Obesity and Diet Research

Mindfulness-based therapy may reduce stress in overweight and obese individuals

July 7, 2017

Science Daily/Wiley

In a randomized clinical trial of women who were overweight or obese, mindfulness-based stress reduction (MBSR) increased mindfulness and decreased stress compared with health education. In addition, fasting blood sugar levels decreased within the MBSR group, but not within the health education group.

 

In the study, 86 women were randomized to 8 weeks of MBSR or health education, and they were followed for 16 weeks. While MBSR significantly reduced stress and had beneficial effects on blood sugar levels, there were no significant changes in blood pressure, weight, or insulin resistance.

 

"Our study suggests that MBSR lowers perceived stress and blood sugar in women with overweight or obesity. This research has wider implications regarding the potential role of MBSR in the prevention and treatment of diabetes in patients with obesity," said Dr. Nazia Raja-Khan, lead author of the Obesity study.

https://www.sciencedaily.com/releases/2017/07/170707070447.htm

Early-life pain may lead to obesity risk, especially in females

July 6, 2017

Science Daily/Georgia State University

Inflammatory pain at birth changes how the hippocampus, a part of the brain associated with memory and eating behavior, works later in life, and this pain also causes adult rats to eat more frequently and in larger amounts, according to a study.

 

The study found early-life inflammatory pain increases sucrose intake in adult male and female rats, and it decreases the expression of a protein that is critical for memory, activity-regulated cytoskeleton-associated protein (Arc), in hippocampal neurons following the consumption of a sweetened solution. In addition, the effects of neonatal pain are more pronounced in female rats and can be reduced in all rats by administering morphine at the time early-life pain is experienced.

 

The findings demonstrate for the first time that one brief episode of inflammatory pain on the day of birth has a long-lasting, sex-dependent effect on the intake of food into adulthood. The results are published in the journal Physiology & Behavior.

 

Previous studies have found a connection between memory and overeating. In humans, disrupting the encoding of the memory of a meal, such as by watching television or playing computer games, increases the amount of food consumed at the next meal. On the contrary, recalling and enhancing the memory of a meal decreases the amount of food ingested at a future meal.

 

In this study, the researchers induced neonatal inflammatory pain by injecting an inflammatory agent into a rat pup's paw on the day of birth. Some of the rats received morphine at the time of the inflammatory pain. Then, rats were trained to consume a sucrose solution at a specific time and location daily, and the researchers measured the rats' sucrose intake and sucrose-associated Arc expression in the dorsal hippocampus into adulthood. Sucrose solution was used as the meal because it's pleasant and rewarding to rats, can't be hoarded and overconsumption of sweetened beverages contributes to the development of obesity.

 

The study found male and female rats that experienced pain on the day of birth ate more of the sucrose solution at each meal than rats that didn't experience pain. However, there were differences between the sexes. Female rats that experienced pain consumed more during each meal and also returned to the sucrose feeding tube sooner after each meal. In addition, female rats exposed to pain at birth showed fewer cells expressing the Arc protein when they consumed sucrose.

 

The researchers suggest that female rats are more vulnerable to pain at birth than males, and this could be related to hormone changes during the period around birth. Male rats experience a surge of testosterone during the early postnatal period, which could protect them from some of the adverse effects of neonatal pain. Female rats don't experience a similar hormone change.

 

Rats that received morphine after experiencing early-life pain didn't show the same eating increases as pain-inflicted rats that didn't receive morphine. This suggests changes in eating behavior resulted from the experience of pain.

 

"Our research may have implications for humans because newborn rats are comparable to third-trimester human infants in terms of brain development and can be used as a model for premature human infants born into the neonatal intensive care unit (NICU)," said Dr. Marise Parent, professor of neuroscience and psychology and associate director of the Neuroscience Institute at Georgia State. "Premature infants in the NICU can undergo numerous painful and invasive procedures each day, more than half without pain relievers. Our study suggests that inflammatory pain experienced by infants in the NICU may contribute to the increased food consumption and obesity observed in this population, and that when possible, preventing pain in NICU infants could reduce the increased risk for obesity in this vulnerable population."

https://www.sciencedaily.com/releases/2017/07/170706072742.htm

Smelling your food makes you fat

Mice that lost sense of smell stayed slim on high fat diet, while littermates ballooned in weight

July 5, 2017

Science Daily/University of California - Berkeley

Researchers developed ways to temporarily eliminate the sense of smell in adult mice, and discovered that those mice that lost smell could eat a high-fat diet and stay a normal weight, while littermates that retained the sense of smell ballooned to twice normal weight. Supersmellers gained more weight than did normal mice on the same high-fat diet. Smell-deficient mice burned excess fat instead of storing it, suggesting a link between smell and metabolism.

 

Our sense of smell is key to the enjoyment of food, so it may be no surprise that in experiments at the University of California, Berkeley, obese mice who lost their sense of smell also lost weight.

 

What's weird, however, is that these slimmed-down but smell-deficient mice ate the same amount of fatty food as mice that retained their sense of smell and ballooned to twice their normal weight.

 

In addition, mice with a boosted sense of smell -- super-smellers -- got even fatter on a high-fat diet than did mice with normal smell.

 

The findings suggest that the odor of what we eat may play an important role in how the body deals with calories. If you can't smell your food, you may burn it rather than store it.

 

These results point to a key connection between the olfactory or smell system and regions of the brain that regulate metabolism, in particular the hypothalamus, though the neural circuits are still unknown.

 

"This paper is one of the first studies that really shows if we manipulate olfactory inputs we can actually alter how the brain perceives energy balance, and how the brain regulates energy balance," said Céline Riera, a former UC Berkeley postdoctoral fellow now at Cedars-Sinai Medical Center in Los Angeles.

 

Humans who lose their sense of smell because of age, injury or diseases such as Parkinson's often become anorexic, but the cause has been unclear because loss of pleasure in eating also leads to depression, which itself can cause loss of appetite.

 

The new study, published this week in the journal Cell Metabolism, implies that the loss of smell itself plays a role, and suggests possible interventions for those who have lost their smell as well as those having trouble losing weight.

 

"Sensory systems play a role in metabolism. Weight gain isn't purely a measure of the calories taken in; it's also related to how those calories are perceived," said senior author Andrew Dillin, the Thomas and Stacey Siebel Distinguished Chair in Stem Cell Research, professor of molecular and cell biology and Howard Hughes Medical Institute Investigator. "If we can validate this in humans, perhaps we can actually make a drug that doesn't interfere with smell but still blocks that metabolic circuitry. That would be amazing."

 

Riera noted that mice as well as humans are more sensitive to smells when they are hungry than after they've eaten, so perhaps the lack of smell tricks the body into thinking it has already eaten. While searching for food, the body stores calories in case it's unsuccessful. Once food is secured, the body feels free to burn it.

 

Zapping olfactory neurons

 

The researchers used gene therapy to destroy olfactory neurons in the noses of adult mice but spare stem cells, so that the animals lost their sense of smell only temporarily -- for about three weeks -- before the olfactory neurons regrew.

 

The smell-deficient mice rapidly burned calories by up-regulating their sympathetic nervous system, which is known to increase fat burning. The mice turned their beige fat cells -- the subcutaneous fat storage cells that accumulate around our thighs and midriffs -- into brown fat cells, which burn fatty acids to produce heat. Some turned almost all of their beige fat into brown fat, becoming lean, mean burning machines.

 

In these mice, white fat cells -- the storage cells that cluster around our internal organs and are associated with poor health outcomes -- also shrank in size.

 

The obese mice, which had also developed glucose intolerance -- a condition that leads to diabetes -- not only lost weight on a high-fat diet, but regained normal glucose tolerance.

 

On the negative side, the loss of smell was accompanied by a large increase in levels of the hormone noradrenaline, which is a stress response tied to the sympathetic nervous system. In humans, such a sustained rise in this hormone could lead to a heart attack.

 

Though it would be a drastic step to eliminate smell in humans wanting to lose weight, Dillin noted, it might be a viable alternative for the morbidly obese contemplating stomach stapling or bariatric surgery, even with the increased noradrenaline.

 

"For that small group of people, you could wipe out their smell for maybe six months and then let the olfactory neurons grow back, after they've got their metabolic program rewired," Dillin said.

 

Dillin and Riera developed two different techniques to temporarily block the sense of smell in adult mice. In one, they genetically engineered mice to express a diphtheria receptor in their olfactory neurons, which reach from the nose's odor receptors to the olfactory center in the brain. When diphtheria toxin was sprayed into their nose, the neurons died, rendering the mice smell-deficient until the stem cells regenerated them.

 

Separately, they also engineered a benign virus to carry the receptor into olfactory cells only via inhalation. Diphtheria toxin again knocked out their sense of smell for about three weeks.

 

In both cases, the smell-deficient mice ate as much of the high-fat food as did the mice that could still smell. But while the smell-deficient mice gained at most 10 percent more weight, going from 25-30 grams to 33 grams, the normal mice gained about 100 percent of their normal weight, ballooning up to 60 grams. For the former, insulin sensitivity and response to glucose -- both of which are disrupted in metabolic disorders like obesity -- remained normal.

 

Mice that were already obese lost weight after their smell was knocked out, slimming down to the size of normal mice while still eating a high-fat diet. These mice lost only fat weight, with no effect on muscle, organ or bone mass.

 

The UC Berkeley researchers then teamed up with colleagues in Germany who have a strain of mice that are supersmellers, with more acute olfactory nerves, and discovered that they gained more weight on a standard diet than did normal mice.

 

"People with eating disorders sometimes have a hard time controlling how much food they are eating and they have a lot of cravings," Riera said. "We think olfactory neurons are very important for controlling pleasure of food and if we have a way to modulate this pathway, we might be able to block cravings in these people and help them with managing their food intake."

https://www.sciencedaily.com/releases/2017/07/170705123007.htm

Prebiotics may help to cope with stress

Prebiotic fibers can help to protect beneficial gut bacteria and restore healthy sleep patterns after a stressful event

February 10, 2017

Science Daily/Frontiers

Probiotics are well known to benefit digestive health, but prebiotics are less well understood. Recent study in rats shows that prebiotic fibers may help to protect beneficial gut bacteria and restore healthy sleep patterns after a stressful event.

 

Probiotics are well known to benefit digestive health, but prebiotics are less well understood. Prebiotics are certain types of non-digestible fibers that probiotic bacteria feed on, such as the fibers found in many plant sources like asparagus, oatmeal, and legumes. Certain bacteria also feed on non-fibers such as the protein lactoferrin, which also acts like a prebiotic and is found in breast milk.

 

According to a new study published in the online journal, Frontiers in Behavioral Neuroscience by Professor Monika Fleshner, PhD, and her team from the University of Colorado, Boulder, regular intake of prebiotics may promote beneficial gut bacteria and recovery of normal sleep patterns after a stressful episode.

 

"Acute stress can disrupt the gut microbiome," explained Dr. Agnieszka Mika, a postdoctoral fellow and one of the authors of the study, "and we wanted to test if a diet rich in prebiotics would increase beneficial bacteria as well as protect gut microbes from stress-induced disruptions. We also wanted to look at the effects of prebiotics on the recovery of normal sleep patterns, since they tend to be disrupted after stressful events."

 

In this experiment, test rats received prebiotic diets for several weeks prior to a stressful test condition and compared with control rats that did not receive the prebiotic-enriched diet. Interestingly, rats that ate prebiotics prior to the stressful event did not experience stress-induced disruption in their gut microbiota, and also recovered healthier sleep patterns sooner than controls.

 

Given that these experiments were done in rats, are these results relevant for humans? "The stressor the rats received was the equivalent of a single intense acute stressful episode for humans, such as a car accident or the death of a loved one," said Dr. Robert S. Thompson, the lead author of the study. "A next set of studies will be looking exactly at that question -- can prebiotics help humans to protect and restore their gut microflora and recover normal sleep patterns after a traumatic event?"

 

In the mean time, should we start including prebiotics in our diets to help cope with stress? "So far no adverse effects from prebiotics have been reported," said Dr. Mika, "and they are found widely in many plants, even present in breast milk, and are already commercially available." Healthy gut bacteria and restful sleep could be your benefits.

https://www.sciencedaily.com/releases/2017/02/170210130951.htm

Poor diet before pregnancy linked with preterm birth

May 23, 2014

Science Daily/University of Adelaide

For the first time, researchers have confirmed that women who eat a poor diet before they become pregnant are around 50% more likely to have a preterm birth than those on a healthy diet. The study shows that women who consistently ate a diet high in protein and fruit prior to becoming pregnant were less likely to have a preterm birth, while those who consistently ate high fat and sugar foods, and take-out food were about 50% more likely to have a preterm birth.

 

It's the first study of its kind to assess women's diet prior to conception and its association with outcomes at birth.

 

The results, published in The Journal of Nutrition, show that women who consistently ate a diet high in protein and fruit prior to becoming pregnant were less likely to have a preterm birth, while those who consistently ate high fat and sugar foods and takeaway were about 50% more likely to have a preterm birth.

 

"Preterm birth is a leading cause of infant disease and death and occurs in approximately one in 10 pregnancies globally. Anything we can do to better understand the conditions that lead to preterm birth will be important in helping to improve survival and long-term health outcomes for children," says the lead author of the paper, Dr Jessica Grieger, Posdoctoral Research Fellow with the Robinson Research Institute, based at the Lyell McEwin Hospital.

 

"In our study, women who ate protein-rich foods including lean meats, fish and chicken, as well as fruit, whole grains and vegetables, had significantly lower risk of preterm birth.

 

"On the other hand, women who consumed mainly discretionary foods, such as takeaway, potato chips, cakes, biscuits, and other foods high in saturated fat and sugar were more likely to have babies born preterm," Dr Grieger says.

 

"It is important to consume a healthy diet before as well as during pregnancy to support the best outcomes for the mum and baby," Dr Grieger says.

 

"Diet is an important risk factor that can be modified. It is never too late to make a positive change. We hope our work will help promote a healthy diet before and during pregnancy. This will help to reduce the number of neonatal deaths and improve the overall health of children," she says.

http://www.sciencedaily.com/releases/2014/05/140523145127.htm

Mothers' sleep, late in pregnancy, affects offspring's weight gain as adults

May 16, 2014

Science Daily/University of Chicago Medical Center

Poor-quality sleep during the third trimester of pregnancy can increase the odds of weight gain and metabolic abnormalities in offspring once they reach adulthood. The effects, caused by epigenetic modifications, impose lasting consequences on the next generation.

 

The researchers linked the excess weight and changes in metabolism to epigenetic modifications that reduce expression of the gene for adiponectin -- a hormone that helps regulate several metabolic processes, including glucose regulation. Lower levels of adiponectin correlate with increased body fat and reduced activity.

 

"Disrupted sleep is a common problem during the final trimester of a pregnancy," said study director, sleep specialist David Gozal, MD, the Herbert T Abelson professor of pediatrics at the University of Chicago. "For some women, sleep fragmentation, especially sleep apnea, can be profound. We wanted to devise a system that enabled us to measure the potential impact of fragmented sleep on the fetus, which is uniquely susceptible so early in life."

 

Adiponectin is usually a "beneficial hormone," Gozal said. "It can reduce cholesterol, make you more sensitive to insulin, protect your heart." As adiponectin levels in adults go up, body-fat percentage tends to go down. Expression of the adiponectin gene was reduced in the offspring of sleep-fragmented mothers, especially in their visceral fat cells.

 

A closer look revealed epigenetic changes, such as methylation and histone modification, which shut down selected genes, often in response to environmental stresses.

 

"We found that the offspring of sleep-deprived mothers had largely inactivated AdipoQ, the adiponectin gene," Gozal said. "Such changes may affect other genes as well; we haven't studied all the potential targets yet. Even so, this is the first example of a perturbation during pregnancy that translates into a genetic risk, in midlife, for the next generation."

 

"This is kind of scary," he added. "Will this generation, the sons of sleep-deprived mice, who are already at increased risk for metabolic syndrome and type 2 diabetes, transmit this inherited risk, perhaps compounded by new stresses, to their offspring?"

http://www.sciencedaily.com/releases/2014/05/140516092305.htm

Women who gain too much or too little weight during pregnancy at risk for having an overweight child

April 14, 2014

Science Daily/Kaiser Permanente

Gaining both too much or too little weight during pregnancy appears to increase the risk of having an overweight or obese child, according to a study. In one of the largest studies to examine current Institute of Medicine recommendations regarding pregnancy weight gain in relation to childhood obesity, researchers reviewed the electronic health records of 4,145 racially diverse females who had completed a health survey between 2007 and 2009 and subsequently had a baby.

 

In one of the largest studies to examine current Institute of Medicine recommendations regarding pregnancy weight gain in relation to childhood obesity, researchers reviewed the electronic health records of 4,145 racially diverse female members of Kaiser Permanente in Northern California who had completed a health survey between 2007 and 2009 and subsequently had a baby.

 

Researchers reviewed the medical records of those children between ages 2 and 5 years old and found that:

 

·      Among all women who gained more than the recommended weight during pregnancy, 20.4 percent of their children were overweight or obese, compared with 19.5 percent in women who gained less than recommended weight and 14.5 percent in women who gained weight within the guidelines.

 

·      Women with a normal Body Mass Index measurement before pregnancy who gained less than the recommended amount were 63 percent more likely to have a child who became overweight or obese.

 

·      Women with a normal BMI before pregnancy with weight gain above recommendations were 80 percent more likely to have an overweight or obese child.

 

"The stronger association we found among normal weight women who gained too much or too little weight during pregnancy suggests that perhaps weight gain in pregnancy may have an impact on the child that is independent of genetic factors," said senior investigator Monique M. Hedderson, PhD, Kaiser Permanente Division of Research in Oakland, Calif.

 

"Gaining either too little or too much weight in pregnancy may permanently affect mechanisms that manage energy balance and metabolism in the offspring, such as appetite control and energy expenditure," said the study's lead author Sneha Sridhar, MPH, Kaiser Permanente Division of Research. "This could potentially have long-term effects on the child's subsequent growth and weight."

http://www.sciencedaily.com/releases/2014/04/140414092115.htm

Late Bedtimes and Less Sleep May Lead to Weight Gain in Healthy Adults

June 28, 2013
Science Daily/American Academy of Sleep Medicine
A new study suggests that healthy adults with late bedtimes and chronic sleep restriction may be more susceptible to weight gain due to the increased consumption of calories during late-night hours.

In the largest, most diverse healthy sample studied to date under controlled laboratory conditions, results show that sleep-restricted subjects who spent only four hours in bed from 4 a.m. to 8 a.m. for five consecutive nights gained more weight than control subjects who were in bed for 10 hours each night from 10 p.m. to 8 a.m. 

The study found an overall increase in caloric intake during sleep restriction, which was due to an increase in the number of meals consumed during the late-night period of additional wakefulness. Furthermore, the proportion of calories consumed from fat was higher during late-night hours than at other times of day.

"Although previous epidemiological studies have suggested an association between short sleep duration and weight gain/obesity, we were surprised to observe significant weight gain during an in-laboratory study," said lead author Andrea Spaeth, a doctoral candidate in the psychology department at the University of Pennsylvania in Philadelphia, Pa.

"Among sleep-restricted subjects, there were also significant gender and race differences in weight gain," said Spaeth. "African Americans, who are at greater risk for obesity and more likely to be habitual short sleepers, may be more susceptible to weight gain in response to sleep restriction. Future studies should focus on identifying the behavioral and physiological mechanisms underlying this increased vulnerability."
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2013/06/130628160840.htm

Stress early in life leads to adulthood anxiety and preference for 'comfort foods'

July 30, 2013
Science Daily/Society for the Study of Ingestive Behavior
New research finds that adult rats reared in a stressful neonatal environment demonstrate more anxiety and stress, and they prefer to eat more foods rich in fat and sugar.

Early-Life Stress increased adulthood anxiety, increased the hormonal response to stress (corticosterone) and increased the preference for comfort foods, even after a period of chronic exposure to this type of food.

"Comfort foods" have been defined as the foods eaten in response to emotional stress, and are suggested to contribute to the obesity epidemic. Hormonal responses to chronic stress in adulthood seem to play a role in the increased preference for this type of food, especially in women.

Early-Life Stress increased adulthood anxiety, increased the hormonal response to stress (corticosterone) and increased the preference for comfort foods, even after a period of chronic exposure to this type of food.

"To our knowledge, this is the first study to demonstrate that comfort food preference could be enhanced by such an early stress exposure," says lead researcher Tania Machado. The anxiety and altered food preferences seen in these rats exposed to neonatal adversity can be related to the described changes in the hormonal response to stress. Therefore, in neonatally stressed rats, a greater consumption of "comfort foods" is possibly used as a way to alleviate anxiety symptoms (self-medication). 

Future studies in this area may have implications for primary care on childhood nutrition in vulnerable populations (e.g. low birth weight or children with a history of neonatal adversities).
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2013/07/130730091401.htm

Weight and diet may help predict sleep quality

Overweight adults spend more of their sleep in REM stage than healthy weight adults do, says Penn Medicine study

June 10, 2016

Science Daily/University of Pennsylvania School of Medicine
The old adage 'you are what you eat,' may be better phrased as 'your sleep relates to what you eat.' An individual's body composition and caloric intake can influence time spent in specific sleep stages, according to results of a new study.

In the study, 36 healthy adults experienced two consecutive nights of 10 hours in bed per night at the Hospital of the University of Pennsylvania. Polysomnography- which records physiological changes that occur during sleep -- was recorded on the second night. Body composition and resting energy expenditure were assessed on the morning following the first night of sleep. Food/drink intake was measured each day.

The Penn team found that body mass index (BMI), body fat percentage and resting energy expenditure were not significant predictors of sleep stage duration, but that overweight adults exhibited a higher percentage of time spent in the rapid-eye movement (REM) stage of sleep -- when dreams typically occur and characterized by faster heart rate and breathing and less restorative sleep than in non-REM stages -- than normal-weight adults.

The group also found that increased protein intake predicted less stage 2 sleep -- the period when a person's heart rate and breathing are relatively normal and his/her body temperature lowers slightly -- and predicted more REM sleep.

"In a culture of increasing pressure to sacrifice sleep to maintain productivity, this research adds to the body of knowledge on how lifestyle behaviors may influence the quality of our sleep" said Andrea M. Spaeth, PhD, postdoctoral fellow and lead author on the study.

Much of this body of knowledge resulted from the same researchers. A 2013 study from the Penn team found that those with late bedtimes and chronic sleep restriction may be more susceptible to weight gain due to the increased consumption of calories during late-night hours. A 2015 study from the group found that eating less late at night may help curb the concentration and alertness deficits that accompany sleep deprivation.

Future research is needed to study whether changing protein intake alters REM sleep duration and to find the biological mechanisms behind this relationship.

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/06/160610173612.htm

Age, obesity, dopamine appear to influence preference for sweet foods

Finding may reveal dysfunction in the brains of individuals with obesity
June 15, 2016


Science Daily/Washington University School of Medicine
As young people reach adulthood, their preferences for sweet foods typically decline. But a research team has found that for people with obesity, the drop-off may not be as steep, and the brain's reward system may be operating differently.
https://images.sciencedaily.com/2016/06/160615110927_1_540x360.jpg
For people with obesity, the brain's reward system may be operating differently than those who are not obese.
Credit: © ematon / Fotolia
"We believe we may have identified a new abnormality in the relationship between reward response to food and dopamine in the brains of individuals with obesity," said the study's first author, M. Yanina Pepino, PhD, an assistant professor of medicine. "In general, people grow less fond of sweet things as they move from adolescence into adulthood. Also, as we age, we have fewer dopamine receptors in a brain structure, called the striatum, that is critical to the reward system. We find that both younger age and fewer dopamine receptors are associated with a higher preference for sweets in those of normal weight. However, in people with obesity, that was not the case in our study."

The researchers studied 20 subjects with healthy weights and compared them with 24 people considered obese, each of whom had a body mass index of 30 or higher. The study volunteers were 20 to 40 years old.

The participants received drinks containing varying levels of sugar to determine the degrees of sweetness each individual preferred. The researchers then conducted positron emission tomography (PET) scans to identify dopamine receptors linked to rewards in each person's brain. Dopamine is the main chemical in the brain that makes us feel good. The PET scans revealed that although there was a relationship between the dopamine receptors, preference for sweet things and age in lean people, that pattern didn't hold true in the brains of obese people.

"We found disparities in preference for sweets between individuals, and we also found individual variations in dopamine receptors -- some people have high levels and some low -- but when we looked at how those things go together, the general trend in people of normal weight was that having fewer dopamine receptors was associated with a higher preference for sweets," said co-investigator Tamara Hershey, PhD, a professor of psychiatry, of neurology and of radiology.

But that wasn't true in the obese subjects. The relationship between their ages, sweetness preferences and dopamine receptors didn't follow the pattern seen in people who weighed less.

Pepino and Hershey explained that it's possible that insulin resistance or some other metabolic change linked to obesity could contribute to the absence of those associations in the obese group. Although none of the obese study participants had diabetes, some had higher blood glucose and insulin concentrations, and some were becoming resistant to insulin. The researchers believe those factors could have altered the brain's response to sweet things.

"There is a relationship between insulin resistance and the brain's reward system, so that might have something to do with what we saw in obese subjects," Hershey said. "What's clear is that extra body fat can exert effects not only in how we metabolize food but how our brains perceive rewards when we eat that food, particularly when it's something sweet."

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/06/160615110927.htm

Childhood binge eating: Families, feeding, and feelings

June 28, 2016

Science Daily/University of Illinois College of Agricultural, Consumer and Environmental Sciences
In order to put childhood binge eating into context, a new systematic review identifies two potential risk factors for binge eating in children under the age of 12. With family being the most proximal and influential setting affecting behaviors and attitudes in children, the study reports that parental non-involvement or emotional unresponsiveness and weight-related teasing in the family are behaviors consistently associated with childhood binge eating.

In order to put childhood binge eating into context, a new systematic review from the University of Illinois identifies two potential risk factors for binge eating in children under the age of 12. With family being the most proximal and influential setting affecting behaviors and attitudes in children, the study reports that parental non-involvement or emotional unresponsiveness and weight-related teasing in the family are behaviors consistently associated with childhood binge eating.

Jaclyn Saltzman, a doctoral researcher in human development and family studies, and a scholar in the Illinois Transdisciplinary Obesity Prevention Program, explains that childhood binge eating can lead to many weight and eating behavior problems as the child grows and in to adulthood. "Intervening early to address binge eating may not only help prevent an eating disorder from emerging but also prevent lifetime habits of unhealthy weight-related behaviors," she says.

Saltzman stresses that binge eating is not the same as feeling you have had too much dessert at dinner. "Binge eating is feeling like you are not in control when you are eating. You are eating past the point of fullness and to the point of discomfort. You are experiencing a lot of emotional distress because of it," she explains.

She adds that binge eating is associated with depression and obesity.

Saltzman and Janet M. Liechty, a professor of medicine and of social work at U of I, reviewed studies on childhood binge eating spanning the last 35 years. They found that very few studies had been done over the last decade on kids and binge eating in the family context.

"We quickly found out that we had to focus specifically on family correlates and risk factors for childhood binge eating, because we were struck by how little research had explored contextual influences, especially in comparison to a much larger body of literature on individual psychological, behavioral, and biological influences. We thought there was a need for a more nuanced understanding of the context in which childhood binge eating develops," Saltzman says.

Initially, the researchers identified over 700 studies, to which they applied strict inclusion criteria to locate studies that looked at outcomes in children under age 12, using reliable instruments, and assessing the constructs of interest. "That left us with 15 studies, which we screened with a tool to assess risk for bias so that we could comment on the strengths and limitations in the studies," she adds.

In their review, the researchers focused on binge eating and loss-of-control eating behavior. Loss of control is traditionally considered a symptom of binge eating in adults, but Saltzman explains that, according to recent research in the field, loss of control is used as a proxy for binge eating in young children, although this is not yet officially recognized in diagnostic manuals.

"Loss of control is something that researchers have used to describe binge eating in young children," she says. "The idea is that the size of the binge--the amount of food they eat--is less important than the feelings of being out of control or the stress about that eating behavior, especially in young kids, because they don't have all that much control over the food that they have access to. But they do have control of their emotions around eating and how much they eat and the sense of being out of control."

Although they found parent ignoring, under-involvement, emotional non-responsiveness and weight-related teasing in the family to be associated with childhood binge eating, Saltzman says that parent weight, education, economic situation, race, or ethnicity, are not correlated. "Actually, no studies found any association between these constructs and childhood binge eating," she says.

"This study found that childhood binge eating is really associated with parents' weight-related beliefs, but not their actual weight, and their emotional availability but not necessarily the income availability," she adds.

Weight teasing is being made fun of, mocked, or "kidded with" about one's weight, usually for being perceived as being overweight, Saltzman explains. "Family-based weight teasing would be any of those behaviors perpetrated by a family member, like a parent or a sibling."

Despite finding that behavior in the family is an important context for childhood binge eating, Saltzman stresses that this does not indicate that parents are to blame for children's binge eating behaviors. "Even though weight-related teasing was a correlate of childhood binge eating, it would be counterproductive and incorrect to blame parents for childhood binge eating behavior. In light of these findings, the large body of literature linking childhood binge eating to psychological factors such as negative affect, and other research studies our lab has done, we want to stress the importance of shifting the paradigm from focusing on weight alone--which is what weight teasing does--to addressing beliefs about weight and emotional coping strategies in the family."

This study was limited in that it focused only on peer-reviewed, English-language articles, and that it could not use meta-analytic techniques to identify the magnitude of associations between the identified correlates and childhood binge eating. Despite these limitations, the review finds evidence to suggest that focus on the emotional context of eating is critical to understanding childhood binge eating.

"We want to emphasize to parents that weight isn't the 'be all end all,' and that focusing on weight too much can be damaging. Instead, focusing on giving kids the tools they need to manage their emotions, particularly emotions around eating and weight, can help strengthen children's coping skills so they are less likely to need binge eating." Saltzman says.

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/06/160628182630.htm

Are brain changes fueling overeating in the obese?

July 12, 2016

Science Daily/Michigan State University
Obese mice are much more likely than lean mice to overeat in the presence of environmental cues, a behavior that could be related to changes in the brain, finds a new study.

The findings offer clues in Alexander Johnson's quest to unpack the interconnected mechanisms of overeating and obesity. Obesity is an epidemic domestically -- more than a third of Americans are considered to be obese -- and a growing health problem in other parts of the world.

"In today's society we are bombarded with signals to eat, from fast-food commercials to the smell of barbecue and burgers, and this likely drives overeating behaviors," said Johnson, MSU assistant professor of psychology. "Our study suggests both a psychological and neurobiological account for why obese individuals may be particularly vulnerable to these signals."

The study involved two groups of mice -- one group that was fed a high-calorie diet until they became obese and a second group that was fed a regular lab chow diet so they stayed lean. Johnson then trained the mice with different auditory cues. Whenever they heard one cue, such as a tone, the mice received a reward of sugar solution; with a second cue, such as a white noise, they received no reward.

All of the mice were then given access to their assigned maintenance diet for three days so they were satiated (i.e., not hungry) for the test phase of the study.

In that test, the sugar solution was available to the mice at all times to see what would trigger them to start eating. When no cue was given, and when the white-noise cue was given (which previously offered no reward), the lean mice and obese mice ate roughly the same amount. When the rewarding tone cue was given, however, the obese mice ate significantly more of the sugar solution than the lean mice.

"From a psychological perspective, this tells us that the obese mice are more vulnerable to the effects of food cues on evoking overeating behavior," Johnson said. "Looking at it through a human lens, this suggests that obese individuals may be more sensitive to, say, the McDonald's Golden Arches."

But why? The final part of the study may offer an explanation.

Johnson also examined the mice's lateral hypothalamus, which is known as a key brain area in appetite and feeding behavior. Using a procedure called immunofluorescence to label neurons in this area of the brain, he found that neurons releasing a certain hormone -- melanin-concentrating hormone, or MCH -- were more abundant in obese mice. But importantly, these MCH-releasing neurons were more active when the obese mice encountered the environmental reminders of sugar.

"In other words, if you become obese, this may lead to increases in MCH expression, and this may make you more sensitive to this form of overeating," Johnson said.

The novel findings, he added, start to paint a picture in the relationship between brain-behavior mechanisms that may underlie learned overeating in obese individuals.

"This could be one of perhaps many reasons why obese people have the urge to eat more when presented with food cues."

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/07/160712110730.htm

Just add water? New MRI technique shows what drinking water does to your appetite, stomach and brain

July 12, 2016


Science Daily/Society for the Study of Ingestive Behavior
Stomach MRI images combined with functional fMRI of the brain activity have provided scientists new insight into how the brain listens to the stomach during eating. Researchers show -- for the first time -- real time data of the brain, the stomach, and people's feelings of satiety measured simultaneously during a meal.
https://images.sciencedaily.com/2016/07/160712093345_1_540x360.jpg
Activation in the insula is increased when the stomach is distended more.
Credit: G CAMPS, R VEIT, M MARS, C DE GRAAF, P SMEETS

In the experiment, participants drank a milk-shake on an empty stomach, which was followed by a small (50 mL) or large glass of water (350 mL). MRI images were used to see how the different amounts of water affected stretching of the stomach: the large glass of water doubled the stomach content compared to the small glass. Together with this larger volume subjects reported to have less hunger and felt fuller.

This novel approach -- combining information obtained simultaneously from MRI images of the stomach, feelings reported by the subjects, and brain scans -- can offer new insights which would otherwise have been unknown, for example that activation in a brain area called the mid-temporal gyrus seems is in some way influenced by the increased water load in this experiment. The Wageningen University scientists developed the combined MRI method as part of the European Nudge-it research project, which seeks to discover simple changes that promote healthier eating. They will use it to search for a brain signature that leads people to decide to stop eating, to determine how strategies like water with a meal can be effective at feeling fuller sooner.

"Combining these types of measurements is difficult, because MRI scanners are usually set-up to perform only one type of scan. We've been able to very quickly switch the scanner from one functionality to another to do this type of research" says Guido Camps, lead author of the study. "In conclusion, we've found that simply adding water increases stomach distension, curbs appetite in the short term and increases regional brain activity."
Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/07/160712093345.htm

Stress relief by 'comfort foods' may vary between sexes and across the estrous cycle

July 12, 2016


Science Daily/Society for the Study of Ingestive Behavior
Researchers have found that the brain networks that mediate stress relief after eating highly palatable foods may vary between males and females, and may also depend on the stage of the estrous cycle. The study used a rodent model of 'comfort food' to investigate the neurocircuitry behind this phenomenon.
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"We know that both men and women eat tasty foods as a strategy to reduce stress, and in fact there is some evidence that suggests that women may be more prone to this 'comfort food' style of eating," explained Egan. "This study is important because it suggests that males and females may be using slightly different brain regions, and the stress relief in females may also be affected by the stage of the estrous cycle. This can help us understand how eating behaviors can affect men and women differently, and how eating behaviors are affected by fluctuating hormone levels."

The researchers used a rodent model that is based on human snacking patterns. Female rats were given twice-daily access to a small amount of a sweet sugar drink for 14 days, while other female rats were only given water as a control. Then rats were subjected to a stress test, and their stress hormone response was measured. Similar to previous studies done in male rats, female rats that had been given the sugar solution had a lower stress hormone response to the stress challenge. However, in the female rats the reduced stress response only occurred if the rats were in the proestrus/estrus stage of their estrous cycle, when levels of estrogen are high.

Previous studies in male rats have identified particular brain regions that are important for the stress relief, including the basolateral amygdala and prefrontal cortex. The researchers looked at protein markers of activity (FosB/deltaFosB and pCREB) in these brain regions to see if the sugar drink altered these protein levels similarly in male and female rats. FosB/deltaFosB was increased in the amygdala of males who were given the sugar drink compared to those drinking only water. Female rats also showed this increase in amygdala FosB/deltaFosB after the sugar drink, but only when they were in the proestrus/estrus stage of their cycle. In contrast, amygdala pCREB was increased by the sugar drink in males but not females. Instead amygdala pCREB varied across the estrous cycle in female rats and was unaffected by sugar drink. These different patterns show that comfort eating has some similar effects in male and female brains, but also has unique effects in the female brain that vary across the hormonal cycle. Pursuing these findings could lead to different strategies that could be useful for women and men who habitually eat to manage stress.

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/07/160712092358.htm

Parenting and Home Environment Influence Children's Exercise and Eating Habits

June 18, 2013

Science Daily/SOURCE :http://www.sciencedaily.com/releases/2013/06/130618113652.htm
Science Daily/Duke Medicine
Kids whose moms encourage them to exercise and eat well, and model those healthy behaviors themselves, are more likely to be active and healthy eaters, according to researchers at Duke Medicine.

"Obesity is a complex phenomenon, which is influenced by individual biological factors and behaviors," said study author Truls Østbye, M.D., PhD, professor of community and family medicine at Duke. "But there are variations in obesity from one society to another and from one environment to another, so there is clearly something in the environment that strongly influences the obesity epidemic."

"If we determine that there is a causal link between chronic sleep and poor dietary choices, then we need to start thinking about how to more actively incorporate sleep hygiene education into obesity prevention and health promotion interventions," she said.
 

 

Overeating in obese mice linked to altered brain responses to food cues

July 12, 2016
Science Daily/Society for the Study of Ingestive Behavior
Obese mice are much more likely than lean mice to overeat in the presence of environmental cues, a behavior that could be related to changes in the brain, finds a new study by neuroscientists.

The findings offer clues in Alexander Johnson's quest to unpack the interconnected mechanisms of overeating and obesity. Obesity is an epidemic domestically -- more than a third of Americans are considered to be obese -- and a growing health problem in other parts of the world.

"In today's society we are bombarded with signals to eat, from fast-food commercials to the smell of barbecue and burgers, and this likely drives overeating behaviors," said Johnson, Assistant Professor of Psychology at Michigan State University. "Our study suggests both a psychological and neurobiological account for why obese individuals may be particularly vulnerable to these signals."

The study involved two groups of mice -- one group that was fed a high-calorie diet until they became obese and a second group that was fed a regular lab chow diet so they stayed lean. Johnson then trained the mice with different auditory cues. Whenever they heard one cue, such as a tone, the mice received sugar reward; with a second cue, such as a white noise, they received no reward.

The mice were then given access to their assigned maintenance diet for three days so they were satiated (i.e., not hungry) for the final test phase of the study. In that test, the sugar solution was available to the mice at all times, to see what would trigger them to start eating. When no cue was given, and when the white-noise cue was given (which previously offered no reward), the lean mice and obese mice ate roughly the same amount. When the rewarding tone cue was given, however, the obese mice ate significantly more of the sugar solution compared to the lean mice.

"From a psychological perspective, this tells us that the obese mice are more vulnerable to the effects of environmental triggers on evoking overeating behavior," Johnson said. "Looking at it through a human lens, this suggests that obese individuals may be more sensitive to overeating food in the presence of say, the McDonald's Golden Arches."
But why? The final part of the study may offer an explanation.

Johnson also examined the mice's lateral hypothalamus, which is known as a key brain area in appetite and feeding behavior. Using a procedure called immunofluorescence to label neurons in this area of the brain, he found that neurons releasing a certain hormone- Melanin-Concentrating Hormone, or MCH -- were more abundant in obese mice. But importantly, these MCH-releasing neurons were more active when the obese mice encountered the environmental reminders of sugar.

"In other words, if you become obese this leads to increases in MCH expression, which may make you more sensitive to this form of overeating," Johnson said.

The novel findings, he added, start to paint a picture of the relationship between brain-behavior mechanisms that may underlie learned overeating in obese individuals.

"This could be one of perhaps many reasons why obese people may have the urge to eat more when presented with food cues."

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/07/160712092351.htm

Brains of overweight people 'ten years older' than lean counterparts at middle-age

August 4, 2016

Science Daily/University of Cambridge
From middle-age, the brains of obese individuals display differences in white matter similar to those in lean individuals ten years their senior, according to new research
https://images.sciencedaily.com/2016/08/160804071223_1_540x360.jpg
Comparison of grey matter (brown) and white matter (yellow) in sex-matched subjects A (56 years, BMI 19.5) and B (50 years, BMI 43.4)
Credit: Lisa Ronan

Our brains naturally shrink with age, but scientists are increasingly recognising that obesity -- already linked to conditions such as diabetes, cancer and heart disease -- may also affect the onset and progression of brain ageing; however, direct studies to support this link are lacking.

In a cross-sectional study -- in other words, a study that looks at data from individuals at one point in time -- researchers looked at the impact of obesity on brain structure across the adult lifespan to investigate whether obesity was associated with brain changes characteristic of ageing. The team studied data from 473 individuals between the ages of 20 and 87, recruited by the Cambridge Centre for Aging and Neuroscience. The results are published in the journal Neurobiology of Aging.

The researchers divided the data into two categories based on weight: lean and overweight. They found striking differences in the volume of white matter in the brains of overweight individuals compared with those of their leaner counterparts. Overweight individuals had a widespread reduction in white matter compared to lean people.

The team then calculated how white matter volume related to age across the two groups. They discovered that an overweight person at, say, 50 years old had a comparable white matter volume to a lean person aged 60 years, implying a difference in brain age of 10 years.

Strikingly, however, the researchers only observed these differences from middle-age onwards, suggesting that our brains may be particularly vulnerable during this period of ageing.

"As our brains age, they naturally shrink in size, but it isn't clear why people who are overweight have a greater reduction in the amount of white matter," says first author Dr Lisa Ronan from the Department of Psychiatry at the University of Cambridge, "We can only speculate on whether obesity might in some way cause these changes or whether obesity is a consequence of brain changes."

Senior author Professor Paul Fletcher, from the Department of Psychiatry, adds: "We're living in an ageing population, with increasing levels of obesity, so it's essential that we establish how these two factors might interact, since the consequences for health are potentially serious.

"The fact that we only saw these differences from middle-age onwards raises the possibility that we may be particularly vulnerable at this age. It will also be important to find out whether these changes could be reversible with weight loss, which may well be the case."

Despite the clear differences in the volume of white matter between lean and overweight individuals, the researchers found no connection between being overweight or obese and an individual's cognitive abilities, as measured using a standard test similar to an IQ test.

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/08/160804071223.htm

Mediterranean diet associated with lower risk of early death in cardiovascular disease patients

Preventing sudden death -- diet or device

August 29, 2016

Science Daily/European Society of Cardiology
The Mediterranean diet is associated with a reduced risk of death in patients with a history of cardiovascular disease, according to results from the observational study.

"The Mediterranean diet is widely recognised as one of the healthier nutrition habits in the world," said Professor Giovanni de Gaetano, head of the Department of Epidemiology and Prevention at the I.R.C.C.S. Neuromed Institute in Pozzilli, Italy. "In fact, many scientific studies have shown that a traditional Mediterranean lifestyle is associated with a lower risk of various chronic diseases and, more importantly, of death from any cause."

"But so far research has focused on the general population, which is mainly composed of healthy people," he added. "What happens to people who have already suffered from cardiovascular disease? Is the Mediterranean diet optimal for them too?"

The answer is yes, according to a study in patients with a history of cardiovascular disease, such as coronary artery disease and stroke. The patients were among the participants enrolled into the Moli-sani project, a prospective epidemiological study that randomly recruited around 25,000 adults living in the Italian region of Molise.

"Among the participants, we identified 1197 people who reported a history of cardiovascular disease at the time of enrolment into Moli-sani," said Dr Marialaura Bonaccio, lead author of the research.

Food intake was recorded using the European Prospective Investigation into Cancer (EPIC) food frequency questionnaire. Adherence to the Mediterranean diet was appraised with a 9-point Mediterranean diet score (MDS). All-cause death was assessed by linkage with data from the office of vital statistics in Molise.

During a median follow up of 7.3 years there were 208 deaths. A 2-point increase in the MDS was associated with a 21% reduced risk of death after controlling for age, sex, energy intake, egg and potato intake, education, leisure-time physical activity, waist to hip ratio, smoking, hypertension, hypercholesterolaemia, diabetes and cancer at baseline.

When considered as a 3-level categorical variable, the top category (score 6-9) of adherence to the Mediterranean diet was associated with 37% lower risk of death compared to the bottom category (0-3).

Professor de Gaetano said: "We found that among those with a higher adherence to the Mediterranean diet, death from any cause was reduced by 37% in comparison to those who poorly adhered to this dietary regime."

The researchers deepened their investigation by looking at the role played by individual foods that make up Mediterranean diet. "The major contributors to mortality risk reduction were a higher consumption of vegetables, fish, fruits, nuts and monounsaturated fatty acids -- that means olive oil," said Dr Bonaccio.

Professor de Gaetano concluded: "These results prompt us to investigate the mechanism(s) through which the Mediterranean diet may protect against death. This was an observational study so we cannot say that the effect is causal. We expect that dietary effects on mediators common to chronic diseases such as inflammation might result in the reduction of mortality from any cause but further research is needed."

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/08/160829094040.htm

Stress and obesity biologically linked

October 5, 2016

Science Daily/The Hebrew University of Jerusalem
Metabolic and anxiety-related disorders both pose a significant healthcare burden, and are in the spotlight of contemporary research and therapeutic efforts. Although intuitively we assume that these two phenomena overlap, the link has not been scientifically demonstrated.

Now, a team of researchers from the Hebrew University of Jerusalem, headed by Prof. Hermona Soreq from the Edmond and Lily Safra Center for Brain Sciences and the Department of Biological Chemistry at the Faculty of Mathematics and Sciences, revealed the molecular elements that bridge anxiety and metabolism -- a type of microRNA that influences shared biological mechanisms.

"We already know that there is a connection between body and mind, between the physical and the emotional, and studies show that psychological trauma affects the activity of many genes. Our previous research found a link between microRNA and stressful situations -- stress and anxiety generate an inflammatory response and dramatically increase the expression levels of microRNA regulators of inflammation in both the brain and the gut, for example the situation of patients with Crohn's disease may get worse under psychological stress, "says Prof. Soreq.

"In the present study, we added obesity to the equation. We revealed that some anxiety-induced microRNA are not only capable of suppressing inflammation but can also potentiate metabolic syndrome-related processes. We also found that their expression level is different in diverse tissues and cells, depending on heredity and exposure to stressful situations," explains Prof. Soreq.

The family of microRNA genes is part of the human genome, which was considered until not too long ago as "junk-DNA." However, microRNAs are now known to fulfill an important role in regulating the production process of proteins by other genes. These tiny RNA molecules, which are one percent of the average size of a protein-coding gene, act as suppressors of inflammation and are able to halt the production of proteins.

The research paper, published in the journal Trends in Molecular Medicine, details the evidence linking microRNA pathways, which share regulatory networks in metabolic and anxiety-related conditions. In particular, microRNAs involved in these disorders include regulators of acetylcholine signaling in the nervous system and their accompanying molecular machinery.

Metabolic disorders, such as abdominal obesity and diabetes, have become a global epidemic. In the USA, the prevalence of metabolic syndrome is as high as 35 percent. In other countries, such as Austria, Denmark and Ireland it affects 20-25 percent of the population.

Anxiety disorders are harder to quantify than metabolic ones. They include obsessive-compulsive disorder (OCD), post-traumatic stress disorder (PTSD) and phobia. The full burden of the anxiety spectrum is difficult to assess, due to under-diagnosis and poorly defined pathophysiological processes.

This newly revealed link offers novel opportunities for innovative diagnoses and treatment of both metabolic and anxiety-related phenomena.

"The discovery has a diagnostic value and practical implications, because the activity of microRNAs can be manipulated by DNA-based drugs," explains Prof. Soreq. "It also offers an opportunity to reclassify 'healthy' and 'unhealthy' anxiety and metabolic-prone states, and inform putative strategies to treat these disorders."

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/10/161005114822.htm

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