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What causes obesity? A major new study is upending common wisdom.

What causes obesity? A major new study is upending common wisdom.

Yahoo3 days ago
Obesity is uncommon among Hadza hunter-gatherers in Tanzania, Tsimane forager-farmers in Bolivia, Tuvan herder-farmers in Siberia, and other people in less-developed nations. But it's widespread among those of us in wealthy, highly industrialized nations.
Why? A major study published this week in PNAS brings surprising clarity to that question. Using objective data about metabolic rates and energy expenditure among more than 4,000 men and women living in dozens of nations across a broad spectrum of socioeconomic conditions, the study quantified how many calories people from different cultures burn most days.
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For decades, common wisdom and public health messaging have assumed that people in highly developed nations, like the United States, are relatively sedentary and burn far fewer daily calories than people in less-industrialized countries, greatly increasing the risk for obesity.
But the new study says no. Instead, it finds that Americans, Europeans and people living in other developed nations expend about the same number of total calories most days as hunter-gatherers, herders, subsistence farmers, foragers and anyone else living in less-industrialized nations.
That unexpected finding almost certainly means inactivity is not the main cause of obesity in the U.S. and elsewhere, said Herman Pontzer, a professor of evolutionary anthropology and global health at Duke University in North Carolina and a senior author of the new study.
What is, then? The study offers provocative hints about the role of diet and some of the specific foods we eat, as well as about the limits of exercise, and the best ways, in the long run, to avoid and treat obesity.
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Is diet or inactivity causing obesity?
'There's still a lively debate in public health about the role of diet and activity' in the development of obesity, Pontzer said, especially in wealthy nations. Some experts believe we're exercising too little, others that we're eating too much, and still more that the two contribute almost equally.
Understanding the relative contributions of diet and physical activity is important, Pontzer noted, because we can't effectively help people with obesity unless we first tease out its origins. But few large-scale studies have carefully compared energy expenditure among populations prone to obesity against those more resistant to it, which would be a first step toward figuring out what drives weight gain.
So, for the new study, Pontzer and his 80-plus co-authors gathered existing data from labs around the world that use doubly labeled water in metabolism studies. Doubly labeled water contains isotopes that, when excreted in urine or other fluids, allow researchers to precisely determine someone's energy expenditure, metabolic rates and body-fat percentage. It's the gold standard in this kind of research.
They wound up with data for 4,213 men and women from 34 countries or cultural groups, running the socioeconomic gamut from tribes in Africa to executives in Norway. They calculated total daily energy expenditures for everyone, along with their basal energy expenditure, which is the number of calories our bodies burn during basic, biological operations, and physical activity energy expenditure, which is how many calories we use while moving around.
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A new theory of how our metabolisms work
After adjusting for body size (since people in wealthy nations tend to have larger bodies, and larger bodies burn more calories), they started comparing different groups. Anyone expecting a wide range of energy expenditures, with hunter-gatherers and farmer-herders at the high end and deskbound American office workers trailing well behind, would be wrong.
Across the board, the total daily energy expenditures of the 4,213 people were quite similar, no matter where they lived or how they spent their lives. Although the hunter-gatherers and other similar groups moved around far more throughout the day than a typical American, their overall daily calorie burns were nearly the same.
The findings, though counterintuitive, align with a new theory about our metabolisms, first proposed by Pontzer. Known as the constrained total energy expenditure model, it says that our brains and bodies closely monitor our total energy expenditure, keeping it within a narrow range. If we start consistently burning extra calories by, for instance, stalking prey on foot for days or training for a marathon, our brains slow down or shut off some tangential biological operations, often related to growth, and our overall daily calorie burn stays within a consistent band.
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The role of ultra-processed foods
The upshot is that 'there is no effect of economic development on size-adjusted physical activity expenditure,' Pontzer says. In which case, the fundamental problem isn't that we're moving too little, meaning more exercise is unlikely to reduce obesity much.
What could, then? 'Our analyses suggest that increased energy intake has been roughly 10 times more important than declining total energy expenditure in driving the modern obesity crisis,' the study authors write.
In other words, we're eating too much. We may also be eating the wrong kinds of foods, the study also suggests. In a sub-analysis of the diets of some of the groups from both highly and less-developed nations, the scientists found a strong correlation between the percentage of daily diets that consists of 'ultra-processed foods' - which the study's authors define as 'industrial formulations of five or more ingredients' - and higher body-fat percentages.
We are, to be blunt, eating too much and probably eating too much of the wrong foods.
'This study confirms what I've been saying, which is that diet is the key culprit in our current [obesity] epidemic,' said Barry Popkin, a professor at the Gillings School of Global Public Health at the University of North Carolina at Chapel Hill and an obesity expert.
'This is a well-done study,' he added.
Other experts agree. 'It's clear from this important new research and other studies that changes to our food, not our activity, are the dominant drivers of obesity,' said Dariush Mozaffarian, director of the Food is Medicine Institute at Tufts University in Boston.
The findings don't mean, though, that exercise is unimportant, Pontzer emphasized. 'We know that exercise is essential for health. This study doesn't change that,' he said.
But the study does suggest that 'to address obesity, public health efforts need to focus on diet,' he said, especially on ultra-processed foods, 'that seem to be really potent causes of obesity.'
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Study reveals primary cause of obesity — and it's not lack of exercise
Study reveals primary cause of obesity — and it's not lack of exercise

Fox News

time2 hours ago

  • Fox News

Study reveals primary cause of obesity — and it's not lack of exercise

Obesity among adults continues to be a major public health issue in the United States and other economically developed countries, according to the Centers for Disease Control and Prevention (CDC) and the World Health Organization (WHO). "It's a mix of poor diet, high stress levels, lack of muscle and lack of frequent movement," Lindsay Allen, a registered dietitian nutritionist and owner of Back in Balance Nutrition in Florida, told Fox News Digital. While both overeating and lack of exercise are often to blame, a new global study suggests that one factor far outweighs the other. Scientists studied more than 4,000 adults from 34 populations, ranging from hunter-gatherer communities to office workers. They analyzed each person's total energy expenditure (TEE), which is the number of calories burned daily, along with body fat percentage and BMI (body mass index). When adjusted for body size, people across all lifestyles and income levels burned similar amounts of energy, even if their daily routines were drastically different. "The differences in body fat that we see across populations likely aren't due to major differences in activity level or total daily energy burned," study authors Amanda McGrosky (from Elon University in North Carolina) and Amy Luke (Loyola University in Illinois) told Fox News Digital. "Rather, excess body fat is likely primarily the product of too many 'calories in,' or eating more calories than are burned." People in more economically developed areas burned more calories, the researchers noted — but that's primarily because they tend to weigh more, and heavier bodies naturally burn more energy. Published in the journal Proceedings of the National Academy of Sciences (PNAS), the study concluded that how much people eat plays a far greater role than the amount of exercise when it comes to putting on weight. "Our analyses suggest that increased energy intake has been roughly 10 times more important than declining activity rates in driving the modern obesity crisis," the authors stated. Dr. Brett Osborn, a Florida neurosurgeon and longevity expert, agrees with the adage that "you can't out-train a bad diet." "Exercise burns far fewer calories than people want to believe," Osborn, who was not involved in the study, told Fox News Digital. "We're not gaining weight because we stopped moving. We're gaining because we're overfed." "This latest data only confirms what I've seen in my clinic: We're not gaining weight because we stopped moving. We're gaining because we're overfed." Allen pointed out that muscle mass should also be considered. "Having sufficient muscle is what drastically improves metabolism and fat-burning capabilities," she told Fox News Digital, also emphasizing the importance of stress levels. "People who live in high-stress societies tend to be fatter because stress hormones change our metabolism and shift us into 'survival mode.'" Another finding involves ultraprocessed foods (UPFs), which have long ingredient lists that are often calorie-dense, shelf-stable and "highly palatable." "As more populations are exposed to increasing amounts of highly processed, highly palatable foods, we will likely see increases in obesity in regions with relatively low rates currently," the study authors predicted. Ultraprocessed foods tend to be easier to overeat due to their flavor and texture, and they also don't keep people feeling full, the study found. They are also more calorie-dense, meaning they pack more energy into smaller volumes, and are more easily absorbed, making it harder for the body to eliminate excess energy. "Ultraprocessed foods are engineered to override our biology, namely our satiety signaling in the brain," Osborn told Fox News Digital. 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Obesity May Bring Intimacy Concerns: How to Help Patients
Obesity May Bring Intimacy Concerns: How to Help Patients

Medscape

time3 hours ago

  • Medscape

Obesity May Bring Intimacy Concerns: How to Help Patients

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From Lab to Landmark Therapy: Meet the Woman Behind GLP-1
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Medscape

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From Lab to Landmark Therapy: Meet the Woman Behind GLP-1

Svetlana Mojsov, PhD Biochemist Svetlana Mojsov, PhD, has been awarded the Frontiers of Knowledge Award in Biology and Biomedicine, presented by Spain's BBVA Foundation, for her collaborative research with Daniel Drucker, Joel Habener, and Jens Holst. Their work revealed the biological function of the hormone GLP-1, a key regulator of glucose metabolism and appetite. These discoveries paved the way for a new generation of therapies that have transformed the management of type 2 diabetes (T2D) and obesity, offering not only improved glycemic control and weight loss but also reduced cardiovascular risk. The findings have also sparked new lines of basic and translational research in multiple disease areas. Speaking to El Médico Interactivo , a Medscape Network platform, during the recent awards ceremony in Bilbao, Spain, Mojsov shared her perspective on the future of research. 'We are witnessing a new paradigm in which clinical experience is guiding future research to help us understand very fundamental concepts,' said Mojsov, currently a research associate professor at Rockefeller University in New York. How does it feel to see that drugs derived from your GLP-1 research are helping millions of people manage diabetes and obesity? I'm very happy to have contributed to something that has helped so many people. These drugs improve not only health outcomes but also overall quality of life. Being a scientist is a profession with many rewards — and certainly more benefits than setbacks — when your work can make a real difference. All scientists are driven by the goal of advancing knowledge and human health. I feel privileged to have been part of the early stages of this long scientific journey. Over the past two decades, GLP-1-based therapies have represented a major breakthrough in the treatment of T2D and obesity, improving both quality of life and clinical outcomes for millions of patients. For the first time, we've seen body weight reductions of up to 20% — which is particularly important because excess weight worsens the prognosis of T2D. Most earlier treatments actually caused weight gain, which limited their effectiveness. GLP-1 therapies, in contrast, help patients lose weight and improve disease outlook at the same time. What led you to investigate gut hormones, particularly GLP-1 and glucose-dependent insulinotropic polypeptide (GIP)? My interest in peptide-based therapies for glucose metabolism goes back to the mid-1970s, when I was a graduate student working with Dr Bruce Merrifield at Rockefeller University. We were studying the biology of glucagon — a hormone that raises blood glucose — and exploring how to synthesize glucagon analogs and inhibitors using solid-phase peptide synthesis. At that time, however, the available synthesis techniques often produced biologically inactive glucagon due to chemical modifications in the amino acid sequence. Merrifield encouraged me to develop new strategies to overcome this limitation, which laid the foundation for my later work on GLP-1. Were these the strategies you went on to explore in your research? Yes. For my doctoral thesis and later during my postdoctoral work, I focused on the amino acid sequence and biology of glucagon. That experience was instrumental in my discovery of GLP-1 in the early 1980s at Massachusetts General Hospital in Boston. In 1983, I identified the biologically active form of GLP-1 as a 31-amino acid peptide, which I named GLP-1 (7-37). I also hypothesized that it functioned as an incretin, a gut-derived peptide that stimulates insulin secretion in response to food intake. You and the other three awardees worked on the same hormone. Did you collaborate directly, or was the work conducted independently? How important is collaboration in this field? To detect GLP-1 (7-37) in the gut, I synthesized it myself in the endocrinology unit of my lab using solid-phase peptide synthesis. I also developed highly specific antibodies, radioimmunoassays, and chromatographic techniques that allowed me to confirm the presence of GLP-1 (7-37) at the site of incretin secretion. Although I conducted this initial work independently as a chemist, that kind of foundational research still requires close collaboration across disciplines. After identifying GLP-1 (7-37), I began working closely with Drs Joel Habener and David Nathan at Massachusetts General Hospital, and with Dr Gordon Weir at the Joslin Diabetes Center. So yes, throughout my work, I collaborated extensively with both biologists and clinical researchers. Your first GLP-1 findings date back to 1986. The first drugs came in 2005, and those widely used today appeared in 2017. Has the translation from discovery to clinic taken too long? What could be done to accelerate this process? You're right. Our early clinical studies with Nathan were the first to demonstrate that GLP-1 (7-37) stimulates insulin secretion and lowers blood glucose in people with T2D, establishing its therapeutic potential. Back at Rockefeller, my colleague Yang Wei and I showed that GLP-1 receptors are expressed not only in the pancreas but also in the brain, heart, and kidneys. This indicated that GLP-1's effects across these organs are mediated by a common receptor. In the 1980s and 1990s, the pharmaceutical industry was skeptical that peptides could become viable drugs because they required injection, and oral medications were strongly preferred by patients. Still, GLP-1 (7-37) held promise. In 2005, researchers discovered a longer-acting GLP-1-like peptide in lizard venom, which allowed Amylin Pharmaceuticals to act quickly since they didn't have to develop a new compound from scratch. That said, many companies were hesitant to invest in a peptide derived from a lizard. Twenty-five years after my original publications, Novo Nordisk and Lilly launched long-acting GLP-1 analogs. These drugs are now used to treat a wide range of conditions beyond T2D and obesity, including cardiovascular and renal disease and potentially even neurodegenerative disorders. It's the first time a single drug class has shown such broad therapeutic utility. Your discoveries are already benefiting millions of patients with obesity and diabetes, but cost remains a significant barrier. Do you think these drugs will become more accessible in low- and middle-income countries? They must become more affordable — otherwise, their usefulness is fundamentally limited. The broader the access, the greater the public health impact. I'm optimistic that continued innovation will help lower costs and improve global accessibility. These therapies shouldn't be reserved only for patients in wealthy nations. The health benefits must be shared more equitably. We also need to prioritize and protect scientific research. Especially given the current climate in the US, it's worth remembering that our longer, healthier lives are built on scientific progress. While the pharmaceutical industry plays a vital role, it all starts with discovery — and discovery starts in academic and research institutions. That's where we need to focus our support. Novo Nordisk did outstanding work, but they built on foundational research that came from the lab. Ultimately, we all have to work together. Every breakthrough starts with knowledge— knowledge, knowledge, and more knowledge. With T2D and obesity rising globally, and GLP-1 therapies now widely available, do you worry that they might shift attention away from prevention? No, quite the opposite. These therapies are most effective when combined with a commitment to overall health. Although some health conditions are unavoidable, I believe these drugs serve as a reminder of the importance of personal well-being. They help people take concrete steps toward better health. GLP-1 receptor agonists are now a key part of the pharmacologic toolkit for managing obesity and diabetes. Do you think they'll prove effective in other conditions, such as cardiovascular disease, neurodegeneration, or addiction? We already know they offer cardiovascular benefits, and physicians are prescribing them for people with diabetes — including those on insulin — because they also support kidney function. So these therapies are already broadly accepted and widely used. When it comes to neurodegenerative diseases, however, it's still too early to draw conclusions. Current findings are anecdotal and based on small patient cohorts. We need a much better understanding of the mechanisms involved. The same applies to addiction. There's speculation that GLP-1 analogs might help prevent addictive behaviors, but we need robust evidence before reaching that conclusion. This is the exciting part of science: knowledge opens the door to new discoveries. We need to return to the lab, use animal models, and uncover the mechanisms at work. Once we do, we'll be in a better position to confirm the full range of effects and explore new indications. You've had to fight for recognition on five patents. Do you believe being a woman made that more difficult? And do young women entering science today have equal opportunities? I grew up in Yugoslavia, where we weren't really taught to think in terms of gender differences. I never believed someone would take advantage of me for being a woman. Whether it happened or not, I can't say, but I never attributed any setbacks to my gender. I knew what I wanted and I fought for it. I pursued the patent issue because the original filing didn't properly reflect my contribution. My work resulted in five patents—four of which I secured after correcting Massachusetts General Hospital's initial application. Today, women are firmly part of the scientific community. Half of all researchers are women, so there should be no room for discrimination. That said, when something isn't right, we must speak up—clearly and confidently—and have the courage to stand our ground. Your perseverance and discipline are admirable. How important are those traits for aspiring researchers? They're both essential. This path is never easy.

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