Thoughts drive dieting plans but feelings drive dieting behavior
May 5, 2015
Science Daily/University at Buffalo
Dieting is a process that involves a plan to change eating behavior and behaving according to that plan. But the factors that guide diet planning differ from those that guide actual diet behavior, according to the results of a new study.
Yet 60 percent of American adults are clinically overweight or obese and more than 16 percent of deaths nationwide are related to diet and physical activity.
"There is clearly a disconnect if we have a majority of the population that has tried to lose weight and a majority of the population that is overweight," says Marc Kiviniemi, a public health researcher at the University at Buffalo. "People are planning to diet and trying to diet, but that's not translating into a successful weight loss effort."
Many issues, from biological to environmental, determine effective weight control, but how people manage their own behavior is a big piece of that puzzle.
Dieting is a process that involves a plan to change eating behavior and behaving according to that plan. But the factors that guide diet planning differ from those that guide actual diet behavior, according to the results of Kiviniemi's new study with Carolyn Brown-Kramer of the University of Nebraska-Lincoln published this month in the Journal of Health Psychology.
"The crux of the disconnect is the divide between thoughts and feelings. Planning is important, but feelings matter, and focusing on feelings and understanding their role can be a great benefit," says Kiviniemi, associate professor of community health and health behavior in the UB School of Public Health and Health Professions.
Plans to change behavior are a function of thoughts, the belief that weight loss is possible by making better food choices. But when it comes to making a food choice and decidingto execute the plan, feelings guide behavior.
"If you're sitting back conceiving a plan you may think rationally about the benefits of eating healthier foods, but when you're in the moment, making a decision, engaging in a behavior, it's the feelings associated with that behavior that may lead you to make different decisions from those you planned to make."
The findings highlight the shortcomings of deprivation diets or diets based on food choices that ignore people's preferences.
"First of all, the deprivation experience is miserable. If you didn't associate negative feelings with it to start, you will after a few days," says Kiviniemi. "The other thing that's important is the distinction between things that require effort and things that are automatic.
"Planning is an effort that demands mental energy, but feelings happen automatically. Deprivation or anything that demands a high degree of self-control is a cognitive process. If you put yourself in a position to use that energy every time you make a food choice that energy is only going to last so long."
Kiviniemi says dieters should seriously consider enjoyment when framing and shaping a behavior change.
"In the dietary domain, eating more fruits and vegetables is fabulous advice. But if you have negative feelings about those food choices, they might not represent elements of a good plan," says Kiviniemi. "It's not just about eating healthy foods. It's about eating the healthy foods you like the most."
It's not easy, and a lot of work is required to move intention to action, which is why Kiviniemi says planning should be broadly based on both thoughts and feelings.
"Think seriously about how you're going to implement the plans you make to change your behavior, and that includes not only the feeling component, but how you plan to overcome a negative reaction that might surface during a diet."
It's not just the knowledge of what we're eating, but consideration of how we'll feel having decided to eat those foods, he says.
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2015/05/150505161617.htm
Late-night snacking: Is it your brain's fault?
May 5, 2015
Science Daily/Brigham Young University
New light has been shed on why you, your friends, neighbors and most everyone you know tend to snack at night: some areas of the brain don't get the same 'food high' in the evening. The study also reports that participants were subjectively more preoccupied with food at night even though their hunger and "fullness" levels were similar to other times of the day.
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Researchers at BYU have shed new light on why you, your friends, neighbors and most everyone you know tend to snack at night: some areas of the brain don't get the same "food high" in the evening.
In a newly published study, exercise sciences professors and a neuroscientist at BYU used MRI to measure how people's brains respond to high- and low-calorie food images at different times of the day. The results showed that images of food, especially high-calorie food, can generate spikes in brain activity, but those neural responses are lower in the evening.
"You might over-consume at night because food is not as rewarding, at least visually at that time of day," said lead author Travis Masterson. "It may not be as satisfying to eat at night so you eat more to try to get satisfied."
The study, which appears in academic journal Brain Imaging and Behavior, also reports that participants were subjectively more preoccupied with food at night even though their hunger and "fullness" levels were similar to other times of the day.
Masterson, who carried out the research for his master's thesis under faculty advisor James LeCheminant, said the intent was to better understand if time of day influences neural responses to pictures of food.
The researchers teamed up with BYU neuroscientist Brock Kirwan to use functional MRI to monitor the brain activity of study subjects while they viewed images of food. The participants viewed 360 images during two separate sessions held one week apart--one during morning hours and one during evening hours.
Subjects looked at images of both low-calorie foods (vegetables, fruits, fish, grains) and high-calorie foods (candy, baked goods, ice cream, fast food). As expected, the researchers found greater neural responses to images of high-calorie foods. However, they were surprised to see lower reward-related brain reactivity to the food images in the evening.
"We thought the responses would be greater at night because we tend to over-consume later in the day," said study coauthor Lance Davidson, a professor of exercise sciences. "But just to know that the brain responds differently at different times of day could have implications for eating."
Nevertheless, researchers noted that the study is preliminary and additional work is needed to verify and better understand the findings. The next research steps would be to determine the extent that these neural responses translate into eating behavior and the implications for weight management.
Masterson, who is heading to Penn State University to work on his PhD in the fall, said the study has helped him pay better attention to how food makes him feel both in the morning and the evening. And as for his late-night eating habits?
"I tell myself, this isn't probably as satisfying as it should be," he said. "It helps me avoid snacking too much at night."
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2015/05/150505121418.htm
Obesity, depression have role in excessive daytime sleepiness
May 7, 2015
Science Daily/Penn State Milton S. Hershey Medical Center
Obesity and depression – not only lack of sleep – are underlying causes for regular drowsiness, according to researchers. They say the findings could lead to more personalized sleep medicine for those with excessive daytime sleepiness (EDS).
As much as 30 percent of the general population experiences EDS -- daytime drowsiness or sleepiness occurring most of the day that can include irresistible sleep attacks. Feeling overly tired during the day can reduce job productivity and increase errors and absenteeism and may lead to more serious issues like car crashes.
Previous research has associated EDS with obesity, depression and sleep apnea, but the new study is the first to use physiologic sleep data to infer causation and investigate mechanisms. It is also the first observational study of EDS over several years.
The researchers measured self-reporting of EDS at baseline and again an average of 7.5 years later in 1,395 men and women. Study participants completed a comprehensive sleep history and physical examination and were evaluated for one night in a sleep laboratory. The researchers also recorded sleep, physical and mental health problems and substance use and determined whether participants were being treated for physical and mental health conditions.
"Obesity and weight gain predicted who was going to have daytime sleepiness," said Julio Fernandez-Mendoza, assistant professor of psychiatry at the Sleep Research and Treatment Center at Penn State College of Medicine. "Moreover, weight loss predicted who was going to stop experiencing daytime sleepiness, reinforcing the causal relationship."
The association between body mass index and sleepiness was independent of sleep duration, meaning obese people may be tired during the day no matter how much they sleep at night.
Obesity is also associated with sleep apnea, a condition in which breathing pauses occur during sleep. A hallmark of sleep apnea is daytime sleepiness. Although it may seem logical to assume that sleep apnea causes fatigue in obese people, the study refutes this. Researchers published their findings in the journal SLEEP.
"Body weight predicted EDS better than sleep apnea," Fernandez-Mendoza said. "This data is also consistent with studies showing that CPAP (continuous positive airway pressure) machines greatly reduce the number of apneas, or pauses in breathing, that a person with sleep apnea experiences during the night, but don't effectively reduce daytime sleepiness -- probably because CPAP does not help reduce weight."
The primary underlying mechanism that makes obese people feel overly tired is likely low-grade chronic inflammation. Fat cells, particularly from abdominal fat, produce immune compounds called cytokines that promote sleepiness, among other effects.
Depressed individuals in the study also had high incidence of EDS. Physiologic sleep disturbances, including taking longer to fall asleep and waking up in the middle of the night, explained their daytime drowsiness.
"People with depression typically ruminate, they have difficulty shutting their minds off and they are more likely to have elevated stress hormones," Fernandez-Mendoza said. "The mechanism that we believe is playing a role here is hyperarousal, which is simply going to bed and being too alert; in other words, people with depression feel fatigued but do not necessarily fall asleep during the day."
The researchers also found that a minority of people with EDS have a physiologic sleepiness disorder of the central nervous system. They actually sleep longer than average at night, in part because they fall asleep faster than normal.
"Excessive daytime sleepiness has huge implications for public health and policy," Fernandez-Mendoza said. "Fatigue and sleepiness are the most common causes of poor work productivity and fatal car crashes. In our study we were able to causally link obesity and depression -- disorders of epidemic proportions -- with daytime sleepiness through different mechanisms; in fact, we found that individuals who lost weight did not complain of daytime sleepiness anymore."
Taken together, the findings indicate that a one-size-fits-all approach to treating EDS -- most often a prescription for sleeping pills and more sleep -- will fail in the long term.
"In the medical field, there is a widespread belief that if you feel sleepy during the day, it's because you didn't get enough sleep," Fernandez-Mendoza said. "We need to start abandoning this idea. If we continue to believe that the only cause of excessive daytime sleepiness is people sleeping too little, we are missing the vast majority of the population. The main causes of a sleepy society are an obese society, a depressed society and, to some extent, people who have a physiological disorder. By looking at our patients more closely, we can start personalizing sleep medicine."
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2015/05/150507093154.htm
Road traffic noise linked to heightened risk of midriff bulge
May 26, 2015
Science Daily/BMJ
Road traffic noise is linked to a heightened risk of developing a mid-riff bulge, indicates new research.
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Exposure to a combination of road traffic, rail, and aircraft noise may pose the greatest risk of acquiring a spare tire -- otherwise known as central obesity, and thought to be one of the most harmful types of fat deposition around the body -- the findings suggest.
The researchers assessed how much road traffic, rail, and aircraft noise 5075 people living in five suburban and rural areas around Stockholm, Sweden, had been exposed to since 1999.
They did this, by using official figures on road and rail traffic noise levels and flow. This included information on ground surfaces, building heights, speed limits and noise barriers from the five municipalities. And they used national data on aircraft noise from Stockholm's main airport, Arlanda.
All the participants and had been part of the Stockholm Diabetes Prevention Program (1992-8), which aimed to look at risk factors for the development of diabetes and how best to prevent it.
Between 2002 and 2006, when they were aged between 43 and 66, they completed a detailed questionnaire covering lifestyle, current state of health, levels of psychological distress, insomnia and job strain. They were also asked about environmental noise pollution from road traffic, trains, and planes.
And they underwent a medical, which included blood pressure and a test for diabetes, as well as measures of central body fat (waist and hips and the waist:hip ratio), and overall obesity (weight and height to define the body mass index or BMI).
The researchers calculated that well over half (62%, 3127) had been regularly exposed to road traffic noise of at least 45 decibels (dB) while one in 20 had been exposed to similar levels of noise from trains. A further 1108 had been exposed to aircraft noise of more than 45 dB.
In all, just over half (54%, 2726) had been exposed to one source of traffic noise; 15% (740) to two sources; and 2% (90) to all three. Around a third (30%, 1519) had been exposed to levels below 45 dB, which were not considered to be harmful.
The analysis indicated no link between road traffic noise and BMI. But there was an association between road traffic noise and waist size, with a 0.21 cm increase for every additional 5 dB increase in exposure, although this was only significant among women.
Similarly, there was a link to waist:hip ratio, with a change of 0.16 for every 5 dB increase in noise exposure to road traffic; this association was stronger in men.
A larger waist was significantly associated with exposure to any of the three sources of noise, but the link was strongest for aircraft noise; a larger waist:hip ratio was associated with road traffic and aircraft noise only.
There seemed to be a cumulative effect, however: the more sources of noise pollution a person was exposed to at the same time, the greater their risk of central obesity seemed to be.
The heightened risk of a larger waist rose from 25% among those exposed to only one source to almost double for those exposed to all three sources.
The findings were not influenced by socioeconomic factors, lifestyle, or exposure to ambient air pollution from local road traffic. But age was an influential factor, with associations between central obesity and road traffic noise only found for those below the age of 60.
This is an observational study so no definitive conclusions can be drawn about cause and effect, nor were the researchers able to assess levels of residential sound insulation or the location of the participants' bedrooms.
But noise exposure may be an important physiological stressor and bump up the production of the hormone cortisol, high levels of which are thought to have a role in fat deposition around the middle of the body, they suggest.
"This may explain why the effects of noise were mainly seen for markers of central obesity, such as waist circumference and waist-hip ratio, rather than for generalised obesity, measured by BMI," they write.
Traffic noise from any of the three sources may also affect metabolic as well as cardiovascular functions, through sleep disturbance, they suggest, altering appetite control and energy expenditure.
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2015/05/150526085736.htm
The less you sleep, the more you eat
June 1, 2015
Science Daily/SAGE Publications
Factors influencing food intake have, and continue to be, a hotly contested subject. A new paper suggests that disrupted sleep could be one factor contributing to excessive food intake and thus leading to long term chronic health damage in both adults and children.
In a special issue on Food, Diets, and Dieting, the paper explores how a bad night's sleep -- something that affects millions of people worldwide -- can affect eating habits and behaviors. Though it is well-known that a bad night's sleep can affect our ability to perform daily duties, what is less known is how disrupted sleep can influence both our food choices and intake.
"It is well recognized that food intake is implicated in many chronic health issues including obesity, diabetes and heart disease, and diet is often a target of treatment to prevent the onset of these conditions," commented the researchers Alyssa Lundahl and Timothy D Nelson of the University of Nebraska- Lincoln, USA. However, they continued: "understanding the mechanisms linking disrupted sleep patterns to increased food intake is important for informing both prevention and treatment interventions for chronic health conditions."
Food intake is driven by biological, emotional, cognitive and environmental factors. Though diet is important to consider in the treatment for chronic health disorders associated with food intake, a closer look should be given to how sleep affects these factors. Lundahl and Nelson argue that these mechanisms are heavily altered and influenced by sleep patterns. For example, after a bad night's sleep, the hormone controlling appetite is affected, emotional stress is greater, more food is desired to compensate for lack of energy and impulsivity is increased, all of which affect the amount of food that you would consume in a day. They conclude:
"Health psychologists should be mindful of the link between sleep and eating, and sleep should be actively considered in efforts to modify dietary behavior."
Dr David Marks, editor of JHP, stated: "The research stimulated by Lundahl and Nelson has important treatment implications for health conditions often treated with dietary interventions and illustrates the need for research to empirically examine the underlying mechanisms of food intake. It is important for people to be aware the findings of this study so that if they suffering from lack of sleep, they can take greater care to consider the quality and quantity of food that they are consuming."
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2015/06/150601104537.htm
Importance of a balanced diet for mental health
June 8, 2015
Science Daily/Asociación RUVID
The importance of nutrition for maintaining mental health has been highlighted by recent research. The human brain needs an adequate intake of key nutrients, such as polyunsaturated fatty acids Omega-3, essential amino acids, B-group vitamins (B12 and folate), vitamin D and minerals like zinc, magnesium and iron. A balanced and high-quality diet, such as the Mediterranean, provides all of these, the researchers note.
Lecturer of Psychiatry Vicent Balanzá, also a psychiatrist at La Fe University Hospital, participated in the scientific review made by members of the International Society for Nutritional Psychiatry Research (ISNPR) on the importance, research and future of nutritional medicine, as "it has been proven that the quality of diet and the deficiencies in certain essential nutrients are determining factors for physical and mental health."
In fact, nutrition "has become a key factor for the high prevalence and incidence of very frequent mental diseases, such as depression. A balanced diet is as important in psychiatry as it is in other medical specialties such as cardiology or endocrinology," says Balanzá.
ISNPR is a scientific society founded in 2013, the purpose of which is to promote high-quality scientific research on the prevention and treatment of psychiatric disorders by means of nutritional interventions. Balanzá is a member of its executive committee and he claims that in order to supply optimum performance, the human brain "needs an adequate intake of key nutrients, such as polyunsaturated fatty acids Omega-3, essential amino acids, B-group vitamins (B12 and folate), vitamin D and minerals like zinc, magnesium and iron. A balanced and high-quality diet, such as the Mediterranean, provides all of these, but in cases of deficiencies, nutritional supplements are advisable."
A broad approach to Psychiatry
With this publication in 'The Lancet Psychiatry', the world's experts in nutritional psychiatry propose a debate on the growing role of diet in psychiatry and mental health. "At the population level, we had scientific evidence that Mediterranean diet is associated with a lower risk of cardiovascular disease, diabetes and cognitive impairment. Now we also know that it reduces the risk of depression. These are strong arguments to preserve a cultural -and wholesome- treasure that has been transmitted over time," stresses Vicent Balanzá.
Moreover, the aetiology of mental illnesses is extremely complex and, therefore, so is their treatment. "Expecting that anyone with mental health problems would recover only with medicines is a very limited view of reality. In our article we argue that the future of psychiatry requires a broader approach in which nutritional factors are essential in order to provide better health outcomes, functioning and quality of life," concludes the researcher.
Vicent Balanzá Martínez is an adjunct lecturer of Psychiatry at the Faculty of Medicine and Dentistry at the University of Valencia since 2005 and is accredited as a lecturer. Since 2002 he has been working as a psychiatrist in the Mental Health Unit in Catarroja, which he coordinates. He is also researcher at the Centre for Biomedical Research in Mental Health Network (CIBERSAM).
His research lines focus on neurocognitive functioning in schizophrenia and bipolar disorder, as well as on interventions aimed at improving cognitive deficits. More recently, he has been concerned with the staging models in bipolar disorder and with nutritional interventions (nutritional psychiatry). He has published over 50 scientific articles in international journals that have received more than a thousand citations and his Hirsch index is 19.
Balanzá has participated in numerous research projects and national and international conferences on psychiatry. He is part of the board of directors of the International Society for Nutritional Research Psychiatry (ISNPR) and of the working group on staging of the International Society for Bipolar Disorders (ISBD).
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2015/06/150608081759.htm
Nuts and peanuts -- but not peanut butter -- linked to lower mortality rates
June 10, 2015
Science Daily/Oxford University Press (OUP)
A study confirms a link between peanut and nut intake and lower mortality rates, but finds no protective effect for peanut butter. Men and women who eat at least 10 grams of nuts or peanuts per day have a lower risk of dying from several major causes of death than people who don't consume nuts or peanuts.
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The reduction in mortality was strongest for respiratory disease, neurodegenerative disease, and diabetes, followed by cancer and cardiovascular diseases. The effects are equal in men and women. Peanuts show at least as strong reductions in mortality as tree nuts, but peanut butter is not associated with lower mortality, researchers from Maastricht University found.
This study was carried out within the Netherlands Cohort Study, which has been running since 1986 among over 120,000 Dutch 55-69 year old men and women. Nut consumption was assessed by asking about portion size and frequency of intake of peanuts, other nuts (tree nuts), and peanut butter. The researchers from Maastricht University analyzed the relationship with overall and cause-specific mortality since 1986.
The associations between nuts and peanut intake and cardiovascular death confirm earlier results from American and Asian studies that were often focused on cardiovascular diseases. However, in this new study, it was found that mortality due to cancer, diabetes, respiratory, and neurodegenerative diseases was also lowered among users of peanuts and nuts. Project leader and epidemiologist Professor Piet van den Brandt commented: "It was remarkable that substantially lower mortality was already observed at consumption levels of 15 grams of nuts or peanuts on average per day (half a handful). A higher intake was not associated with further reduction in mortality risk. This was also supported by a meta-analysis of previously published studies together with the Netherlands Cohort Study, in which cancer and respiratory mortality showed this same dose-response pattern."
Peanuts and tree nuts both contain various compounds such as monounsaturated and polyunsaturated fatty acids, various vitamins, fiber, antioxidants, and other bioactive compounds, that possibly contribute to the lower death rates. In contrast to peanuts, no association was found between peanut butter intake and mortality risk. However, besides peanuts, peanut butter contains also added components like salt and vegetable oils. In the past, it has been shown that peanut butter contains trans fatty acids and therefore the composition of peanut butter is different from peanuts. The adverse health effects of salt and trans fatty acids could inhibit the protective effects of peanuts.
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2015/06/150610190920.htm
Body fat can send signals to brain, affecting stress response
July 23, 2015
Science Daily/University of Florida
The brain's effect on other parts of the body has been well established. Now, a group of researchers has found that it's a two-way street: Body fat can send a signal that affects the way the brain deals with stress and metabolism.
While the exact nature of those signals remains a mystery, researchers say simply knowing such a pathway exists and learning more about it could help break a vicious cycle: Stress causes a desire to eat more, which can lead to obesity. And too much extra fat can impair the body's ability to send a signal to the brain to shut off the stress response.
The findings are important and unique because they show that it's not simply the brain that drives the way the body responds to stress, said James Herman, Ph.D., a co-author of the paper and a professor in the department of psychiatry and behavioral neuroscience at the University of Cincinnati,.
"It moved our understanding of stress control to include other parts of the body. Before this, everyone thought that the regulation of stress was mainly due to the brain. It's not just in the brain. This study suggests that stress regulation occurs on a much larger scale, including body systems controlling metabolism, such as fat," Herman said.
The findings, which reveal a novel fat-to-brain feedback network, were published in the June edition of the journal Psychoneuroendocrinology by a group that included Annette D. de Kloet, Ph.D., a research assistant professor in the UF College of Medicine's department of physiology and functional genomics, and Eric Krause, Ph.D., an assistant professor in the UF College of Pharmacy's department of pharmacodynamics.
Researchers found that a glucocorticoid receptor in fat tissue can affect the way the brain controls stress and metabolism. Initially, such signals from the receptor can be lifesavers, directing the brain to regulate its energy balance and influencing stress responses in a beneficial way.
"The stress response in the short term is adaptive. It's going to help you cope with stress," Krause said. "The idea that fat is actually talking to the brain to dampen stress is new."
The researchers found that steroid hormones known as glucocorticoids activate their receptors within fat tissue in a way that affects a main component of the metabolic stress response. Using mouse models, they found a unique connection between glucocorticoid signaling in fat tissue and the brain's regulation of energy balance and stress response. Because glucocorticoid signaling is crucial to regulating the hypothalamic-pituitary-adrenal axis, fat tissue can directly affect central nervous system functions that link obesity, metabolic disease and stress-related problems, researchers concluded.
Understanding fat-to-brain signaling is a first step toward someday being able to influence the broad, complex relationship between stress, obesity and metabolism. Herman credited de Kloet for pressing the search for a fat-to-brain signaling network.
Now that researchers have established that a fat-to-brain signaling pathway exists, a fuller understanding of how it functions could someday lead to drugs or other therapies that ward off the negative effects of long-term stress.
"The big question is the nature of that signal to the brain. We need to learn how to go in and break that cycle of stress, eating and weight gain," Herman said.
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2015/07/150723111359.htm
A high fat diet leads to overeating because of faulty brain signaling
Offering low fat foods could help prevent obesity, say researchers
September 21, 2015
Science Daily/Elsevier
Defective signaling in the brain can cause overeating of high fat foods in mice, leading to obesity, according to a new article. The body controls food intake by balancing a need for food to survive with a desire for food for pleasure. By shifting the balance between these systems, defective brain signaling can cause pleasure to take over, resulting in overeating and obesity.
The researchers, from the Neuroscience Program in Substance Abuse (N-PISA) at Vanderbilt University, USA, say understanding the mechanisms behind overeating could help prevent it and reduce the incidence of obesity.
"We have always been struck by how much animals -- and even people -- will over-consume tasty high-fat foods, even though they might be technically feeling full," said Dr. Aurelio Galli, one of the authors of the study. "A high fat diet causes people to eat more, which ultimately impairs the ability of obese people to successfully control their caloric intake, lose weight and maintain weight loss. We have conducted several studies trying to understand why a high fat diet has this effect."
Worldwide, obesity has more than doubled since 1980. Today around two billion people are overweight, and 600 million of these are obese. A number of factors contribute to the obesity epidemic, including economic stresses, changes in the built environment and changing food trends.
Biologically, obesity is the result of defects in the central nervous system that mean the body can't match its energy intake through food with its energy expenditure. The amount we eat is controlled by survival and reward (hedonic eating) the body's metabolism and our pleasure senses, like taste and smell. When specific signals in the brain are impaired, these two systems can fall out of balance, resulting in overeating.
The new study reveals a novel mechanism behind overeating high fat foods for pleasure. A specific signaling pathway in brain cells that control motivation, movement and attention determines the amount of high fat foods consumed. When the signaling is defective, the person only overeats high fat foods.
"We distilled the neurobiological mechanisms involved specifically in overeating for fat," said Dr. Kevin Niswender, one of the authors of the study. "We defined the why, where, and how of 'hedonic' obesity and found that disrupting a specific signaling pathway in the brain can lead to overeating specifically food high in fat."
The researchers studied one particular signaling pathway in the brain -- insulin signaling -- and the way it works in specific brain cell circuits. Defects in insulin signaling can override the body's natural homeostatic mechanisms in favor of the reward mechanisms, leading to obesity.
Rapamycin complex 2 (mTORC2) is a group of proteins involved in insulin signaling in the brain. The researchers wanted to find out how insulin signaling and mTORC2 affect how rewarding high fat foods are. They genetically altered brain cells in mice by taking out a part of mTORC2 and found that the mice without a functioning mTORC2 ate high-fat food excessively. However, when provided only with low-fat food they did not overeat.
Furthermore, they found that the mice whose mTORC2 does not function also had less dopamine in specific regions of the brain. Lower dopamine transmission in brain cells is associated with obesity in humans and animals, and also in escalating substance abuse.
"Our findings reveal a system that is designed to control eating of rewarding foods that are high in fat and possibly sugar," said Dr. Galli. "This system can be hijacked by the very foods that it is designed to control. Eating a high-fat or high-carbohydrate diet feels rewarding, but also appears to cause changes in the brain areas that are involved in controlling eating, by causing for example insulin resistance. Our study shows that when specific signaling in these areas of the brain is disrupted, it leads to a vicious cycle of increasing, escalating high-fat diet intake that likely further cements changes in these brain areas."
The researchers now plan to find out whether the effect of disrupting the signaling system works. They plan to restore mTORC2 signaling in obese mice to see whether it leads to them eating a normal amount of calories.
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2015/09/150921090147.htm
More obesity among the less educated in rich countries
September 30, 2015
Science Daily/Norwegian Institute of Public Health
In rich countries, obesity is more common among the lower educated, whilst in poor countries, obesity is more common among the higher educated, confirms new research. Previous studies have shown that the number of people with obesity increases with the gross domestic product (GDP) of a country. Previous research has also indicated that education can be an important factor in this context. The aim of this new study was to explore the assumption from previous studies that obesity is linked to GDP and education, and to include new data from several different countries.
Previous studies have shown that the number of people with obesity increases with the gross domestic product (GDP) of a country. Previous research has also indicated that education can be an important factor in this context. The aim of this new study was to explore the assumption from previous studies that obesity is linked to GDP and education, and to include new data from several different countries.
The researchers have included more extensive and up-to-date data than what has been done in previous studies. In total, data from 70 countries was included. Previous research as focused mostly on low -- and medium-cost countries. The present study also included a number of high-cost countries.
Relationship between education, obesity and GDP
The results from this study confirm that there is an association between obesity, education and GDP. The prevalence of obesity increases with rising GDP, but only among individuals with lower levels of education. There is no significant increase in obesity among those with higher education.
This means that:
• In countries with low GDP there is more obesity among those with high education.
• In countries with high GDP there is more obesity among those with low education.
The study also found that the relationship was somewhat more marked among women than among men.
Possible explanations
"When countries become richer, changes in living conditions occur that predominantly affect the weight of those with low education," says lead author Jonas Minet Kinge.
Kinge is a researcher at the Norwegian Institute of Public Health and also Associate Professor at the Department of Health Management and Health Economics at the University of Oslo.
"For example, earlier literature suggests that low education in poorer countries is associated with limited resources available for excess food consumption, and more physically demanding work. These conditions limit obesity among those with low education in developing countries," says Kinge.
"In rich countries with economies based largely on service and technology industries, most people can afford calorie-rich foods and there are, overall, fewer jobs with physically demanding work. This boosts the prevalence of obesity among those with lower education in high GDP countries," explains Kinge.
The reason why the association was found to be more pronounced in women than in men is less clear. The study did not test whether the differences between the sexes are significant. But it may be that women and men often have different educational backgrounds and professions, and that they experience different norms and ideals from their society.
About the study
The researchers collected data about individuals' education, age, gender, height and weight from 70 different countries. They used different statistical methods to analyze the association between obesity and GPD by education.
A major strength of this study is that it included many countries and that it has used both absolute and relative educational categories.
It is important to emphasize that the study has not studied causality. The researchers cannot determine, for example, whether it is education and GDP that affect obesity or vice versa. Neither can they rule out that the results are influenced by other factors not included in the study. Another limitation of the study is that it used self-reported height and weight, which is not optimal.
Nevertheless, Kinge believes the results from this study may be useful for health promotion work, emphasizing the interplay between social and economic factors and obesity. Perhaps especially in developing countries, health promotion efforts should take these factors into consideration.
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2015/09/150930074433.htm
Short sleep linked to distracted secondary eating, drinking
December 11, 2015
Science Daily/University of Alabama at Birmingham
Research suggests a link between short sleep and obesity from secondary eating and drinking while engaged in another activity. Investigators assessed time spent on secondary eating and drinking as well as primary eating and drinking, with sleep duration as the principal independent variable.
Gabriel S. Tajeu, DrPH, a postdoctoral fellow in UAB's Department of Epidemiology, in collaboration with Bisakha Sen, Ph.D., professor in the Department of Health Care Organization and Policy, found "short sleep is associated with more time spent in secondary eating and, in particular, secondary drinking. This potentially suggests a pathway from short sleep to increased caloric intake in the form of beverages and distracted eating and thus potential increased obesity risk, although more research is needed."
"The association between short sleep and obesity risk is well-established," Tajeu said. "However, we are looking at whether short sleep is linked to more time spent in secondary eating or drinking, that is, eating or drinking beverages other than water -- such as sugar-sweetened beverages -- while primarily engaged in another activity, such as television watching."
Using data from 28,150 American adults (55.8 percent female) ranging in ages from 21 to 65 who participated in the American Time Use Survey between 2006 and 2008, the investigators assessed time spent on secondary eating and drinking as well as primary eating and drinking, with sleep duration as the principal independent variable.
The authors estimated multivariable regression models, an analysis technique that uses multiple variables including participants' demographic characteristics like race and gender, socioeconomic characteristics. and weekday versus weekend participation in ATUS, in order to determine the association of short sleep and eating and drinking behaviors. Compared with participants reporting having experienced normal sleep -- between seven and eight hours -- those reporting short sleep engaged in secondary eating an additional 8.7 minutes a day as well as an additional 28.6 and 31.28 minutes daily of secondary drinking on weekdays and weekends, respectively.
"New Pathways From Short Sleep to Obesity? Associations Between Short Sleep and 'Secondary' Eating and Drinking Behavior" was published online in November in the American Journal of Health Promotion.
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2015/12/151211154105.htm
Weight loss through diet changes can improve sleep at any body weight
December 16, 2015
Science Daily/Perelman School of Medicine at the University of Pennsylvania
Weight loss due to dietary changes can improve sleepiness at any weight, according to a new. The findings offer new insights into how weight fluctuations impact numerous aspects of sleep independent of body weight.
Previous studies have linked obesity with persistent sleepiness, lack of energy during the day, and poor sleep quality, all of which can be successfully combatted with weight loss treatment. But until now, researchers have known little about the link between excessive weight, poor dietary habits, and sleep/wake abnormalities.
Nearly 185 million adults and 24 million children in the United States are overweight or obese. In Philadelphia, an estimated 68 percent of adults are overweight or obese. Beyond impaired cognitive function, poor sleep is associated with a host of chronic health problems including depression, obesity, and hypertension. Additionally, the Centers for Disease Control and Prevention estimates that 50 to 70 million U.S. adults experience sleep or wakefulness disorders.
In the current research, obesity was studied using diet-induced obese mice. Half the mice were randomly chosen to receive regular chow (RC) while the other mice were fed a high-fat diet (HFD, more than three times higher in fat content) for eight weeks. At the end of that period, some of the mice were switched to the alternative diet for one week, causing newly-fed HFD mice to gain weight and newly-fed RC mice to lose weight, while the rest of the mice continued to consume their current diet.
After the ninth week, mice maintained on HFD weighed 30 percent more, slept more than one hour longer per day, and suffered from increased wake fragmentation (frequently slipping into sleep) compared to mice maintained on RC. The "diet switch" groups, however, had similar body weight at week nine, but completely different sleep/wake profiles when compared to each other.
"Our findings suggest body weight is a less important factor than changes in weight for regulating sleepiness," said the study's lead author, Isaac Perron, a PhD student in Neuroscience at the University of Pennsylvania. "Diet-induced obese mice that ate a regular chow diet for only one week showed the same sleep/wake profile as mice that ate a regular chow diet for nine weeks."
The findings have implications for the lean population as well, since mice consuming the low-fat diet for eight weeks followed by only one week of HFD had similar sleep as those eating a HFD for nine weeks.
"The diet consumed during the final week was key to driving the sleep effects, independent of the starting body weight," said Perron. "If you're overweight and often feel tired, you may not need to lose all the weight to improve sleep, but rather just beginning to lose that excess weight may improve your sleep abnormalities and wake impairments."
As individuals pursue these dietary changes, they may start to feel more awake during the day and be motivated to live a healthier lifestyle.
"This study has mapped a completely novel food and sleep interaction," said co-author Sigrid Veasey, MD, DABSM, a professor in the division of Sleep Medicine and a member of Penn's Center for Sleep and Circadian Neurobiology. "That changing to a healthier diet can acutely improve alertness and sleep, is extremely important and certainly an interaction to now test in humans."
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2015/12/151216110200.htm
Midnight munchies mangle memory
Eating at the wrong time impairs learning, memory
December 23, 2015
Science Daily/eLife
Modern schedules can lead us to eat around the clock so it is important to understand how this could dull some of the functions of the brain. New research in mice shows that clocks in different regions of the brain start working out of step, altering the brain's physiology.
https://images.sciencedaily.com/2015/12/151223141445_1_540x360.jpg
Eating at times normally reserved for sleep causes a deficiency in the type of learning and memory controlled by the hippocampal area of the brain, according to new research.
Credit: © LoloStock / Fotolia
Eating at times normally reserved for sleep causes a deficiency in the type of learning and memory controlled by the hippocampal area of the brain, according to findings in the journal eLife.
Researchers from the Semel Institute in the David Geffen School of Medicine at University of California, Los Angeles (UCLA) became interested in the cognitive effects of eating at inappropriate hours because it is already known to have an impact on metabolic health, for example leading to a pre-diabetic state.
"We have provided the first evidence that taking regular meals at the wrong time of day has far-reaching effects for learning and memory," says first author Dawn Loh from the UCLA Laboratory of Circadian and Sleep Medicine.
"Since many people find themselves working or playing during times when they'd normally be asleep, it is important to know that this could dull some of the functions of the brain."
The researchers stress that their findings have not been confirmed in humans, but highlight the fact that shift workers have been shown to perform less well on cognitive tests.
The current study shows that some learned behaviours are more affected than others. The team tested the ability of mice to recognise a novel object. Mice regularly fed during their sleep-time were significantly less able to recall the object. Long-term memory was also dramatically reduced, demonstrated during a fear conditioning experiment.
Both long-term memory and the ability to recognise a novel object are governed by the hippocampus. The hippocampus plays an important role in our ability to associate senses and emotional experiences with memory and our ability to organise and store new memories.
During an experience, nerve impulses are activated along specific pathways and, if we repeat the experience, the same pathways increase in strength. However, this effect was reduced when food was made available to mice during a six-hour window in the middle of their normal sleep time instead of a six-hour daytime window when the mice were active.
Some genes involved in both the circadian clock and in learning and memory are regulated by a protein called CREB (cAMP response element-binding protein). When CREB is less active, it decreases memory, and may play a role in the onset of Alzheimer's disease. In the mice fed at the wrong time, the total activity of CREB throughout the hippocampus was significantly reduced, with the strongest effects in the day.
However, the master pacemaker of the circadian system, the suprachiasmatic nucleus located in the hypothalamus, is unaffected. This leads to desynchrony between the clocks in the different brain regions (misalignment), which the authors suggest underlies the memory impairment.
"Modern schedules can lead us to eat around the clock so it is important to understand how the timing of food can impact cogitation" says Professor Christopher Colwell from the Department of Psychiatry and Biobehavioral Sciences at UCLA.
"For the first time, we have shown that simply adjusting the time when food is made available alters the molecular clock in the hippocampus and can alter the cognitive performance of mice."
Eating at the wrong time also disrupted sleep patterns. The inappropriate feeding schedule resulted in the loss of the normal day/night difference in the amount of sleep although the total time spent asleep over 24 hours was not changed. Sleep became fragmented, with the mice catching up on sleep by grabbing more short naps throughout the day and night.
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2015/12/151223141445.htm
Eat less and be happy: Is it possible?
January 7, 2016
Science Daily/Cornell Food & Brand Lab
Small, uncertain incentives stimulate the same reward center of the brain as food, new brain-imaging research reveals. In a new article, the authors offer food for thought on why we overeat and how we can be just as happy not doing it.
According to functional magnetic resonance imaging (fMRI) studies, the brain responds to a small toy, gift card, or lottery ticket in the same way it does to a mouthwatering burger or cheese-slathered pizza.
Martin Reimann, assistant professor of marketing at the Eller College of Management at the University of Arizona, Deborah MacInnis, and Ramona I. Hilliard Professor of Business Administration and professor of marketing at USC Marshall; Antoine Bechara, professor of psychology at USC Dornsife, published their paper -- the culmination of Reimann's doctoral research in psychology at USC --in the Journal of the Association for Consumer Research.
In "Can Smaller Meals Make You Happy? Behavioral, Neurophysiological and Psychological Insights Into Motivating Smaller Portion Choice," the authors offer food for thought on why we overeat and how we can be just as happy not doing it.
"Clearly, eating less is not fun for many people (and may even be a source of short-term unhappiness), as portion size restriction requires discipline and self-control," the authors wrote. "Yet, by combining one shorter-term desire (to eat) with another shorter-term desire (to play) that in combination also address a longer-term desire (to be healthy), different sources of happiness become commensurable."
In a series of experiments, the researchers found that the majority of children and adults chose a half-sized portion paired with a toy or monetary prize over a full-sized portion without a toy or monetary prize. The price of the two options was kept the same.
Great, right? But it gets better. Not only can a small prize motivate the healthier meal choice, but, in fact, the mere prospect of getting it is more motivating than the prize itself. In other words, the researchers found that people were more likely to choose a smaller meal for the chance to win a $10 lottery than to get a guaranteed reward. The premiums in the study were the chance to win $10, $50 or $100.
"The fact that participants were willing to substitute part of a tangible food item for the mere prospect of a relatively small monetary premium is intriguing," said Martin Reimann. "Unlike the Happy Meal, which offers a toy every time, adults were willing to sacrifice calories for a gamble," commented Deborah MacInnis
While participants identified their choices with various foods and incentives, researchers collected neuroimaging data with fMRIs. The results showed that the combination of half-sized portion and nonfood premium activates similar areas of the brain (specifically, the striatum which is associated with reward, desire and motivation) as the full-sized portion alone.
What's more, people were strongly motivated to choose half a burger or pizza even if they were hungry. And they didn't compensate by eating more calories later.
Desirability of the prize also impacts motivation, the researchers found. While uncertain prizes are highly motivating, further research showed that a vague possibility of winning frequent flyer miles (You could win!) was more effective than a probable contest that listed the odds (You have a 1 in 5 chance of winning.).
"One explanation for this finding is that possible premiums may be more emotionally evocative than certainty premiums," said Reimann. "This emotional evocation is clearly present in gambling or sports contexts, where the uncertainty of winning provides added attraction and desirability through emotional 'rushes' and 'thrills.' The possibility of receiving a premium also evokes a state of hope for the premium's receipt -- a state that is in itself psychologically rewarding."
MacInnis, Reimann and Bechara wrote that these findings imply that individuals can reward themselves for eating less food with nonfood items. "This substitution of rewards assists consumers in staying happy and satisfied," they said.
Individuals could also celebrate other achievements, like a job promotion, with something other than food and still be happy.
"Similarly, we recommend that parents could reward and, thus, reinforce their children's achievements with nonfood incentives, even uncertain ones, rather than with food," the authors wrote. "As such, parents lessen the likelihood of linking good behavior to food intake, but instead link good behavior to the receipt of a nonfood incentive and, thus, avoid overeating."
This research suggests a win-win solution for both consumers and firms.
"Restaurants and food manufacturers are, more often than not, interested in selling more food, not less," Antoine Bechara said. "Our research provides a simple but powerful solution to unite these two, seemingly contradictory goals of selling more versus eating less."
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2016/01/160107094422.htm
What you eat can influence how you sleep
Daily intake of fiber, saturated fat and sugar may impact sleep quality
January 14, 2016
Science Daily/American Academy of Sleep Medicine
A new study found that eating less fiber, more saturated fat and more sugar is associated with lighter, less restorative, and more disrupted sleep.
Results show that greater fiber intake predicted more time spent in the stage of deep, slow wave sleep. In contrast, a higher percentage of energy from saturated fat predicted less slow wave sleep. Greater sugar intake also was associated with more arousals from sleep.
"Our main finding was that diet quality influenced sleep quality," said principal investigator Marie-Pierre St-Onge, PhD, assistant professor in the department of medicine and Institute of Human Nutrition at Columbia University Medical Center in New York, N.Y. "It was most surprising that a single day of greater fat intake and lower fiber could influence sleep parameters."
Study results are published in the January issue of the Journal of Clinical Sleep Medicine.
"This study emphasizes the fact that diet and sleep are interwoven in the fabric of a healthy lifestyle," said American Academy of Sleep Medicine President Dr. Nathaniel Watson, who was not involved in the study. "For optimal health it is important to make lifestyle choices that promote healthy sleep, such as eating a nutritious diet and exercising regularly."
The study also found that participants fell asleep faster after eating fixed meals provided by a nutritionist, which were lower in saturated fat and higher in protein than self-selected meals. It took participants an average of 29 minutes to fall asleep after consuming foods and beverages of their choice, but only 17 minutes to fall asleep after eating controlled meals.
"The finding that diet can influence sleep has tremendous health implications, given the increasing recognition of the role of sleep in the development of chronic disorders such as hypertension, diabetes and cardiovascular disease," said St-Onge.
The randomized, crossover study involved 26 adults -- 13 men and 13 women -- who had a normal weight and an average age of 35 years. During 5 nights in a sleep lab, participants spent 9 hours in bed from 10 p.m. to 7 a.m., sleeping for 7 hours and 35 minutes on average per night. Objective sleep data were gathered nightly by polysomnograhy. Sleep data were analyzed from night 3, after 3 days of controlled feeding, and night 5, after one day of ad libitum food intake.
According to the authors, the study suggests that diet-based recommendations might be used to improve sleep in those with poor sleep quality. However, future studies are needed to evaluate this relationship.
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2016/01/160114213443.htm
Brain function differs in obese children
January 25, 2016
Science Daily/Vanderbilt University Medical Center
The brains of children who are obese function differently from those of children of healthy weight, and exhibit an "imbalance" between food-seeking and food-avoiding behaviors, researchers have found. Because of this, mindfulness, a practice used as a therapeutic technique to focus awareness, should be studied as a way to encourage healthy eating and weight loss in children, the new research suggests.
Diet and exercise may not be enough to restore normal weight or prevent overweight children from becoming obese, they conclude. It may be necessary to change their brain function.
In a paper published in the journal Heliyon, the researchers suggest that mindfulness, a practice used as a therapeutic technique to focus awareness, should be studied as a way to encourage healthy eating and weight loss in children.
"Adults, and especially children, are primed towards eating more," said senior author Kevin Niswender, M.D., Ph.D. "This is great from an evolutionary perspective ... but in today's world, full of readily available, highly advertised, energy dense foods, it is putting children at risk of obesity."
"We think mindfulness could recalibrate the imbalance in the brain connections associated with childhood obesity," added co-senior author Ronald Cowan, M.D., Ph.D. "Mindfulness has produced mixed results in adults ... So far there have been few studies showing its effectiveness for weight loss in children."
Childhood obesity in the United States has nearly doubled during the past 30 years, and among adolescents it has tripled. In 2010, a third of U.S. children were considered obese or overweight.
The Vanderbilt study included 38 children, five who were considered obese and six who were overweight. Their eating behaviors were assessed using a questionnaire, and their brain function was assessed using magnetic resonance imaging (MRI).
Three brain regions in adults are potent modulators of eating habits: the nucleus accumbens, associated with reward-motivated behaviors; the frontal pole, associated with impulsivity; and the inferior parietal lobe (IPL), associated with response inhibition, the ability to inhibit or override a response such as overeating.
The researchers used MRI to determine the balance of functional neural connectivity between these eating-related brain regions in children of various weights.
"We wanted to look at the way (their) brains function in more detail so we can better understand what is happening neurologically in children who are overweight and obese," said first author and Vanderbilt graduate student BettyAnn Chodkowski.
They found that as weight increased among children, the connectivity between the inhibition-associated IPL and reward-associated nucleus accumbens decreased, while connectivity between the nucleus accumbens and the impulsivity-associated frontal pole increased.
This suggests that unhealthy eating behaviors and obesity could reflect an imbalance in the functional connectivity of brain areas associated with response inhibition, impulsivity and reward.
The practice of mindfulness can increase response inhibition and decrease impulsivity. Mindfulness has been used to encourage healthy responses to everyday adversities, although few studies have tested its use in the area of healthy eating or weight loss among children.
Among adults, mindfulness has had mixed results when used for weight loss and weight control, which may reflect "the extreme tenaciousness of adult obesity," as well as age-related loss of brain plasticity, the researchers noted.
This supports the importance of early identification of children at risk for obesity, and the need to develop novel methods to treat and prevent it, they concluded.
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2016/01/160125185035.htm
How obesity makes memory go bad
January 26, 2016
Science Daily/University of Alabama at Birmingham
Obesity is associated with epigenetic changes that dysregulate memory-associated genes, and a particular enzyme in brain neurons of the hippocampus appears to be a link between chronic obesity and cognitive decline.
They have found that epigenetic changes dysregulate memory-associated genes, and a particular enzyme in brain neurons of the hippocampus appears to be a link between chronic obesity and cognitive decline. Their work is published in the Jan. 27 issue of Journal of Neuroscience.
Obesity plagues developed nations, and among the numerous negative health outcomes associated with obesity is a memory impairment that is seen in middle-aged and older obese people. The cause of this decline? Experiments with obese rodents have given a clue: altered gene expression in the hippocampus area of the brain. Until now, the reasons gene expression was changed, as well as the mechanism by which obesity leads to pathogenic memory impairment, have not been known.
There was one suspect: epigenetic dysregulation in neurons of the hippocampus. Foundational experiments over the past decade have linked the creation of long-term memories to changes in DNA methylation and hydroxymethylation -- changes caused by epigenetic mechanisms that sit above the level of the genes.
Such lasting molecular changes to DNA appear to play an important role in promoting or suppressing memory formation through their ability to increase or reduce the expression of genes that help brain neurons create new synaptic connections.
UAB researchers have now shown that epigenetic changes are indeed associated with changes in the expression of memory-associated genes within the hippocampus of obese mice, and these epigenetic changes correlate with diminished object location spatial memory in the obese mice. The UAB researchers have also implicated reduced amounts of one particular memory-associated gene product -- SIRT1 -- as the principal pathogenic cause of obesity-induced memory impairment. The hippocampus subregion of the brain is important for consolidation of long-term memory.
Corresponding author J. David Sweatt, Ph.D., first author Frankie D. Heyward, Ph.D., and colleagues in the UAB Department of Neurobiology, Evelyn F. McKnight Brain Institute, write that these data "provide the first evidence that high-fat-diet-induced obesity leads to the time-dependent development of aberrant epigenetic modifications within the hippocampus, as well as corresponding reduction in the expression of various memory-related genes."
Sweatt noted, "We feel this is a very exciting finding that identifies a new linkage between diet, epigenetics and cognitive function, especially in light of the burgeoning obesity epidemic in the U.S. and elsewhere."
This work, they write, "offers a novel working model that may serve as a conceptual basis for the development of therapeutic interventions for obesity-induced memory impairment."
In details about the cause of altered gene expression, the UAB researchers found that:
• Mice with diet-induced obesity at 20 weeks had impaired performance in object location memory tests, and their hippocampus had impaired synaptic plasticity, as measured by long-term potentiation.
• Four memory-associated genes -- Ppargc1a, Ppp1cb, Reln and Sirt1 -- showed significantly decreased gene expression at 23 weeks of diet-induced obesity, as has been seen before, and the latter three had significantly increased DNA methylation in their gene promoter regions. Increased methylation is known to decrease gene expression. Furthermore, the Sirt1 promoter region also had significantly decreased DNA hydroxymethylation. Gene expression increases or decreases as DNA hydroxymethylation increases or decreases.
• Obesity-induced memory impairment develops over time. At just 13 weeks of diet-induced obesity, seven weeks earlier than the experiments above, mice did not have significant object location memory impairment, and at 16 weeks of diet-induced obesity, also seven weeks earlier than above, none of the genes showed significant increases in DNA methylation. Only one gene at 16 weeks -- Ppargc1a -- showed significant decreases in gene expression and DNA hydroxymethylation.
To probe the mechanism by which obesity leads to pathogenic memory impairment, the UAB researchers focused on the gene Sirt1, which makes an enzyme that is active in the neuron during energy expenditure and fat mobilization. This enzyme appears to be depleted and dysfunctional in obesity, and the deletion of the Sirt1 gene in the brain shortly after birth is known to impair memory and the ability to form new neural synapses. These roles for the SIRT1 gene product -- in both high-fat-diet-induced molecular pathology and in memory impairment -- suggest that it might be a link between chronic obesity and cognitive decline.
Heyward, Sweatt and colleagues found that the hippocampus of obese mice had significantly diminished protein expression of SIRT1, and a substrate of the enzyme, acetlylated-p53, was significantly increased, suggesting reduced enzymatic activity. Also, a targeted deletion of Sirt1 in the forebrain region that includes the hippocampus at age 8-12 weeks showed decreased Sirt1 mRNA and protein in the hippocampus, and these mice showed impaired object-location memory when tested two weeks later.
Furthermore, chemical activation of SIRT1 in diet-induced obese mice by feeding them resveratrol showed decreased levels of acetylated-p53, suggesting increased SIRT1 enzymatic activity, and the resveratrol-fed obese mice had a normal object-location memory, as compared with the control obese mice. The resveratrol-fed obese mice did not show an enhanced memory compared with normal mice. This suggests that resveratrol preserved their hippocampus-dependent spatial memory and SIRT1 function in the hippocampus.
Besides Heyward and Sweatt, co-authors of the paper, "Obesity weighs down memory through a mechanism involving the neuroepigenetic dysregulation of Sirt1," are Daniel Gilliam, Mark Coleman, Cristin Gavin, Ph.D., Jing Wang, Ph.D., Garrett Kaas, Ph.D., Richard Trieu, John Lewis and Jerome Moulden, all of the UAB Department of Neurobiology.
Heyward is now a postdoctoral fellow at Harvard Medical School, the Broad Institute and Beth Israel Deaconess Medical Center. While at UAB, Heyward was supported by a UNCF/Merck Graduate Science Research Dissertation Fellowship that helps train and develop African-American biomedical scientists.
About 10 years ago, Sweatt's lab made the seminal discovery that everyday experiences tap into epigenetic mechanisms in subregions of the brain, and the resulting epigenetic changes in DNA are critically important for long-term memory formation and the stable storage of long-term memory. The 2007 Neuron paper "Covalent modification of DNA regulates memory formation," by Courtney Miller, Ph.D., and Sweatt, was the first to show that active regulation of the chemical structure of DNA is involved in learning and experience-driven changes in the brain.
Obesity and cognitive decline
Evidence that suggests a link between the two includes:
• People ages 40-45 who were obese had a 74 percent increased risk of dementia 21 years later, and those who were overweight had a 35 percent greater risk. This study cohort had 10,276 men and women. Whitmer, RA, et al., BMJ 2005.
• A study of 2,223 healthy workers found that a higher body-mass index was associated with lower cognitive scores, after adjustment for age, sex, educational level, blood pressure, diabetes and other co-variables. Also, a higher BMI at baseline was associated with higher cognitive decline at a follow-up five years later. Cournot, M., et al., Neurology 2006.
• Metabolic syndrome in 73 people with an average age of 60 was associated with significant reductions in recall and overall intellectual functioning, compared with age- and education-matched controls. Hassenstab, J.J., et al., Dementia and Geriatric Cognitive Disorders 2010.
• A study of 8,534 twin individuals who were 65 or older showed that being overweight or obese at mid-life, with an average age of 43, was related to later dementia at the older age. Xu, W.L., et al., Neurology 2011.
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2016/01/160126175513.htm
Being overweight linked to poorer memory
February 26, 2016
Science Daily/University of Cambridge
Overweight young adults may have poorer episodic memory -- the ability to recall past events -- than their peers, suggests new research, adding to increasing evidence of a link between memory and overeating. Researchers found an association between high body mass index and poorer performance on a test of episodic memory.
In a preliminary study published in The Quarterly Journal of Experimental Psychology, researchers from the Department of Psychology at Cambridge found an association between high body mass index (BMI) and poorer performance on a test of episodic memory.
Although only a small study, its results support existing findings that excess bodyweight may be associated with changes to the structure and function of the brain and its ability to perform certain cognitive tasks optimally. In particular, obesity has been linked with dysfunction of the hippocampus, an area of the brain involved in memory and learning, and of the frontal lobe, the part of the brain involved in decision making, problem solving and emotions, suggesting that it might also affect memory; however, evidence for memory impairment in obesity is currently limited.
Around 60% of UK adults are overweight or obese: this number is predicted to rise to approximately 70% by 2034. Obesity increases the risk of physical health problems, such as diabetes and heart disease, as well as psychological health problems, such as depression and anxiety.
"Understanding what drives our consumption and how we instinctively regulate our eating behaviour is becoming more and more important given the rise of obesity in society," says Dr Lucy Cheke. "We know that to some extent hunger and satiety are driven by the balance of hormones in our bodies and brains, but psychological factors also play an important role -- we tend to eat more when distracted by television or working, and perhaps to 'comfort eat' when we are sad, for example.
"Increasingly, we're beginning to see that memory -- especially episodic memory, the kind where you mentally relive a past event -- is also important. How vividly we remember a recent meal, for example today's lunch, can make a difference to how hungry we feel and how much we are likely to reach out for that tasty chocolate bar later on."
The researchers tested 50 participants aged 18-35, with body mass indexes (BMIs) ranging from 18 through to 51 -- a BMI of 18-25 is considered healthy, 25-30 overweight, and over 30 obese. The participants took part in a memory test known as the 'Treasure-Hunt Task', where they were asked to hide items around complex scenes (for example, a desert with palm trees) across two 'days'. They were then asked to remember which items they had hidden, where they had hidden them, and when they were hidden. Overall, the team found an association between higher BMI and poorer performance on the tasks.
The researchers say that the results could suggest that the structural and functional changes in the brain previously found in those with higher BMI may be accompanied by a reduced ability to form and/or retrieve episodic memories. As the effect was shown in young adults, it adds to growing evidence that the cognitive impairments that accompany obesity may be present early in adult life.
This was a small, preliminary study and so the researchers caution that further research will be necessary to establish whether the results of this study can be generalised to overweight individuals in general, and to episodic memory in everyday life rather than in experimental conditions.
"We're not saying that overweight people are necessarily more forgetful," cautions Dr Cheke, "but if these results are generalizable to memory in everyday life, then it could be that overweight people are less able to vividly relive details of past events -- such as their past meals. Research on the role of memory in eating suggests that this might impair their ability to use memory to help regulate consumption.
"In other words, it is possible that becoming overweight may make it harder to keep track of what and how much you have eaten, potentially making you more likely to overeat."
Dr Cheke believes that this work is an important step in understanding the role of psychological factors in obesity. "The possibility that there may be episodic memory deficits in overweight individuals is of concern, especially given the growing evidence that episodic memory may have a considerable influence on feeding behaviour and appetite regulation," she says.
Co-author Dr Jon Simons adds: "By recognising and addressing these psychological factors head-on, not only can we come to understand obesity better, but we may enable the creation of interventions that can make a real difference to health and wellbeing."
Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/02/160226133801.htm
Sleep loss boosts hunger, unhealthy food choices
February 29, 2016
Science Daily/University of Chicago Medical Center
Cutting back on sleep boosts levels of a chemical signal that can enhance the pleasure of eating snack foods and increase caloric intake, report investigators. It may be part of a mechanism that encourages overeating, leading to weight gain, they say.
Skimping on sleep has long been associated with overeating, poor food choices and weight gain. Now a new study shows how sleep loss initiates this process, amplifying and extending blood levels of a chemical signal that enhances the joy of eating, particularly the guilty pleasures gained from sweet or salty, high-fat snack foods.
The findings were published Feb. 29, 2016, in the journal SLEEP.
Sleep-deprived participants in this study -- all young, healthy volunteers -- were unable to resist what the researchers called "highly palatable, rewarding snacks," meaning cookies, candy and chips, even though they had consumed a meal that supplied 90 percent of their daily caloric needs two hours before. The effects of sleep loss on appetite were most powerful in the late afternoon and early evening, times when snacking has been linked to weight gain.
"We found that sleep restriction boosts a signal that may increase the hedonic aspect of food intake, the pleasure and satisfaction gained from eating," said Erin Hanlon, PhD, a research associate in endocrinology, diabetes and metabolism at the University of Chicago. "Sleep restriction seems to augment the endocannabinoid system, the same system targeted by the active ingredient of marijuana, to enhance the desire for food intake."
This chemical signal is the endocannabinoid 2-arachidonoylglycerol (2-AG). Blood levels of 2-AG are typically low overnight. They slowly rise during the day, peaking in the early afternoon.
When the study subjects were sleep-deprived, however, endocannabinoid levels rose higher and remained elevated through the evening, beyond the typical 12:30 p.m. peak. During that period, sleep-restricted study subjects reported higher scores for hunger and stronger desire to eat. When given access to snacks, they ate nearly twice as much fat as when they had slept for eight hours.
This increase in circulating endocannabinoid levels, the authors note, "could be a mechanism by which recurrent sleep restriction results in excessive food intake, particularly in the form of snacks, despite minimal increases in energy need."
"The energy costs of staying awake a few extra hours seem to be modest," explained Hanlon. "One study has reported that each added hour of wakefulness uses about 17 extra calories. That adds up to about 70 calories for the four hours of lost sleep. But, given the opportunity, the subjects in this study more than made up for it by bingeing on snacks, taking in more than 300 extra calories. Over time, that can cause significant weight gain."
Obesity and sleep restriction have become extremely common. According to the Centers for Disease Control and Prevention, about a third of Americans get less than seven hours of sleep a night and more than a third of adults in the United States are obese. A 2013 Gallup poll found that U.S. adults sleep an average of 6.8 hours per night. Forty percent of adults report sleeping six hours or less.
Hanlon and colleagues designed the study to help understand how the endocannabinoid system connected short sleep with weight gain. Her team recruited 14 healthy men and women in their 20s as volunteers. The researchers monitored the subjects' hunger and eating habits in two situations: one four-day stay in the University's Clinical Research Center during which they spent 8.5 hours in bed each night (averaging 7.5 hours of sleep), and another four-day stay when they spent only 4.5 hours in bed (4.2 hours asleep).
The participants ate identical meals three times a day, at 9 a.m., 2 p.m., and 7 p.m. Researchers measured levels of the hormone ghrelin, which boosts appetite, and leptin, which signals fullness, in their blood. Previous studies have linked high ghrelin and low leptin levels to reduced sleep time and increased appetite.
For the first time, however, they also measured blood levels of endocannabinoids. After a normal night's sleep, 2-AG levels were low in the morning. They peaked in the early afternoon, soon after lunchtime, then decreased.
After restricted sleep, however, 2-AG levels rose to levels about 33 percent higher than those seen after normal sleep. They also peaked about 90 minutes later, at 2 p.m., and remained elevated until about 9 p.m.
After the period of restricted sleep, study subjects reported a significant increase in hunger levels. This was prominent soon after their second meal of the day, the time when 2-AG levels were highest. Sleep deprived study subjects expressed greater desire to eat. When asked, they estimated that they could eat much more than they predicted the day after a full night's sleep.
After the fourth night of restricted sleep, subjects were offered an array of snack foods. Despite having eaten a large meal less than two hours before being offered snacks, subjects in the restricted sleep phase of the study had trouble limiting their snack consumption. They chose foods that provided 50 percent more calories, including twice the amount of fat, as when they were completing the normal sleep phase.
These results support "the novel insight that sleep restriction leads not only to increased caloric intake," but also to "changes in the hedonic aspects of food consumption," wrote Frank Scheer, PhD, of the Medical Chronobiology Program at Harvard University's Brigham and Women's Hospital, in a commentary. The increase in 2-AG following sleep restriction, he added, "may be part of the mechanism by which people overeat."
Despite the study's limitations -- small size, short duration, limited sampling frequency -- the findings are clearly significant and consistent with the epidemiologic evidence, the authors note. They are also "relevant to normal life conditions."
This tells us that "if you have a Snickers bar, and you've had enough sleep, you can control your natural response," Hanlon explained. "But if you're sleep deprived, your hedonic drive for certain foods gets stronger, and your ability to resist them may be impaired. So you are more likely to eat it. Do that again and again, and you pack on the pounds."
Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/02/160229221045.htm
Can mindful eating help lower risk of type 2 diabetes, cardiovascular disease?
New research suggests mindfulness could improve glucose levels, heart health
March 9, 2016
Science Daily/Wiley
Given the high stress levels, extended periods of screen time and regular social outings many Americans experience day-to-day in environments where high-calorie foods are readily available, it can be easy to fall into the habit of mindless eating -- where we're too distracted to pay attention to how much, what and why we're eating.
Given the high stress levels, extended periods of screen time and regular social outings many Americans experience day-to-day in environments where high-calorie foods are readily available, it can be easy to fall into the habit of mindless eating -- where we're too distracted to pay attention to how much, what and why we're eating. Research suggests that practicing mindfulness -- or taking the time to bring awareness to present-moment experiences with an open attitude of curiosity and non-judgment -- can be effective in allowing us to make more thoughtful food choices and recognize when we are hungry, satisfied or full. The latest research in this area led by Jennifer Daubenmier, PhD, Assistant Professor at the Osher Center for Integrative Medicine at the University of California, San Francisco, suggests that the impact of mindful eating could be even greater.
"Whether eating snacks while watching the game or grazing by the dessert tray at the office event, we often find ourselves overeating not because we're hungry, but because the food looks delicious, we're distracted, or we wish to soothe away unpleasant feelings," explains Dr. Daubenmier. "Our study suggests that mindful eating can go further than making healthy food choices and recognizing when we're full; it could improve glucose levels and heart health to a greater extent than behavioral weight-loss programs that do not teach mindful eating."
Dr. Daubenmier and her colleagues evaluated the effects of a mindfulness-based weight-loss intervention on adults with obesity, and although no statistically significant differences in weight loss were found compared to the control group, the mindfulness intervention showed greater improvements in certain cardiometabolic outcomes tied to Type 2 Diabetes and cardiovascular disease up to one year after the intervention ended. The research is published in the March issue of Obesity, the scientific journal of The Obesity Society.
To conduct the study, the researchers randomized nearly 200 adults with obesity to a mindfulness intervention or an active attention control group over a five-and-a-half month period, with a subsequent one-year follow up. Both groups were given identical diet and exercise guidelines. Participants in the mindfulness intervention received added training on mindfulness meditation and how to practice awareness of their thoughts, feelings, and bodily sensations during eating and exercise. At 18 months after the start of the intervention, participants in the mindfulness program lost an estimated 4.3% of body weight on average, which was 3.7 pounds more than those in the control group but not enough to reach statistical significance. Nevertheless, the authors found that the mindfulness program had more positive effects on fasting blood glucose at 18 months and a ratio of triglycerides to HDL-cholesterol levels at 12 months (a difference of -4.1 mg/dL and -0.57, respectively), both of which are linked to Type 2 Diabetes and cardiovascular disease.
"Most behavioral weight-loss interventions do not place as much emphasis on managing mindless eating, and previous studies on the topic have not included attention controls or long term follow-up to better study the contribution of mindfulness components over time," said Deborah Tate, PhD, spokesperson for The Obesity Society. "This research points to some of the potential benefits of enhancing the mindfulness components of behavioral weight loss."
Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/03/160309082810.htm