Posts tagged obesity

ScienceDaily (July 3, 2012) — As the United States confronts the growing epidemic of obesity among children and adults, a team of University of Colorado School of Medicine obesity researchers concludes that what the nation needs is a new battle plan — one that replaces the emphasis on widespread food restriction and weight loss with an emphasis on helping people achieve “energy balance” at a healthy body weight.

In a paper published in the July 3 issue of the journal Circulation, James O. Hill, PhD. and colleagues at the Anschutz Health and Wellness Center take on the debate over whether excessive food intake or insufficient physical activity cause obesity, using the lens of energy balance — which combines food intake, energy expended through physical activity and energy (fat) storage — to advance the concept of a “regulated zone,” where the mechanisms by which the body establishes energy balance are managed to overcome the body’s natural defenses towards preserving existing body weight. This is accomplished by strategies that match food and beverage intake to a higher level of energy expenditure than is typical in America today, enabling the biological system that regulates body weight to work more effectively. Additional support for this concept comes from many studies showing that higher levels of physical activity are associated with low weight gain whereas comparatively low levels of activity are linked to high weight gain over time.

"A healthy body weight is best maintained with a higher level of physical activity than is typical today and with an energy intake that matches," explained Hill, professor of pediatrics and medicine and executive director of the Anschutz Health and Wellness Center at the University of Colorado Anschutz Medical Campus and the lead author of the paper. "We are not going to reduce obesity by focusing only on reducing food intake. Without increasing physical activity in the population we are simply promoting unsustainable levels of food restriction. This strategy hasn’t worked so far and it is not likely to work in the future.

As Dr. Hill explains, “What we are really talking about is changing the message from ‘Eat Less, Move More” to ‘Move More, Eat Smarter.’ “

The authors argue that preventing excessive weight gain is a more achievable goal than treating obesity once it is present. Here, the researchers stress that reducing calorie intake by 100 calories a day would prevent weight gain in 90 percent of the adult population and is achievable through small increases in physical activity and small changes in food intake.

People who have a low level of physical activity have trouble achieving energy balance because they must constantly use food restriction to match energy intake to a low level of energy expenditure. Constant food restriction is difficult to maintain long-term and when it cannot be maintained, the result is positive energy balance (when the calories consumed are greater than the calories expended) and an increase in body mass, of which 60 percent to 80 percent is usually body fat. The increasing body mass elevates energy expenditure and helps reestablish energy balance. In fact, the researchers speculate that becoming obese may be the only way to achieve energy balance when living a sedentary lifestyle in a food-abundant environment.

Using an exhaustive review of the energy balance literature as the basis, the researchers also refuted the popular theory that escalating obesity rates can be attributed exclusively to two factors — the change in the American diet and the rise in overall energy intake without a compensatory increase in energy expenditure. Using rough estimates of increases in food intake and decreases in physical activity from 1971 to 2000, the researchers calculated that were it not for the physiological processes that produce energy balance, American adults would have experienced a 30 to 80 fold increase in weight gain during that period, which demonstrates why it is not realistic to attribute obesity solely to caloric intake or physical activity levels. In fact, energy expenditure has dropped dramatically over the past century as our lives now require much less physical activity just to get through the day. The authors argue that this drop in energy expenditure was a necessary prerequisite for the current obesity problem, which necessitates adding a greater level of physical activity back into our modern lives.

"Addressing obesity requires attention to both food intake and physical activity, said co-author John Peters, PhD., assistant director of the Anschutz Health and Wellness Center. "Strategies that focus on either alone will not likely work."

In addition, the researchers conclude that food restriction alone is not effective in reducing obesity, explaining that although caloric restriction produces weight loss, this process triggers hunger and the body’s natural defense to preserve existing body weight, which leads to a lower resting metabolic rate and notable changes in how the body burns calories. As a result, energy requirements after weight loss can be reduced from 170 to 250 calories for a 10 percent weight loss and from 325 to 480 calories for a 20 percent weight loss. These findings provide insight concerning weight loss plateau and the common occurrence of regaining weight after completing a weight loss regimen.

Recognizing that energy balance is a new concept for to the public, the researchers call for educational efforts and new information tools that will teach Americans about energy balance and how food and physical activity choices affect energy balance.

Source: Science Daily

ScienceDaily (July 2, 2012) — Investigators from Boston University School of Medicine (BUSM) and Boston University’s Slone Epidemiology Center report research findings that may shed light on influences on obesity during adulthood. Appearing in the journal Pediatrics, the study found an association of severity of sexual and physical abuse during childhood and adolescence with obesity during adulthood.

The findings were based on the ongoing Black Women’s Health Study, which has followed a large cohort of African-American women since 1995. Information provided in 2005 by more than 33,000 participants on early life experiences of abuse was assessed in relation to two measures of obesity: body mass index of 30 kg/m2 or more as a measure of overall obesity and waist circumference greater than 35 inches as a measure of central obesity.

The risk of obesity in 2005 by either measure was estimated to be approximately 30 percent greater among women in the highest category of physical and sexual abuse than in women who reported no abuse. The association was dampened but not fully explained by allowance for reproductive history, diet, physical activity and depressive symptoms, which might have been intermediates between abuse and weight gain.

According to the researchers, the findings add to growing evidence that experiences during childhood may have long-term health consequences. “Abuse during childhood may adversely shape health behaviors and coping strategies, which could lead to greater weight gain in later life,” explained Renee Boynton-Jarrett, MD, the lead investigator of the study and a pediatric primary care physician at Boston Medical Center. She also noted that metabolic and hormonal disruptions resulting from abuse could have that effect and that childhood abuse could be a marker for other adversities. “Ultimately, greater understanding of pathways between early life abuse and adult weight status may inform obesity prevention and treatment approaches.” Boynton-Jarrett cautioned that further studies are needed to clarify just which factors are responsible for the association of abuse with obesity and noted there is a consensus that pediatric providers should screen for abuse.

Source: Science Daily

ScienceDaily (June 25, 2012) — Researchers have discovered how a hormone in the gut slows the rate at which the stomach empties and thus suppresses hunger and food intake. Results of the animal study were presented June 25 at The Endocrine Society’s 94th Annual Meeting in Houston.

"The gut hormone glucagon-like peptide 2, or GLP-2, functions as a neurotransmitter and fine-tunes gastric emptying through — as suspected — its receptor action in the brain," said the lead investigator, Xinfu Guan, PhD, assistant professor of pediatrics and medicine at Baylor College of Medicine in Houston.

The researchers found that this action occurs in the GLP-2 receptor specifically in a key group of nerve cells in the brain, called pro-opiomelanocortin, or POMC, neurons. These neurons are in the hypothalamus, the part of the brain that produces appetite-controlling neuropeptides.

In their study using molecular methods, mice lacking this GLP-2 receptor in the POMC neurons showed late-onset obesity and higher food intake compared with normal wild-type mice. The mutant, or GLP-2 receptor “knockout,” mice also had accelerated gastric emptying after a liquid meal, as found on a noninvasive breath test. The faster the gastric emptying, the higher the food intake, scientists know.

Therefore, obese people may have something wrong with this hormone receptor, which alters their gastric emptying rate, Guan speculated. Many studies have shown that nondiabetic, obese humans have accelerated gastric emptying.

The researchers also found that this receptor quickly activated the PI3K intracellular signaling pathway in the POMC neurons. This, in turn, induces neuronal excitation (transmission of signals) and gene expression, according to Guan.

These findings, Guan said, show that in the central nervous system the GLP-2 receptor plays an important physiological role in the control of food intake and gastric emptying.

"This study has advanced our understanding of the brain-gut neural circuits that mediate eating behavior via modulating gastric emptying, which contributes to the control of body weight," he said.

Source: Science Daily

ScienceDaily (June 14, 2012) — An international team of researchers’ study of the spatial patterns of the spread of obesity suggests America’s bulging waistlines may have more to do with collective behavior than genetics or individual choices. The team, led by City College of New York physicist Hernán Makse, found correlations between the epidemic’s geography and food marketing and distribution patterns.

Supermarket. Physicists found correlations between the obesity epidemic’s geography and food marketing and distribution patterns. (Credit: © flashpics / Fotolia)

"We found there is a relationship between the prevalence of obesity and the growth of the supermarket economy," Professor Makse said. "While we can’t claim causality because we don’t know whether obesity is driven by market forces or vice versa, the obesity epidemic can’t be solved by focus on individual behavior."

The teams findings, published online this week in Scientific Reports, come as a policymakers are starting to address the role of environmental factors in obesity. For example, in New York Mayor Michael Bloomberg wants to limit serving sizes of soda sweetened with sugar to 16 ounces as a way to combat obesity.

The World Health Organization considers obesity a global epidemic similar to cancer or diabetes. It is a non-communicable disease for which no prevention strategy has been able to contain the spread.

Because obesity is related to increased calorie intake and physical inactivity, prevention has focused on changing individuals’ behaviors. However, prevalence of non-communicable diseases shows spatial clustering, and the spread of obesity has shown “high susceptibility to social pressure and global economic drivers.”

Professor Makse and his colleagues hypothesized that these earlier findings suggest collective behavior plays a more significant role in the spread of the epidemic than individual factors such as genetics and lifestyle choices. To study collective behavior’s role, they implemented a statistical clustering analysis based on the physics on the critical phenomena.

Using county-level microdata provided by the U.S. Centers for Disease Control Behavior Risk Factor Surveillance Systems for 2004 through 2008, they investigated spatial correlations for specific years. Over that time span, the pattern of the spreading of the epidemic, which has Greene County, Ala., as its epicenter, has shown that two clusters spanning distances of 1,000 kilometers have emerged; one along the Appalachian Mountains, the second in the lower Mississippi River valley.

The spatial map of obesity prevalence in the United States shows that neighboring areas tend to have similar percentages of their populations considered obese, i.e. have a body mass index greater than or equal to 30. Such areas are considered obesity clusters, and their spread can be seen in the maps from 2004 to 2008.

To assess the properties of these spatial arrangements, the researchers calculated an equal-time, two-point correlation function that measured the influence of a set of characteristics in one county on another county at a given distance. The characteristics studied were population density, prevalence of adult obesity and diabetes, cancer mortality rates and economic activity.

The researchers said the form of the correlations in obesity were reminiscent of those in physical systems at a critical point of second-order phase transition. Such systems are uncorrelated and characterized by short-range vanishing fluctuations when they are not at a critical stage.

However, at critical points long-range correlations appear, and these may signal the emergence of strong critical fluctuations in the spreading of obesity and diabetes. Consequently, they concluded the clustering patterns found in obesity were the result of “collective behavior, which may not merely be the consequence of fluctuations in individual habits.”

Professor Makse and his colleagues believe the correlations of fluctuations in the prevalence of obesity may be linked to demographic and economic variables. To test this hypothesis, they compared the spatial characteristics of industries associated with food production and sales, e.g. supermarkets, food and beverage stores, restaurants and bars, to other sectors of the economy.

Their analysis of spatial fluctuations in food economic activity gave rise to the same anomalous values as obesity and diabetes. Areas with above-average concentrations of food-related businesses had high-than-normal prevalence of obesity and diabetes.

In future studies, Professor Makse plans to apply physics concepts to measure the spread of cancer and diabetes. “The basic idea is that if a non-communicable disease is spreading like a virus, then environmental factors have to be at work,” he said. “If only genetics determined obesity, we wouldn’t have seen the correlations.”

Source: Science Daily

ScienceDaily (June 13, 2012) — Wake up, America, and lose some weight — it’s keeping you tired and prone to accidents. Three studies being presented June 13 at sleep 2012 conclude that obesity and depression are the two main culprits making us excessively sleepy while awake.

Researchers at Penn State examined a random population sample of 1,741 adults and determined that obesity and emotional stress are the main causes of the current “epidemic” of sleepiness and fatigue plaguing the country. Insufficient sleep and obstructive sleep apnea also play a role; both have been linked to high blood pressure, heart disease, stroke, depression, diabetes, obesity and accidents.

"The ‘epidemic’ of sleepiness parallels an ‘epidemic’ of obesity and psychosocial stress," said Alexandros Vgontzas, MD, the principal investigator for the three studies. "Weight loss, depression and sleep disorders should be our priorities in terms of preventing the medical complications and public safety hazards associated with this excessive sleepiness."

In the Penn State cohort study, 222 adults reporting excessive daytime sleepiness (EDS) were followed up 7½ years later. For those whose EDS persisted, weight gain was the strongest predicting factor. “In fact, our results showed that in individuals who lost weight, excessive sleepiness improved,” Vgontzas said.

Adults from that same cohort who developed EDS within the 7½-year span also were studied. The results show for the first time that depression and obesity are the strongest risk factors for new-onset excessive sleepiness. The third study, of a group of 103 research volunteers, determined once again that depression and obesity were the best predictors for EDS.

"The primary finding connecting our three studies are that depression and obesity are the main risk factors for both new-onset and persistent excessive sleepiness," Vgontzas said.

In the Penn State cohort study, the rate of new-onset excessive sleepiness was 8 percent, and the rate of persistent daytime sleepiness was 38 percent. Like insufficient sleep and obstructive sleep apnea, EDS also is associated with significant health risks and on-the-job accidents.

Source: Science Daily

ScienceDaily (June 7, 2012) — Researchers at Columbia University Medical Center (CUMC) have identified a brain receptor that appears to play a central role in regulating appetite. The findings, published June 7 in the online edition of Cell, could lead to new drugs for preventing or treating obesity.

"We’ve identified a receptor that is intimately involved in regulating food intake," said study leader Domenico Accili, MD, professor of Medicine at CUMC. "What is especially encouraging is that this receptor is belongs to a class of receptors that turn out to be good targets for drug development, making it a highly ‘druggable’ target. In fact, several existing medications already seem to interact with this receptor. So, it’s possible that we could have new drugs for obesity sooner rather than later."

In their search for new targets for obesity therapies, scientists have focused on the hypothalamus, a tiny brain structure that regulates appetite. Numerous studies suggest that the regulatory mechanism is concentrated in neurons that express a neuropeptide, or brain modulator, called AgRP. But the specific factors that influence AgRP expression are not known.

The CUMC researchers found new clues to appetite control by tracing the actions of insulin and leptin. Both hormones are involved in maintaining the body’s energy balance, and both are known to inhibit AgRP. “Surprisingly, blocking either the insulin or leptin signaling pathway has little effect on appetite,” says Dr. Accili. “We hypothesized that both pathways have to be blocked simultaneously in order to influence feeding behavior.”

To test their hypothesis, the researchers created a strain of mice whose AgRP neurons lack a protein that is integral to both insulin and leptin signaling. As the researchers hypothesized, removing this protein — Fox01 — had a profound effect on the animals’ appetite. “Mice that lack Fox01 ate less and were leaner than normal mice,” said lead author Hongxia Ren, PhD, associate research scientist in Medicine. “In addition, the Fox01-deficient mice had better glucose balance and leptin and insulin sensitivity — all signs of a healthier metabolism.”

Since Fox01 is a poor drug target, the researchers searched for other ways to inhibit the action of this protein. Using gene-expression profiling, they found a gene that is highly expressed in mice with normal AgRP neurons but is effectively silenced in mice with Fox01-deficient neurons. That gene is Gpr17 (for G-protein coupled receptor 17), which produces a cell-surface receptor called Gpr17.

To confirm that the receptor is involved in appetite control, the researchers injected a Gpr17 activator into normal mice, and their appetite increased. Conversely, when the mice were given a Gpr17 inhibitor, their appetite decreased. Similar injections had no effect on Fox01-deficient mice.

According to Dr. Accili, there are several reasons why Gpr17, which is also found in humans, would be a good target for anti-obesity medications. Since Grp17 is part of the so-called G-protein-coupled receptor family, it is highly druggable. About a third of all existing drugs work through G-protein-coupled receptors. In addition, the receptor is abundant in AgRP neurons but not in other neurons, which should limit unwanted drug side effects.

Source: Science Daily

ScienceDaily (May 23, 2012) — Blame it on your genes? Researchers from The Miriam Hospital’s Weight Control and Diabetes Research Center say individuals with variations in certain “obesity genes” tend to eat more meals and snacks, consume more calories per day and often choose the same types of high fat, sugary foods.

Blame it on your genes? Researchers say individuals with variations in certain “obesity genes” tend to eat more meals and snacks and consume more calories per day. (Credit: © Gennadiy Poznyakov / Fotolia)

Their study, published online by the American Journal of Clinical Nutrition and appearing in the June issue, reveals certain variations within the FTO and BDNF genes — which have been previously linked to obesity — may play a role in eating habits that can cause obesity.

The findings suggest it may be possible to minimize genetic risk by changing one’s eating patterns and being vigilant about food choices, in addition to adopting other healthy lifestyle habits, like regular physical activity.

"Understanding how our genes influence obesity is critical in trying to understand the current obesity epidemic, yet it’s important to remember that genetic traits alone do not mean obesity is inevitable," said lead author Jeanne M. McCaffery, Ph.D., of The Miriam Hospital’s Weight Control and Diabetes Research Center.

"Our lifestyle choices are critical when it comes to determining how thin or heavy we are, regardless of your genetic traits," she added. "However, uncovering genetic markers can possibly pinpoint future interventions to control obesity in those who are genetically predisposed."

Previous research has shown individuals who carry a variant of the fast mass and obesity-associated gene FTO and BDNF (or brain-derived neurotrophic factor gene) are at increased risk for obesity. The genes have also been linked with overeating in children and this is one of the first studies to extend this finding to adults. Both FTO and BDNF are expressed in the part of the brain that controls eating and appetite, although the mechanisms by which these gene variations influence obesity is still unknown.

As part of the Look AHEAD (Action in Health and Diabetes) trial, more than 2,000 participants completed a questionnaire about their eating habits over the past six months and also underwent geneotyping. Researchers focused on nearly a dozen genes that have been previously associated with obesity. They then examined whether these genetic markers influenced the pattern or content of the participants’ diet.

Variations in the FTO gene specifically were significantly associated with a greater number of meals and snacks per day, greater percentage of energy from fat and more servings of fats, oils and sweets. The findings are largely consistent with previous research in children.

Researchers also discovered that individuals with BDNF variations consumed more servings from the dairy and the meat, eggs, nuts and beans food groups. They also consumed approximately 100 more calories per day, which McCaffery notes could have a substantial influence on one’s weight.

"We show that at least some of the genetic influence on obesity may occur through patterns of dietary intake," she said. "The good news is that eating habits can be modified, so we may be able to reduce one’s genetic risk for obesity by changing these eating patterns."

McCaffery says that while this research greatly expands their knowledge on how genetics may influence obesity, the data must be replicated before the findings can be translated into possible clinical measures.

Source: Science Daily

May 14, 2012

Why does one person become anorexic and another obese? A study recently published by a University of Colorado School of Medicine researcher shows that reward circuits in the brain are sensitized in anorexic women and desensitized in obese women. The findings also suggest that eating behavior is related to brain dopamine pathways involved in addictions.

Guido Frank, MD, assistant professor director of the Developmental Brain Research Program at the CU School of Medicine and his colleagues used functional magnetic resonance imaging (fMRI) to examine brain activity in 63 women who were either anorexic or obese. Scientists compared them to women considered “normal” weight. The participants were visually conditioned to associate certain shapes with either a sweet or a non-sweet solution and then received the taste solutions expectedly or unexpectedly. This task has been associated with brain dopamine function in the past.

The authors found that during these fMRI sessions, an unexpected sweet-tasting solution resulted in increased neural activation of reward systems in the anorexic patients and diminished activation in obese individuals. In rodents, food restriction and weight loss have been associated with greater dopamine-related reward responses in the brain.

"It is clear that in humans the brain’s reward system helps to regulate food intake" said Frank. "The specific role of these networks in eating disorders such as anorexia nervosa and, conversely, obesity, remains unclear.”

Scientists agree that more research is needed in this area. The study was published in Neuropsychopharmacology.

Provided by University of Colorado Denver

Source: medicalxpress.com

April 3, 2012

The brains of people with anorexia and obesity are wired differently, according to new research. Neuroscientists for the first time have found that how our brains respond to food differs across a spectrum of eating behaviors – from extreme overeating to food deprivation. This study is one of several new approaches to help better understand and ultimately treat eating disorders and obesity.

Eating disorders have the highest mortality rate of any mental illness. And more than two-thirds of the U.S. population are overweight or obese – a health factor associated with cardiovascular issues, diabetes, and cancer. “This body of work not only increases our understanding of the relationship between food and brain function but can also inform weight loss programs,” says Laura Martin of Hoglund Brain Imaging Center at the University of Kansas Medical Center, one of several researchers whose work being presented today at a meeting of cognitive neuroscientists in Chicago.

"One of the most intriguing aspects of these studies of the brain on food," Martin says, is that they show "consistent activations of reward areas of the brain that are also implicated in studies of addiction." However, how those reward areas respond to food differs between people depending on their eating behaviors, according to the new brain imaging study by Laura Holsen of Harvard Medical School and Brigham and Women’s Hospital and colleagues.

Holsen’s team conducted fMRI brain scans of individuals with one of three eating conditions – anorexia nervosa, simple obesity, and Prader-Willi syndrome (extreme obesity) – as well as healthy control subjects. When hungry, those with anorexia, who severely restrict their food intake, showed substantially decreased responses to various pictures of food in regions of their brains associated with reward and pleasure. For those who chronically overeat, there were significantly increased responses in those same brain regions.

"Our findings provide evidence of an overall continuum relating food intake behavior and weight outcomes to food reward circuitry activity," Holsen says. Her work also has implications, she says, for everyday eating decisions in healthy individuals. "Even in individuals who do not have eating disorders, there are areas of the brain that assist in evaluating the reward value of different foods, which in turn plays a role in the decisions we make about which foods to eat."

Kyle Simmons of the Laureate Institute studies the neural mechanisms that govern such everyday eating decisions. His work with fMRI scans has found that as soon as people see food, their brains automatically gather information about how they think it will taste and how that will make them feel. The brain scans showed an apparent overlap in the region on the insula that responds to seeing food pictures and the region of the insula that processes taste, the “primary gustatory cortex.”

Simmons is currently expanding this work to better understand the differences in taste preferences between lean, healthy individuals and obese ones. “We simply don’t know yet if differences exist between lean and obese participants,” he says. “And knowing which brain regions underlie inferences about food taste and reward is critical if we are going to develop efficacious interventions for obesity and certain eating disorders, both of which are associated with enormous personal and public health costs.”

Provided by Cognitive Neuroscience Society

Source: medicalxpress.com