, tempting slice of pie? A new study provides timely, if cautionary, clues. The study, which involved overweight, sedentary men and women and several types of moderate exercise, found that people who worked out did not overeat afterward at an enticing buffet lunch. However, they also did not skip dessert or skimp on portions. The findings offer a reminder during the holidays that while exercise has countless health benefits, helping us eat less or lose weight may not be among them. For most of us, exercise affects our weight and hunger in unexpected and sometimes contradictory ways. According to multiple scientific studies, few people who start to exercise drop as many pounds as the number of calories they burn working out would foretell. Some recent research suggests this occurs because our bodies stubbornly try to hang on to our fat stores, an evolutionary adaptation that protects us against (unlikely) future famines. So, if we burn calories during exercise, our bodies might nudge us to sit more afterward or reallocate energy from some bodily systems to others, reducing our overall daily energy expenditure. In this way, our bodies unconsciously compensate for many of the calories we burn exercising, reducing our chances of dropping pounds by working out. But that caloric compensation happens slowly, over the course of weeks or months, and involves energy expenditure. It has been less clear whether and how exercise influences our energy intake — that is, how many servings of food we consume — especially in the hours immediately after a workout. The evidence so far has been mixed. © 2021 The New York Times Company

'It's not your fault': Changing the conversation about obesity

For years, Theresa Babb blamed herself for her obesity. "It was always my fault," she told The Current. "Who else's fault would it be?" She says she spent thousands of dollars trying to lose weight, even going so far as to try commercial weight-loss programs like Weight Watchers and Jenny Craig. She also sought medical help from health-care providers, but she found some of them weren't willing to discuss her weight with her aside beyond uttering clichés about eating less or working out more. "I don't understand why a health-care professional would be afraid of talking to somebody or be uncomfortable about talking with a patient about health," she said. Nothing seemed to work for Babb, and she said she felt like a "failure" for not succeeding. That was until she met obesity specialist Dr. Laura Reardon two years ago. "One of the very first things that Dr. Reardon said to me … was 'It's not your fault,'" she said. "And it was hearing those words for the first time in my life that changed everything for me." According to Statistics Canada data from 2018, 7.3 million Canadian adults reported heights and weights classified as obese. Another 9.9 million Canadian adults were classified as overweight. Combined, these numbers represent 63.1 per cent of the Canadian adult population. Reardon said Babb's journey is one shared with millions of Canadians. "A lot of patients who come to see me probably have experiences like lots of the people out there, which is they've tried everything," she said. "They've gone to all these commercial weight loss programs. They've hired personal trainers. They've gone to the gym." ©2021 CBC/Radio-Canada.

Diet soda may prompt food cravings, especially in women and people with obesity

Allison Aubrey The "diet" in diet drinks may be a false promise for some soda lovers. True, they deliver the fizz and taste of a soda experience, without the calories. Yet, new research shows they also can leave people with increased food cravings. A study published recently in JAMA Network Open adds to the evidence that drinks made with sucralose may stimulate the appetite, at least among some people, and the study gives some clues as to why. "We found that females and people with obesity had greater brain reward activity" after consuming the artificial sweetener, says study author Katie Page, a physician specializing in obesity at the University of Southern California. Both groups also had a reduction in the hormone that inhibits appetite, and they ate more food after they consumed drinks with sucralose, compared with after regular sugar-sweetened drinks. In contrast, the study found males and people of healthy weight did not have an increase in either brain reward activity or hunger response, suggesting they're not affected in the same way. The study notes that most earlier research focused on males and people of normal weight. But this finding suggests that diet drinks sweetened with sucralose could be disadvantageous to the people who could benefit most from an effective diet strategy. © 2021 npr

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 8: Hormones and Sex
Link ID: 28027 - Posted: 10.09.2021

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