Links for Keyword: Obesity

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Do gut bacteria make a second home in our brains?

By Kelly Servick SAN DIEGO, CALIFORNIA—We know the menagerie of microbes in the gut has powerful effects on our health. Could some of these same bacteria be making a home in our brains? A poster presented here this week at the annual meeting of the Society for Neuroscience drew attention with high-resolution microscope images of bacteria apparently penetrating and inhabiting the cells of healthy human brains. The work is preliminary, and its authors are careful to note that their tissue samples, collected from cadavers, could have been contaminated. But to many passersby in the exhibit hall, the possibility that bacteria could directly influence processes in the brain—including, perhaps, the course of neurological disease—was exhilarating. “This is the hit of the week,” said neuroscientist Ronald McGregor of the University of California, Los Angeles, who was not involved in the work. “It’s like a whole new molecular factory [in the brain] with its own needs. … This is mind-blowing.” The brain is a protected environment, partially walled off from the contents of the bloodstream by a network of cells that surround its blood vessels. Bacteria and viruses that manage to penetrate this blood-brain barrier can cause life-threatening inflammation. Some research has suggested distant microbes—those living in our gut—might affect mood and behavior and even the risk of neurological disease, but by indirect means. For example, a disruption in the balance of gut microbiomes could increase the production of a rogue protein that may cause Parkinson’s disease if it travels up the nerve connecting the gut to the brain. © 2018 American Association for the Advancement of Science

Related chapters from BN8e: 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: 25664 - Posted: 11.10.2018

When an FDA Ruling Curbed Fecal Transplants, I Performed My Own

/ By Susan D’Agostino I’d had intestinal distress before, but never like this. I was excreting not just waste, but blood and bits of my colon’s lining — up to 30 times per day. My abdominal pain hit deeper and felt less productive than the pain of giving birth, epidural-free, to my second child. Even shingles, which stung like a dental drill against my face, paled in comparison. Such was the agony of Clostridium difficile. Commonly known as C. diff., Clostridium difficile is an antibiotic-resistant superbug carried by approximately 5 percent of the adult population. The harmful gut bacterium is normally kept in check by other, good bacteria in the gut’s microbiome. But when the microbial balance is upset — for example, by a dose of antibiotics — C. diff. can gain a foothold. Left to multiply unchecked, it may kill its human host. In 2013, the Centers for Disease Control and Prevention estimated that 14,000 Americans die each year from C. diff. Thanks to an ill-considered decision by the U.S. Food and Drug Administration, and the willful ignorance of a string of doctors charged with my care, I was nearly one of them. Things started innocently enough. In early 2013, my doctor diagnosed me with a bacterial infection and prescribed an antibiotic. I had lived antibiotic-free for nearly four decades — a streak I was not inclined to break. But my doctor insisted on antibiotics, and I reluctantly complied. Soon after, my stomach turned against me. I went to an emergency room and was sent home with a prescription for vancomycin, an antibiotic reserved for serious bacterial infections. But the drug proved little match for the microbes that had bum-rushed my colon. My weight and fluid loss accelerated. My colon risked perforation. Copyright 2018 Undark

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 25663 - Posted: 11.10.2018

Yes exercise really does play a role in weight loss

By David Prologo “Exercise isn’t really important for weight loss” has become a popular sentiment in the weight-loss community. “It’s all about diet,” many say. “Don’t worry about exercise so much.” This idea crept out amid infinite theories about dieting and weight loss, and it quickly gained popularity, with one article alone citing 60 studies to support and spread this notion like wildfire. The truth is that you absolutely can — and should — exercise your way to weight loss. So why is anyone saying otherwise? For 10 years, I have been studying the epidemic of failed weight-loss attempts and researching the phenomenon of hundreds of millions of people embarking on weight-loss attempts — then quitting. Meanwhile, exercise remains the most common practice among nationally tracked persons who are able to maintain weight loss over time. Ninety percent of people who lose significant weight and keep it off exercise at least one hour a day, on average. There are a few reasons that exercise for weight loss gets a bad rap. First, the public is looking, in large part, for a quick fix — and the diet and weight-loss industry exploits this consumer desire for an immediate solution. Many studies have shown that exercise changes your body’s composition, improves your resting metabolism and alters your food preferences. These plain and simple facts have stood the test of time, but go largely unnoticed compared to most sensationalized diet products (change through exercise over time is a much tougher sell than a five-day “cleanse”). Moreover, many people consider one hour a day for exercise to be unreasonable or undoable, and find themselves looking elsewhere for an easier fix. © 1996-2018 The Washington Post

Alzheimer’s Gene Affects Energy Consumption in Mouse Brains

Sukanya Charuchandra L. Wu et al., “Human ApoE isoforms differentially modulate brain glucose and ketone body metabolism: Implications for Alzheimer’s disease risk reduction and early intervention,” J Neurosci, 38:6665–81, 2018. Humans carry three different isoforms of the ApoE gene, which affects Alzheimer’s risk. Liqin Zhao of the University of Kansas and her colleagues previously found that the gene plays a role in brain metabolism when expressed in mice; in a new study, they looked for the pathways involved. LEAVING AN IMPRESSION Zhao’s team engineered female mice to express the human versions of either ApoE2, ApoE3, or ApoE4, and analyzed expression of 43 genes involved in energy metabolism in their cortical tissue. BLOCKADE Mice with ApoE2 showed higher levels of proteins needed for glucose uptake and metabolism in their brains relative to animals harboring the most common isoform in humans, ApoE3. Mice with ApoE4 had lower levels of such proteins. The brain tissue’s glucose transport efficiency also varied across the genotypes, and levels of a key glucose-metabolizing enzyme, hexokinase, were reduced in ApoE4 brains. However, ApoE2 and ApoE4 brains contained similar levels of proteins involved in using ketone bodies, a secondary source of energy, while ApoE3 brains had lower levels of those proteins. “Brain glycolytic function may serve as a significant mechanism underlying the differential impact of ApoE genotypes,” Zhao says. © 1986 - 2018 The Scientist.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 25613 - Posted: 10.25.2018

Messing with fruit flies’ gut bacteria turns them into speed walkers

Laura Sanders Researchers have found a new link between gut and brain. By signaling to nerve cells in the brain, certain microbes in the gut slow a fruit fly’s walking pace, scientists report. Fruit flies missing those microbes — and that signal — turn into hyperactive speed walkers. With the normal suite of gut microbes, Drosophila melanogaster fruit flies on foot cover an average of about 2.4 millimeters a second. But fruit flies without any gut microbes zip along at about 3.5 millimeters a second, Catherine Schretter, a biologist at Caltech, and her colleagues report October 24 in Nature. These flies with missing microbes also take shorter breaks and are more active during the day. “Our work suggests that microbes assist in maintaining a certain level of locomotion,” Schretter says. An enzyme made by Lactobacillus brevis bacteria normally serves as the brakes, the researchers found. When researchers supplied the enzyme, called xylose isomerase, to flies lacking bacteria, the flies began walking at a slower, more normal pace. Xylose isomerase acts on a sugar that’s thought to influence nerve cells in fruit flies’ brains that control walking. For still mysterious reasons, the bacterial influence on walking speed occurred only in female fruit flies, not males. Studying that difference will be “a very interesting potential direction for this work,” Schretter says. |© Society for Science & the Public 2000 - 2018

Self-Control Center in the Brain Linked to Weight Loss

Ashley P. Taylor The activity in a cortical area involved in self-regulation was the best correlate of weight loss in a study published today (October 18) in Cell Metabolism. Previously, scientists thought that challenges to losing weight stemmed from imbalances between the hormones leptin, which produces a feeling of satiety, and ghrelin, which stimulates hunger. When people go on a diet, ghrelin levels go up and leptin levels go down. To see how brain activity fits into dieting physiology, Alain Dagher, a neurologist at McGill University, worked with 24 overweight and obese people who were starting a 1,200-calories-per-day diet at a weight-loss clinic. Before starting the regimen, participants had fMRIs—imaging scans that show brain activity—while looking at pictures of either appetizing, sometimes high-calorie food, or of scenery. The researchers repeated the scans one month and three months into the diet. Typically, food pictures activate the ventral medial prefrontal cortex, linked to desire, motivation, and value, Dagher says in a press release. Further, this region stimulates hunger when the body is burning more calories than it’s taking in, Dagher tells HealthDay. Over the course of the study, the ventral medial prefrontal cortex responded less and less to the pictures of food, but the decline in activity was greatest in people who lost the most weight, Dagher says in the release. On the other hand, activity in the lateral prefrontal cortex, involved in self-regulation, increased over the course of the diet, and the more it was active, the more weight people lost. © 1986 - 2018 The Scientist

Gene mutation points to new way to fight diabetes, obesity, heart disease

Researchers say they have discovered a gene mutation that slows the metabolism of sugar in the gut, giving people who have the mutation a distinct advantage over those who do not. Those with the mutation have a lower risk of diabetes, obesity, heart failure, and even death. The researchers say their finding could provide the basis for drug therapies that could mimic the workings of this gene mutation, offering a potential benefit for the millions of people who suffer with diabetes, heart disease, and obesity. The study, which is largely supported by the National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health, appears in the Journal of the American College of Cardiology (link is external). “We’re excited about this study because it helps clarify the link between what we eat, what we absorb, and our risk for disease. Knowing this opens the door to improved therapies for cardiometabolic disease,” said Scott D. Solomon, M.D., a professor of medicine at Harvard Medical School and a senior physician at Brigham and Women’s Hospital in Boston, who led the research. He explained that the study is the first to fully evaluate the link between mutations in the gene mainly responsible for absorbing glucose in the gut — SGLT-1, or sodium glucose co-transporter-1 — and cardiometabolic disease. People who have the natural gene mutation appear to have an advantage when it comes to diet, Solomon noted. Those who eat a high-carbohydrate diet and have this mutation will absorb less glucose than those without the mutation. A high-carbohydrate diet includes such foods as pasta, breads, cookies, and sugar-sweetened beverages.

Belly Fat Has a Role to Play in Fighting Infections

Selene Meza-Perez, Troy D. Randall Fat is a loaded tissue. Not only is it considered unsightly, the excess flab that plagues more than two-thirds of adults in America is associated with many well-documented health problems. In fact, obesity (defined as having a body mass index of 30 or more) is a comorbidity for almost every other type of disease. But, demonized as all body fat is, deep belly fat known as visceral adipose tissue (VAT) also has a good side: it’s a critical component of the body’s immune system. VAT is home to many cells of both the innate and adaptive immune systems. These cells influence adipocyte biology and metabolism, and in turn, adipocytes regulate the functions of the immune cells and provide energy for their activities. Moreover, the adipocytes themselves produce antimicrobial peptides, proinflammatory cytokines, and adipokines that together act to combat infection, modify the function of immune cells, and maintain metabolic homeostasis. Unfortunately, obesity disrupts both the endocrine and immune functions of VAT, thereby promoting inflammation and tissue damage that can lead to diabetes or inflammatory bowel disease. As researchers continue to piece together the complex connections between immunity, gut microbes, and adipose tissues, including the large deposit of fat in the abdomen known as the omentum, they hope not only to gain an understanding of how fat and immunity are linked, but to also develop fat-targeted therapeutics that can moderate the consequences of infectious and inflammatory diseases. © 1986 - 2018 The Scientist

Are We Wired to Sit?

By Gretchen Reynolds Are we born to be physically lazy? A sophisticated if disconcerting new neurological study suggests that we probably are. It finds that even when people know that exercise is desirable and plan to work out, certain electrical signals within their brains may be nudging them toward being sedentary. The study’s authors hope, though, that learning how our minds may undermine our exercise intentions could give us renewed motivation to move. Exercise physiologists, psychologists and practitioners have long been flummoxed by the difference between people’s plans and desires to be physically active and their actual behavior, which usually involves doing the opposite. Few of us exercise regularly, even though we know that it is important for health and well being. Typically, we blame lack of time, facilities or ability. But recently an international group of researchers began to wonder whether part of the cause might lie deeper, in how we think. For an earlier review, these scientists had examined past research about exercise attitudes and behavior and found that much of it showed that people sincerely wished to be active. In computer-based studies, for example, they would direct their attention to images of physical activity and away from images related to sitting and similar languor. But, as the scientists knew, few people followed through on their aims to be active. So maybe, the scientists thought, something was going on inside their skulls that dampened their enthusiasm for exercise. To find out, they recruited 29 healthy young men and women. All of the volunteers told the scientists that they wanted to be physically active, although only a few of them regularly were. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 5: The Sensorimotor System
Link ID: 25526 - Posted: 10.04.2018

A Nerve Pathway Links the Gut to the Brain’s Pleasure Centers

By Diana Kwon How do we decide what we like to eat? Although tasty foods typically top the list, a number of studies suggest preferences about consumption go beyond palatability. Scientists have found both humans and animals can form choices about what to consume based on the caloric content of food, independent of taste. Research spanning many decades has shown nutrients in the gastrointestinal tract can shape animals’ flavor preferences. One of the earliest findings of this effect dates back to the 1960s, when Garvin Holman of the University of Washington reported hungry rats preferred consuming a liquid paired with food injected into the stomach rather than a solution coupled with a gastric infusion of water. More recently Ivan de Araujo, a neuroscientist at the Icahn School of Medicine at Mount Sinai, and his colleagues have shown calories can trump palatability: Their work has demonstrated mice prefer consuming bitter solutions paired with a sugar infusion injected in the gut rather than a calorie-free sweet solution. Advertisement For years De Araujo and his group have been working to tease apart how the contents of the gut produce pleasure in the brain. In mice they have found sugar in the digestive tract can activate the brain’s reward centers. In animals bred without the ability to taste sweetness, sugary snacks still triggered activity in the ventral striatum, a brain region involved in reward processing. But according to De Araujo, the specific pathway that relayed signals between the gut and the brain remained a mystery. © 2018 Scientific American

The Gut of Mice Communicates with the Brain Through the Vagus Nerve

Sukanya Charuchandra Previous research has shown that the gut-brain connection, which refers to signaling between the digestive and the central nervous systems, is based on the transport of hormones, but a study published today (September 21) in Science suggests there may be a more direct link—the vagus nerve. This research presents “a new set of pathways that use gut cells to rapidly communicate with . . . the brain stem,” Daniel Drucker, who studies gut disorders at the Lunenfeld-Tanenbaum Research Institute in Toronto, Canada, and was not involved with the project, tells Science. Building on an earlier study in which the team found that gut cells had synapses, the researchers injected a rabies virus, expressing green fluorescence, into the stomachs of mice and watched it travel speedily from the intestines to the rodents’ brainstems. When they grew sensory gut cells together with neurons from the vagus nerve, the neurons moved across the dish to form synapses with the gut cells and began electrically coupling with them. Adding sugar to the dish sped up the rate of signaling between the gut and brain cells, a finding that suggests glutamate, a neurotransmitter involved in sensing taste, may be key to the process. Blocking glutamate secretion in gut cells brought these signals to a grinding halt. © 1986 - 2018 The Scientist.

Your gut is directly connected to your brain, by a newly discovered neuron circuit

By Emily Underwood The human gut is lined with more than 100 million nerve cells—it’s practically a brain unto itself. And indeed, the gut actually talks to the brain, releasing hormones into the bloodstream that, over the course of about 10 minutes, tell us how hungry it is, or that we shouldn’t have eaten an entire pizza. But a new study reveals the gut has a much more direct connection to the brain through a neural circuit that allows it to transmit signals in mere seconds. The findings could lead to new treatments for obesity, eating disorders, and even depression and autism—all of which have been linked to a malfunctioning gut. The study reveals “a new set of pathways that use gut cells to rapidly communicate with … the brain stem,” says Daniel Drucker, a clinician-scientist who studies gut disorders at the Lunenfeld-Tanenbaum Research Institute in Toronto, Canada, who was not involved with the work. Although many questions remain before the clinical implications become clear, he says, “This is a cool new piece of the puzzle.” In 2010, neuroscientist Diego Bohórquez of Duke University in Durham, North Carolina, made a startling discovery while looking through his electron microscope. Enteroendocrine cells, which stud the lining of the gut and produce hormones that spur digestion and suppress hunger, had footlike protrusions that resemble the synapses neurons use to communicate with each other. Bohórquez knew the enteroendocrine cells could send hormonal messages to the central nervous system, but he also wondered whether they could “talk” to the brain using electrical signals, the way that neurons do. If so, they would have to send the signals through the vagus nerve, which travels from the gut to the brain stem. © 2018 American Association for the Advancement of Science

Microglia Cause Cognitive Decline in Obese Mice

Diana Kwon Obesity is on the rise across the globe. The worldwide prevalence of the condition has nearly tripled over the last four decades, and approximately 13 percent of adults were obese in 2016. This staggering rise poses a public health concern: not only is obesity tied to bodily ailments such as cardiovascular disease and diabetes, epidemiological investigations have revealed that it is also linked to cognitive decline—and higher chances of developing dementia and other brain-related disorders later in life. Researchers have recently started to shed light on how weight gain affects the brain, and over the last few years, microglia, the brain’s resident immune cells, have emerged as the key culprit. Several rodent studies paint a picture of activated microglia gobbling up dendritic spines that form synapses in obese animals’ brains as the cause of cognitive decline. A study published today (September 10) in the Journal of Neuroscience provides strong new support for this theory. While prior studies have drawn robust associations between microglia and obesity-related cognitive decline, Elise Cope, a postdoc at Princeton University, says none had yet addressed whether those cells were actually causing the behavioral changes. “The novelty of our study was where we decided to see if blocking microglia using three different methods could actually prevent the dendritic spine loss and improve cognitive function,” Cope says. © 1986 - 2018 The Scientist.

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 25443 - Posted: 09.13.2018

How obesity may harm memory and learning

Laura Sanders Obesity can affect brainpower, and a study in mice may help explain how. In the brains of obese mice, rogue immune cells chomp nerve cell connections that are important for learning and memory, scientists report September 10 in the Journal of Neuroscience. Drugs that stop this synapse destruction may ultimately prove useful for protecting the brain against the immune cell assault. Like people, mice that eat lots of fat quickly pack on pounds. After 12 weeks of a high-fat diet, mice weighed almost 40 percent more than mice fed standard chow. These obese mice showed signs of diminished brainpower, neuroscientist Elizabeth Gould of Princeton University and colleagues found. Obese mice were worse at escaping mazes and remembering an object’s location than mice of a normal weight. On nerve cells, microscopic knobs called dendritic spines receive signals. Compared with normal-sized mice, obese mice had fewer dendritic spines in several parts of the mice’s hippocampi, brain structures important for learning and memory. The dendritic spine destruction comes from immune cells called microglia, the results suggest. In obese mice, higher numbers of active microglia lurked among these sparser nerve cell connections compared with mice of normal weights. When the researchers interfered with microglia in obese mice, dendritic spines were protected and the mice’s performance on thinking tests improved. |© Society for Science & the Public 2000 - 2018.

Longer daily fasting times improve health and longevity in mice

Increasing time between meals made male mice healthier overall and live longer compared to mice who ate more frequently, according to a new study published in the Sept. 6, 2018 issue of Cell Metabolism. Scientists from the National Institute on Aging (NIA) at the National Institutes of Health, the University of Wisconsin-Madison, and the Pennington Biomedical Research Center, Baton Rouge, Louisiana, reported that health and longevity improved with increased fasting time, regardless of what the mice ate or how many calories they consumed. “This study showed that mice who ate one meal per day, and thus had the longest fasting period, seemed to have a longer lifespan and better outcomes for common age-related liver disease and metabolic disorders,” said NIA Director Richard J. Hodes, M.D. “These intriguing results in an animal model show that the interplay of total caloric intake and the length of feeding and fasting periods deserves a closer look.” The scientists randomly divided 292 male mice into two diet groups. One group received a naturally sourced diet that was lower in purified sugars and fat, and higher in protein and fiber than the other diet. The mice in each diet group were then divided into three sub-groups based on how often they had access to food. The first group of mice had access to food around the clock. A second group of mice was fed 30 percent less calories per day than the first group. The third group was meal fed, getting a single meal that added up to the exact number of calories as the round-the-clock group. Both the meal-fed and calorie-restricted mice learned to eat quickly when food was available, resulting in longer daily fasting periods for both groups.

Limited Meal Times Prevent Obesity in Mice Prone to Gaining Weight

Abby Olena Mice with faulty circadian clocks are prone to obesity and diabetes. So are mice fed a diet high in fat. Remarkably, animals that have both of these obesity-driving conditions can stay lean and metabolically healthy by simply limiting the time of day when they eat. In a study published today (August 30) in Cell Metabolism, researchers report that restricting feeding times to mice’s active hours can overcome both defective clock genes and an unhealthy diet, a finding that may have an impact in the clinic. The work corroborates previous research showing how powerful restricted feeding can be to improve clock function, says Kristin Eckel-Mahan, a circadian biologist at the University of Texas Health Science Center at Houston who did not participate in the study. Over the last 20 years, biologists have found circadian clocks keeping physiologic time in almost every organ. They have also shown that mice with disrupted clocks often develop metabolic diseases, such as obesity, and that circadian clock proteins physically bind to the promoters of many metabolic regulators and instruct them when to turn on and off. For Satchidananda Panda of the Salk Institute, these lines of evidence came together in 2009, when his group published a study showing that in mice without the clock component Cryptochrome, feeding and fasting could drive the expression of some, but not all, of the metabolic regulators throughout the body. Other groups have also confirmed that even in the absence of the clock it is still possible to drive some genetic rhythms. In this latest study, he and colleagues wanted to look more closely at how the cycling of clock and metabolic transcripts induced by time-restricted feeding, rather than normal genetic rhythms, influences the health of mice. © 1986 - 2018 The Scientist

Weight-loss pill hailed as 'holy grail' in fight against obesity

A weight-loss pill has been hailed as a potential “holy grail” in the fight against obesity after a major study showed it did not increase the risk of serious heart problems. Researchers say lorcaserin is the first weight-loss drug to be deemed safe for heart health with long-term use. Taken twice a day, the drug is an appetite suppressant which works by stimulating brain chemicals to induce a feeling of fullness. A US study saw 12,000 people who were either obese or overweight given the pills or a placebo – with those who took the drug shedding an average of 4kg (9lbs) in 40 months. Further analysis showed no big differences in tests for heart valve damage. Tam Fry, of Britain’s National Obesity Forum, said the drug is potentially the “holy grail” of weight-loss medicine. “I think it is the thing everybody has been looking for,” he said. “I think there will be several holy grails, but this is a holy grail and one which has been certainly at the back of the mind of a lot of specialists for a long time. “But all of the other things apply – lifestyle change has got to be root and branch part of this.” Prof Jason Halford, an obesity expert at the University of Liverpool, told the Daily Telegraph newspaper that the drug’s availability in the UK would depend on whether it is approved by National Health Service regulators. “We don’t have any appetite suppressants available on the NHS. We have a massive great gap between lifestyle modification and surgery,” he said. © 2018 Guardian News and Media Limited

A Molecular Reason Why Obese People Have Trouble Losing Weight

By Bret Stetka Obesity rates in the U.S. and abroad have soared: The world now has more overweight people than those who weigh too little. One reason relates to the way the body reacts to its own fat stores by setting in motion a set of molecular events that impede the metabolic process that normally puts a damper on hunger. A new study published August 22 in Science Translational Medicine provides details of how this process occurs, giving new insight into why obese individuals have trouble shedding pounds. It also suggests a possible treatment approach that targets obesity in the brain, not in the belly. Scientists have long known that a hormone called leptin is instrumental in regulating the human diet. Produced by fat cells, the molecule communicates with a brain region called the hypothalamus, which reins in hunger cravings when our energy stores are full. Yet as we gain weight our bodies become less sensitive to leptin, and it becomes harder and harder to slim down. In other words, weight gain begets more weight gain. In an experiment using mice that became obese on a high-fat diet, an international team found obesity increases the activity of an enzyme called matrix metalloproteinase-2, or MMP-2. By using a technique called western blot analysis—separating and identifying all the proteins in a tissue sample—the authors found MMP-2 cleaves off a portion of the leptin receptor in the hypothalamus, impairing the hormone’s signaling and its ability to suppress appetite. © 2018 Scientific American

Low-carb diets could shorten life, study suggests

By Alex Therrien Health reporter, BBC News A low-carb diet could shorten life expectancy by up to four years, a study suggests. Low-carb diets, such as Atkins, have become increasingly popular for weight loss and have shown promise for lowering the risk of some illnesses. But a US study over 25 years indicates that moderate carb consumption - or switching meat for plant-based protein and fats - is healthier. The study relied on people remembering the amount of carbohydrates they ate. 'Gaining widespread popularity' In the study, published in The Lancet Public Health, 15,400 people from the US filled out questionnaires on the food and drink they consumed, along with portion sizes. From this, scientists estimated the proportion of calories they got from carbohydrates, fats, and protein. After following the group for an average of 25 years, researchers found that those who got 50-55% of their energy from carbohydrates (the moderate carb group and in line with UK dietary guidelines) had a slightly lower risk of death compared with the low and high-carb groups. Carbohydrates include vegetables, fruit and sugar but the main source of them is starchy foods, such as potatoes, bread, rice, pasta and cereals. The NHS Eatwell Guide provides details on how to achieve this kind of healthy, balanced diet and reduce the risk of serious illnesses in the long term. Researchers estimated that, from the age of 50, people in the moderate carb group were on average expected to live for another 33 years. © 2018 BBC

Any Weight Loss Can Be Healthful, but More Can Be Much Better

By Nicholas Bakalar When it comes to losing weight, more can be better. A lot better, according to a new study. Researchers studied 7,670 overweight or obese people who wanted to lose weight. Using data on current weight, weight a year ago and maximum lifetime weight, they tested the association of long-term weight loss with lowering the risk for metabolic syndrome — a constellation of unhealthy conditions that includes high blood pressure, insulin resistance, excess fat around the waist, high triglycerides and low HDL, or “good,” cholesterol. Compared to people who maintained less than a 5 percent weight loss for one year, those who lost 5 to 10 percent lowered their risk for metabolic syndrome by 22 percent. A 15 to 19 percent loss was associated with a 37 percent lower risk, and those who maintained a loss of 20 percent or more had a 53 percent lower risk. The study is in the Mayo Clinic Proceedings. Only 5.5 percent of the participants succeeded in holding a 20 percent or greater weight loss for one year. “Any weight loss is beneficial,” said the lead author, Gregory Knell of the University of Texas School of Public Health in Houston. “You don’t have to reach 20 percent to have a benefit. But if you are able to lose more weight, you get some really significant numbers related to metabolic health.” © 2018 The New York Times Company

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