Jogging and five other exercises ward off weight gain despite 'obesity genes'

August 1, 2019

Science Daily/PLOS

For people who inherited genes that increase their chance of becoming obese, there is hope for keeping the weight off. A study by Wan-Yu Lin of National Taiwan University and colleagues, published 1st August in PLOS Genetics, identified the types of exercise that are especially effective at combating genetic effects that contribute to obesity.

 

Worldwide, obesity is a challenging condition to control because it results from interactions between a person's genetics and lifestyle. Doctors often recommend exercise, but it is not clear which kinds are best for curbing weight gain in individuals whose genetics make them more likely to become obese. A new study of 18,424 Han Chinese adults, aged 30 to 70 years, examined the interactions between the individuals' genetics and their self-reported exercise routines. The researchers looked specifically at five measures of obesity, such as body mass index (BMI), body fat percentage and waist-to-hip ratio. They found that regular jogging was the best type of exercise for managing obesity, according to the five measures. Moreover, mountain climbing, walking, power walking, certain types of dancing, and long yoga practices also reduce BMI in individuals predisposed to obesity. Surprisingly, cycling, stretching exercises, swimming and Dance Dance Revolution did not counteract the genetic effects on obesity.

 

Overall, the study suggests that when it comes to obesity, genetics are not destiny, and the effects can be lessened by several kinds of regular exercise. Previous research has shown that frequent physical activity blunts the genetic effects on obesity, but these studies focused only on BMI. The new study also considers four other measures of obesity that are more closely linked to metabolic problems. As obesity continues to be a serious public health challenge, the benefits of exercise cannot be overstated.

https://www.sciencedaily.com/releases/2019/08/190801142527.htm

Weight stigma in men associated with harmful health consequences

July 30, 2019

Science Daily/UConn Rudd Center for Food Policy and Obesity

As many as 40% of men report experiencing weight stigma, but little is known about how this stigma affects their health. This study found that men experiencing weight stigma have more depressive symptoms, are more likely to binge eat, and have lower self-rated health.

 

Men's health may be compromised by weight stigma, finds the latest research from the Rudd Center for Food Policy and Obesity at the University of Connecticut.

 

Weight stigma is pervasive against people with obesity, and can contribute to both physical and emotional health problems for those targeted. As many as 40% of men report experiencing weight stigma, but when it comes to how this stigma affects their health, men have received less attention in research compared to women.

 

"It's often assumed that conversations about weight loss, poor body image, and dieting are more salient for women. Men are frequently overlooked, but that does not necessarily mean that men are less affected by weight stigma or less likely to internalize negative biases," says Mary Himmelstein, lead author of the study.

 

The research, published in the journal Obesity, involved two groups of men: 1,249 men from a diverse national survey panel, and 504 men from an online data collection service. Both groups of men completed identical surveys about their experiences of weight-based stigma, how much they internalized these experiences (e.g., blamed themselves), as well as their psychological wellbeing and health behaviors.

 

Key findings include:

 ·     Both experienced and internalized weight stigma were associated with more depressive symptoms and more dieting behaviors.

·     Men who experienced weight stigma had increased odds of engaging in binge eating.

·     Men who internalized weight stigma had lower self-rated health.

 

These findings suggest the need for increased attention to men not only in research on links between weight stigma and health, but also among health professionals treating men for various health conditions, in which weight stigma may play a contributing role. In particular, it may be useful for health care providers to ask men about weight stigma to help identify those who may be vulnerable to depression or disordered eating behaviors, which are underdiagnosed in men.

 

"Our study shows that weight stigma is not a gendered issue. It can affect men's health in the same damaging ways in which we already know that it harms women's health, and neglecting these issues in men, either in research or clinical practice, may put them at a serious disadvantage in treatment," says Himmelstein. "Opportunities for supportive interventions should be available for men, women, and non-binary individuals alike to help them cope with weight stigma in less harmful ways."

https://www.sciencedaily.com/releases/2019/07/190730083717.htm

Individuals with obesity get more satisfaction from their food

July 30, 2019

Science Daily/Elsevier

A new study found no significant difference in taste perceptions between participants of normal weight and those who were overweight. However, participants with obesity had initial taste perceptions that were greater than participants who were not obese, which declined at a more gradual rate than participants who were not obese. This quantification of satisfaction from food may help explain why some people eat more than others.

 

The propensity to overeat may, in part, be a function of the satisfaction derived from eating. A new study in the Journal of the Academy of Nutrition and Dietetics, published by Elsevier, found no significant difference in taste perceptions between participants of normal weight and those who were overweight. However, participants with obesity had initial taste perceptions that were greater than participants who were not obese, which declined at a more gradual rate than participants who were not obese. This quantification of satisfaction from food may help explain why some people eat more than others.

 

"Obesity is a major public-health problem. Thirty percent of the US population is obese, and obesity-related health problems (diabetes, hypertension, etc.) are increasing. Causes of obesity are varied, but food consumption decisions play an important role, especially decisions about what foods to eat and how much to consume. Taste perceptions may lead to overeating. If people with obesity have different taste perceptions than nonobese people, it could lead to better understanding of obesity and possibly designing new approaches to prevent obesity," explained lead investigator Linnea A. Polgreen, PhD, Department of Pharmacy Practice and Science, University of Iowa, Iowa City, IA, USA.

 

As individuals consume more of a food item, they experience diminishing marginal taste perception, which means their level of perceived taste from additional consumption may tend to decline (ie, additional consumption may become less pleasurable). The relationship between perceived taste and quantity consumed has traditionally been referred to as sensory-specific satiety.

 

In order to determine if marginal taste perceptions differ among participants of normal-weight, those who are overweight and those with obesity, and whether knowledge of nutritional information affects marginal taste perception, researchers at the University of Iowa conducted a non-clinical, randomized controlled trial of 290 adults (161 with normal BMI, 78 considered overweight, and 51 considered obese) to measure instantaneous taste perceptions. Eighty percent of the participants were female, and ages ranged from 18 to 75 years. Participants were offered and rated one piece of chocolate at a time in a controlled environment and could eat as much as they wanted without feeling uncomfortable. They consumed between two and 51 pieces. Half of the study participants received nutritional information about the chocolate before the chocolate tasting began.

 

The study identified a consistent association between taste from food, specifically chocolate, and BMI by directly observing instantaneous taste changes over a period of time, rather than just at the beginning and end of a period of consumption, as in prior studies.

 

Typically, the appeal of a specific food may decline as more of that food is eaten: the first bite of chocolate is better than the 10th, a phenomenon consistent with the concept of sensory-specific satiety. As anticipated, researchers found that ratings generally went down after each piece of chocolate consumed with no significant difference in taste perceptions between normal and overweight participants reported. However, participants with obesity had higher levels of initial taste perception, rated subsequent pieces higher than their counterparts without obesity, and their ratings declined at a more gradual rate compared to participants with normal weight and those with obesity. People hungrier prior to the study had greater taste perception; women's taste perceptions declined faster than men's; and providing nutritional information prior to chocolate consumption did not affect taste perception.

 

"In our study population, people with obesity reported a higher level of satisfaction for each additional piece of chocolate compared to nonobese people. Thus, their taste preferences appear markedly different," noted co-investigator Aaron C. Miller, PhD, Department of Epidemiology, University of Iowa, Iowa City, IA, USA. "Our findings further indicate that obese participants needed to consume a greater quantity of chocolate than nonobese participants to experience a similar decline in taste perceptions. Specifically, obese women needed to eat 12.5 pieces of chocolate to fall to the same level of taste perception as nonobese women who ate only 10 pieces, which corresponds to a difference of 67.5 calories. This may, in part, explain why obese people consume more than nonobese people."

 

These findings suggest that understanding and manipulating taste perceptions, in addition to targeting nutritional awareness, may be crucial to understanding and preventing obesity. Strategies that work for individuals of normal-weight or those who are overweight may not work as effectively for individuals with obesity if they derive more satisfaction from eating additional amounts of food. If these findings are generalizable to other foods, they may help inform future interventions.

https://www.sciencedaily.com/releases/2019/07/190730083710.htm

Meal timing strategies appear to lower appetite, improve fat burning

July 24, 2019

Science Daily/The Obesity Society

Researchers have discovered that meal timing strategies such as intermittent fasting or eating earlier in the daytime appear to help people lose weight by lowering appetite rather than burning more calories, according to a report published online today in the journal Obesity, the flagship journal of The Obesity Society. The study is the first to show how meal timing affects 24-hour energy metabolism when food intake and meal frequency are matched.

 

"Coordinating meals with circadian rhythms, or your body's internal clock, may be a powerful strategy for reducing appetite and improving metabolic health," said Eric Ravussin, PhD, one of the study's authors and associate executive director for clinical science at Louisiana State University's Pennington Biomedical Research Center in Baton Rouge.

 

"We suspect that a majority of people may find meal timing strategies helpful for losing weight or to maintain their weight since these strategies naturally appear to curb appetite, which may help people eat less," said Courtney M. Peterson, PhD, lead author of the study and an assistant professor in the Department of Nutrition Sciences at the University of Alabama at Birmingham.

 

Peterson and her colleagues also report that meal timing strategies may help people burn more fat on average during a 24-hour period. Early Time-Restricted Feeding (eTRF) -- a form of daily intermittent fasting where dinner is eaten in the afternoon -- helped to improve people's ability to switch between burning carbohydrates for energy to burning fat for energy, an aspect of metabolism known as metabolic flexibility. The study's authors said, however, that the results on fat-burning are preliminary. "Whether these strategies help people lose body fat need to be tested and confirmed in a much longer study," said Peterson.

 

For the study, researchers enrolled 11 adult men and women who had excess weight. Participants were recruited between November 2014 and August 2016. Adults, in general good health, aged 20-to-45-years old were eligible to participate if they had a body mass index between 25 and 35 kg/m2 (inclusive), body weight between 68 and 100 kg, a regular bedtime between 9:30 p.m. and 12 a.m., and for women, a regular menstrual cycle.

 

Participants tried two different meal timing strategies in random order: a control schedule where participants ate three meals during a 12-hour period with breakfast at 8:00 a.m. and dinner at 8:00 p.m. and an eTRF schedule where participants ate three meals over a six-hour period with breakfast at 8:00 a.m. and dinner at 2:00 p.m. The same amounts and types of foods were consumed on both schedules. Fasting periods for the control schedule included 12 hours per day, while the eTRF schedule involved fasting for 18 hours per day.

 

Study participants followed the different schedules for four days in a row. On the fourth day, researchers measured the metabolism of participants by placing them in a respiratory chamber -- a room-like device -- where researchers measured how many calories, carbohydrates, fat and protein were burned. Researchers also measured the appetite levels of participants every three hours while they were awake, as well as hunger hormones in the morning and evening.

 

Although eTRF did not significantly affect how many calories participants burned, the researchers found that eTRF did lower levels of the hunger hormone ghrelin and improved some aspects of appetite. It also increased fat-burning over the 24-hour day.

 

"By testing eTRF, we were able to kill two birds with one stone," said Peterson, adding that the researchers were able to gain some insight into daily intermittent fasting (time restricted-feeding), as well as meal timing strategies that involve eating earlier in the daytime to be in sync with circadian rhythms. The researchers believe that these two broader classes of meal timing strategies may have similar benefits to eTRF.

 

Hollie Raynor, PhD, RD, LDN, who was not associated with the research, said "this study helps provide more information about how patterns of eating, and not just what you eat, may be important for achieving a healthy weight." Raynor is a professor and interim dean of research in the Department of Nutrition, College of Education, Health, and Human Sciences at The University of Tennessee, Knoxville.

 

Peterson and colleagues said prior research was conflicted on whether meal timing strategies help with weight loss by helping people burn more calories or by lowering appetite. Studies in rodents suggest such strategies burn more calories, but data from human studies were conflicting -- some studies suggested meal timing strategies increase calories burned, but other reports showed no difference. The study's authors said, however, that previous studies did not directly measure how many calories people burned or were imperfect in other ways.

https://www.sciencedaily.com/releases/2019/07/190724103702.htm

Offering children a wide variety and large quantities of snack food encourages them to eat more

Less focus on plate size and more on reducing quantity and variety of food key to getting children to snack less

July 19, 2019

Science Daily/Murdoch Childrens Research Institute

Offering children a wide variety and large quantities of snack food encourages them to eat more - and may contribute to weight problems, a new study has found. The research also found that how snacks are presented (in a large or small container) has little influence on how much children snack.

 

A new study has found that offering children a wide variety and large quantities of snack food encourages them to eat more -- and this practice may be contributing to Australia's weight problem.

 

The research*, led by the Murdoch Children's Research Institute and published in the latest International Journal of Obesity, also found that how snacks are presented (in a large or small container) has little influence on how much children snack.

 

Lead researcher Dr Jessica Kerr said their study found children weren't greatly affected by container size, with food consumption mainly driven by the quantity/variety of snacks on offer.

 

"There has been a popular push by nutritionists and public health officials towards replacing large dishware with smaller versions to nudge people towards healthier decisions," she said. "But we have found dishware size has very little effect on the amount of food consumed."

 

Dr Kerr said while the overconsumption of snack foods is an important contributor to obesity, most people do not recognise the impact it has on their calorie intake.

 

"Children and adults should only consume energy-dense snacks occasionally -- they do not need to be part of daily energy intake," she said. "But the reality is that Australians typically get around 30-40 per cent of their energy intake from snack foods."

 

Dr Kerr said three times as many children in Australia are now overweight or obese compared to 30 years ago.

 

"About 20 per cent (1 in 5) of children are overweight or obese," she said. "There are many complications of children being overweight such as type 2 diabetes, orthopaedic and respiratory disorders, liver problems and sleep apnoea."

 

Dr Kerr said until now studies into snacking behavior were limited by self-reported data or small sample sizes.

 

"Past dietary studies have mostly focused on main meals," Dr Kerr said. "It is important to determine on a larger scale how dishware size and the quantity, variety, and energy density of snacks affect both child and adult snacking behavior when apart from each other outside of the family environment," she said.

 

For the study, participants ate during a 15-minute snack break between 20 other health assessments at the Child Health CheckPoint, which looked at the health of 1800 children, aged 11-12 years, and their parents across a variety of factors from physical activity to sleep.

 

The children and parents were given a snack box containing non-perishable items such as crackers, cheese, a muesli bar, biscuits, a tub of peaches and chocolate.

 

The quantity/number and variety of snack food items and the container sizes that the food was presented in varied. Children and parents ate separately and at different times.

 

Researchers recorded how much food each child and parent left in the box uneaten, and calculated the total grams and kilojoules consumed.

 

"Children who were offered more snack items consumed considerably more energy and a slightly higher food mass. Manipulating box/container size had little effect on consumption," she said.

 

The impact on adults was little, however Dr Kerr said adults were more aware that they were being observed and this may have impacted their eating behaviour.

 

Dr Kerr said further research should be done with parents and community leaders to better understand the use and purpose of snack food items in the face of time pressures, marketing, and child preferences.

 

"Although there is sometimes a place for snack items to bridge the gap between main meals, our results reinforce calls to educate parents and schools about appropriate snack items and amounts of food to offer children," she said.

 

"Our research indicates that more attention and resources should be directed to toward offering children smaller amounts of food and, specifically, fewer and less variety of energy-dense foods and pre-packaged items. Interventions should not solely invest in reducing dishware size in the expectation that this will lead to reduced intake of snack foods."

https://www.sciencedaily.com/releases/2019/07/190719105511.htm

Should obesity be recognized as a disease?

July 17, 2019

Science Daily/BMJ

With obesity now affecting almost a third (29%) of the population in England, and expected to rise to 35% by 2030, should we now recognise it as a disease? Experts debate the issue in The BMJ today.

 

Obesity, in which excess body fat has accumulated to such an extent that health may be adversely affected, meets the dictionary definition of disease, argue Professor John Wilding at the University of Liverpool and Vicky Mooney, representing the European Coalition for People living with Obesity (ECPO).

 

They point out that more than 200 genes influence weight, and most of these are expressed in the brain or in adipose tissue. "Thus body weight, fat distribution, and risk of complications are strongly influenced by biology -- it is not an individual's fault if they develop obesity."

 

They argue that the recent rapid increase in obesity is not due to genetics but to an altered environment (food availability and cost, physical environment, and social factors).

 

Yet the widespread view is that obesity is self inflicted and that it is entirely the individual's responsibility to do something about it, while healthcare professionals seem ill informed on the complexity of obesity and what patients with obesity want.

 

Recognising obesity as a chronic disease with severe complications rather than a lifestyle choice "should help reduce the stigma and discrimination experienced by many people with obesity," they add.

 

They disagree that labelling a high proportion of the population as having a disease removes personal responsibility or may overwhelm health services, pointing out that other common diseases, such as high blood pressure and diabetes, require people to take action to manage their condition.

 

They suggest that most people with obesity will eventually develop complications, and those who do not could be considered as not having disease. "But unless we accept that obesity is a disease, we are not going to be able to curb the epidemic," they conclude.

 

But Dr Richard Pile, a GP with a special interest in cardiology and Clinical Lead for Prevention for Herts Valleys Clinical Commissioning Group, argues that adopting this approach "could actually result in worse outcomes for individuals and society."

 

He believes that the dictionary definition of disease "is so vague that we can classify almost anything as a disease" and says the question is not whether we can, but whether we should, and to what end.

 

If labelling obesity as a disease was harmless then it wouldn't really matter, he writes. But labelling obesity as a disease "risks reducing autonomy, disempowering and robbing people of the intrinsic motivation that is such an important enabler of change."

 

There is an important difference psychologically between having a risk factor that you have some responsibility for and control over and having a disease that someone else is responsible for treating, he says.

 

What's more, making obesity a disease "may not benefit patients, but it will benefit healthcare providers and the pharmaceutical industry when health insurance and clinical guidelines promote treatment with drugs and surgery," he warns.

 

While self determination is key in enabling change, "we should acknowledge that the origins of obesity for most people are social, and so too is the solution," he adds. "If people meet, shop, cook, eat, and engage in activities together the end result will be improved wellbeing and reducing obesity will be a consequential beneficial side effect."

 

Classifying obesity as a disease is neither essential nor beneficial. It's much more complicated than that, he concludes.

https://www.sciencedaily.com/releases/2019/07/190717195401.htm

Early and ongoing experiences of weight stigma linked to self-directed weight shaming

New study identifies key characteristics of people who internalize weight bias

July 15, 2019

Science Daily/University of Pennsylvania School of Medicine

Weight bias is a common form of prejudice against people who are viewed as having excess weight. Some individuals who struggle with weight may internalize the stigma directed toward them, blaming and devaluing themselves because of their weight. While it's known that weight "self-stigma" is associated with poor mental and physical health, it isn't clear who is most prone to this internalization. In a new study published today in Obesity Science and Practice, researchers at Penn Medicine and the University of Connecticut Rudd Center for Food Policy and Obesity surveyed more than 18,000 adults enrolled in the commercial weight management program WW International (formerly Weight Watchers Inc.), and found that participants who internalized weight bias the most tended to be younger, female, have a higher body mass index (BMI), and have an earlier onset of their weight struggle. Participants who were black or had a romantic partner had lower levels of internalization.

 

"We don't yet know why some people who struggle with their weight internalize society's stigma and others do not," said the study's lead author Rebecca Pearl, PhD, an assistant professor of Psychology in Psychiatry in the Perelman School of Medicine at the University of Pennsylvania. "These findings represent a first step toward helping us identify, among people trying to manage their weight, who may be most likely to self-stigmatize. People who are trying to lose weight may be among the most vulnerable to weight self-stigma, but this issue is rarely discussed in treatment settings."

 

Research has found that, beyond the effects of BMI and depression, self-directed weight stigma is associated with increased risk for cardiovascular and metabolic disease. In this study -- the largest investigation of weight self-stigma in the world -- researchers surveyed adults to identify key characteristics and experiences of people who internalize weight bias.

 

Participants recalled when in their life they experienced weight stigma from other people, how frequent and how upsetting the experiences were, and who it was that called them names, rejected them, or denied them an opportunity simply because of their weight. Results showed that almost two-thirds of the participants reported experiencing weight stigma at least once in their life, and almost half reported experiencing these events when they were children or teens. The researchers examined the relationships between these experiences and levels of self-directed stigma.

 

Participants who reported experiencing weight stigma from others had higher levels of internalized weight bias than those who reported no experiences of weight stigma. Researchers say this was particularly true for participants who had weight-stigmatizing experiences early in life and continued to have these upsetting experiences as adults. People who experienced weight stigma from family members or friends, or from those in their workplace, community, or health care setting, also had greater evidence of weight self-stigma compared to participants who did not encounter weight stigma from those sources.

 

"Our findings can inform ways to support people who are experiencing or internalizing weight stigma, including opportunities to address weight stigma as part of weight management and healthy lifestyle programs," said the study's principal investigator Rebecca Puhl, PhD, a professor of Human Development and Family Sciences at the University of Connecticut.

 

The study sample, although the largest to date, represented only a small percentage of WW members, so the findings may not generalize to all members or to adults trying to lose weight in other ways. Some prior research has suggested that people who internalize weight bias may have worse long-term weight loss outcomes, but more research on this topic is needed.

 

In addition, Pearl's team is developing a psychological intervention for weight self-stigma that can be incorporated into weight management.

https://www.sciencedaily.com/releases/2019/07/190715075424.htm

Seeing greenery linked to less intense and frequent unhealthy cravings

July 12, 2019

Science Daily/University of Plymouth

New research shows that being able to see green spaces from your home is associated with reduced cravings for alcohol, cigarettes and harmful foods.

 

Being able to see green spaces from your home is associated with reduced cravings for alcohol, cigarettes and harmful foods, new research has shown.

 

The study, led by the University of Plymouth, is the first to demonstrate that passive exposure to nearby greenspace is linked to both lower frequencies and strengths of craving.

 

It builds on previous research suggesting exercising in nature can reduce cravings, by demonstrating the same may be true irrespective of physical activity.

 

Researchers say the findings add to evidence that points to the need to protect and invest in green spaces within towns and cities, in order to maximise the public health benefits they may afford. They also suggest the causality of this link needs to be investigated further.

 

The study, published in the journal Health & Place, is the first to investigate the relationship between exposure to natural environments, craving for a range of appetitive substances and the experiencing of negative emotions or feelings.

 

It involved academics from the University's School of Psychology, with support from the European Centre for Environment and Human Health at the University of Exeter.

 

Leanne Martin, who led the research as part of her Master's degree in Plymouth, said: "It has been known for some time that being outdoors in nature is linked to a person's wellbeing. But for there to be a similar association with cravings from simply being able to see green spaces adds a new dimension to previous research. This is the first study to explore this idea, and it could have a range of implications for both public health and environmental protection programmes in the future."

 

For the research, participants completed an online survey that explored the relationships between various aspects of nature exposure, cravings.

 

Among other things, it measured the proportion of greenspace in an individual's residential neighbourhood, the presence of green views from their home, their access to a garden or allotment; and their frequency of use of public greenspaces.

 

The results showed that having access to a garden or allotment was associated with both lower craving strength and frequency, while residential views incorporating more than 25% greenspace evoked similar responses.

 

The study also measured physical activity undertaken within the same time frame that cravings were assessed, showing the reduced craving occurred irrespective of physical activity level.

 

Dr Sabine Pahl, Associate Professor (Reader) in Psychology, added: "Craving contributes to a variety of health-damaging behaviours such as smoking, excessive drinking and unhealthy eating. In turn, these can contribute to some of the greatest global health challenges of our time, including cancer, obesity and diabetes. Showing that lower craving is linked to more exposure to green spaces is a promising first step. Future research should investigate if and how green spaces can be used to help people withstand problematic cravings, enabling them to better manage cessation attempts in the future."

https://www.sciencedaily.com/releases/2019/07/190712120211.htm

Exercise improves brain function in overweight and obese individuals

July 9, 2019

Science Daily/Society for the Study of Ingestive Behavior

New findings out of the University of Tübingen show that, on top of its benefits for metabolism, mood, and general health, exercise also improves brain function. In recent studies, researchers learned that obese and overweight individuals are prone to insulin resistance in the brain, where it provides information about current nutritional status, as well as the rest of the body. So researchers wanted to know whether exercise can improve insulin sensitivity in the brain and improve cognition in overweight individuals.

 

In the current study, led by Dr. Stephanie Kullmann, 22 sedentary adults with overweight or obesity (an average BMI of 31) underwent two brain scans before and after an 8-week exercise intervention, including cycling and walking. Brain function was measured before and after using an insulin nasal spray to investigate insulin sensitivity of the brain. Participants were also assessed for cognition, mood, and peripheral metabolism.

 

Even though the exercise intervention only resulted in a marginal weight loss, brain functions important for metabolism "normalized" only after 8-weeks. Exercise increased regional blood flow in areas of the brain important for motor control and reward processes, both of which depend on the neurotransmitter dopamine. Dopamine is an important neurotransmitter for learning new motor skills and in reward-related learning and this research shows that exercise significantly improves dopamine-related brain function. One area in particular, the striatum, had enhanced sensitivity to insulin after the 8-weeks of exercise such that the brain response of a person with obesity after exercise training resembled the response of a person with normal-weight. Interestingly, the greater the improvement in brain function, the more belly fat a person lost during the course of the exercise intervention. Behaviorally, participants reported an improvement in mood and task switching, which is an indicator for improved executive function.

 

"The bottom line is that exercise improves brain function," said Kullmann. "And increasing insulin sensitivity in dopamine-related brain regions through exercise may help decrease the risk of a person to develop type 2 diabetes, along with the benefits for mood and cognition."

https://www.sciencedaily.com/releases/2019/07/190709171815.htm

'Lentils will help you run faster:' Communicating food benefits gets kids to eat healthier

May 8, 2019

Science Daily/Washington State University

Communicating food benefits to children that they can relate to may get them to eat healthier.

 

That's according to a study published today in the Journal of Nutrition Education and Behavior by Washington State University and Florida State University scientists.

 

The researchers found affirming statements like 'eat your lentils if you want to grow bigger and run faster' were more effective at getting kids to make healthy food choices than presenting the food repeatedly without conversation.

 

In fact, kids ate twice as much healthy food when they were told how it would benefit them in terms they could understand as opposed to when they were given the food with no contextual information.

 

"Every child wants to be bigger, faster, able to jump higher," said Jane Lanigan, associate professor in the WSU Department of Human Development and lead author of the study. "Using these types of examples made the food more attractive to eat."

 

Previous research shows that offering foods repeatedly increases the likelihood that kids will try something new. But that research didn't look at the context of those offerings, Lanigan said.

 

In their study, Lanigan and her colleagues wanted to see if child-centered nutrition phrases (CCNPs), affirmative statements that simply convey the benefits of healthy food, influenced young children to make healthier food choices. The phrases focus on goals children have and are based on accurate nutrition information.

 

The WSU and FSU research team ran an experiment where they offered healthy foods to a group of three-to-five-year old children for six weeks.

 

Before beginning, the 87 children in the experiment ranked how much they liked four foods chosen from different food groups including, green peppers (vegetable), tomatoes (vegetables), quinoa (grain), and lentils (protein).

 

The kids were then offered two of the foods they liked the least twice a week. Over the six-week experiment, the researchers presented the children one of their low-rated foods with pre-selected age-appropriate facts about the benefits of the food. The other food was merely given to them to taste. A coin flip determined which food would be paired with the CCNP. The experiment was built into the kids' normal class routine, Lanigan said.

 

The researchers then measured how much the kids ate at three times: pre-test, post-test, and one month after the study ended. The immediate post-test showed no result, likely because the kids "got sick of eating the same foods," Lanigan said.

 

Results and impact

 

The month-after measurement told a different story.

 

"We found that a month later, the kids ate twice as much of their CCNP food with the repeated exposure compared to the food without the positive words," Lanigan said. "For example, when we presented lentils we would say, 'This will help you grow bigger and run faster."

 

Over time, Lanigan and colleagues' study shows that using CCNPs is likely to increase the amount of healthy food that children eat.

 

"I have two kids and I probably could have done things differently when trying to get them to eat healthier," Lanigan said. "We wanted to fill a gap, where parents are often told what their kids should be eating but not how to get them to eat it. And that's really important."

https://www.sciencedaily.com/releases/2019/05/190508093734.htm

Fat fruit flies: High-sugar diet deadens sweet tooth; promotes overeating, obesity in flies

May 7, 2019

Science Daily/University of Michigan

Some research suggests that one reason people with obesity overeat is because they don't enjoy food -- especially sweets -- as much as lean people.

 

But it's not understood if obesity itself or eating certain foods causes taste changes, or how those changes impact appetite and obesity.

 

For clues, University of Michigan researchers turned to Drosophila melanogaster -- fruit flies -- in a study appearing May 7 in Cell Reports.

 

They discovered that after feeding fruit flies a high-sugar diet, the flies' taste neurons triggered a molecular chain-reaction that hampered their ability to taste sweets, which in turn fueled overeating and obesity. Further, eating sugar caused the taste changes, not the metabolic consequences of obesity or the sweet taste of food.

 

The fly findings are significant because if people respond similarly to sugar, researchers are closer to understanding how too much sugar contributes to overeating and obesity. And, because these are molecular changes, it supports the idea that overeating is at least partly beyond our control.

 

While it's impossible to measure fruit flies' "enjoyment" of food, they certainly ate more on the high-sugar diet, said principal investigator Monica Dus, U-M associate professor of molecular, cellular, and developmental biology.

 

And yes -- fruit flies do become obese, said Christina May, first author of the study and a doctoral student in Dus' lab. Flies and humans share other surprising similarities: Both love sugar and fat and produce dopamine upon eating it, and their brain cells use many of the same proteins and molecules humans do, for the same things.

 

The researchers tested their findings in several ways. First, they fed flies that were genetically obese but never exposed to high dietary sugar, and their taste didn't change. However, when they fed sugar equivalent to a cookie to flies unable to store fat, they stayed thin but still lost the ability to taste sweets.

 

"That's really amazing because it tells you their ability to taste sweets changed because of what they're eating, not because they're becoming obese," May said.

 

To find out if the sugar or the sweet taste of food caused taste changes, the researchers fed flies a diet similar to artificially sweetened diet soda. Only the files eating real sugar lost their sweet-tasting ability.

 

"We know it's something specific about the sugar in the diet that's making them lose their taste," Dus said.

 

The researchers identified the molecule O-GlcNAc transferase, a sugar sensor located in the flies' taste buds that keeps track of how much sugar is in the cells. OGT has previously been implicated in obesity-related conditions like diabetes and heart disease in humans.

 

They also manipulated flies' taste cells so that even on a high-sugar diet they wouldn't lose taste, and those flies didn't overeat despite loads of sugar.

 

"This means the changes in taste, at least in flies, are pretty important to drive overconsumption and weight gain," Dus said. "Do changes in taste also play a role in the overconsumption that we see when humans and other animals find themselves in food environments high in sugar?"

 

Study co-author Anoumid Vaziri, a doctoral student in Dus' lab, said the findings "not only shed light on sugar-diet-dependent neural mechanisms of overeating and obesity, but provide a platform to study the underlying molecular mechanisms that drive changes in neural activity."

 

So what's this mean for people who are overweight, dieting or feel addicted to sugar? It's possible that in the long-term, a drug or other intervention that corrects dietary sweetness and preserves the sweet taste sensation could someday help curb obesity and the associated chronic diseases. But that is years away, May said.

 

More importantly, if humans respond the same way as the flies, the research suggests that changing the amount of sugar in the diet can help regulate our food intake, Dus said. Much of the sugar we eat is hidden in processed food, and it's important to keep it to a minimum, she added.

 

"I think if you try to keep added sugars out of your diet, you'll probably be totally fine, you won't have problems with changing taste and overeating," May said. "All of us try to avoid the added sugars. That's important."

 

Dus said that future research will examine sugar's impact on the brain's reward circuits to learn what causes overeating, and how sugar changes the brain on a molecular level.

https://www.sciencedaily.com/releases/2019/05/190507121423.htm

Being a car commuter with obesity linked to a 32% increased early death risk

April 27, 2019

Science Daily/European Association for the Study of Obesity

New research presented at this year's European Congress on Obesity in Glasgow, Scotland (28 April -- 1 May) shows that individuals with obesity who commute by car have a 32% higher risk of death, from any cause, compared with those individuals with a normal weight and commute via cycling and walking. The study is by Edward Toke-Bjolgerud, University of Glasgow, UK, and colleagues.

 

Previous work, using UK Biobank data, has shown that active commuting, mainly cycling, was associated with a 50% lower risk of death, from any cause, and heart disease compared to car commuting. Since 57% of men and 66% of women in the UK are overweight or obese -- a condition linked with a range of poor health outcomes -- the authors of this new research aimed to investigate how different modes of active commuting (car, cycling, walking, mixed-mode) might alter the association between obesity and adverse health outcomes.

 

Their analysis includes 163,149 UK Biobank participants who have been followed up for a mean of 5 years. The age range was 37 to 73 years and 50.8% were women. Obesity was defined as a body mass index (BMI) (kg/m2) of greater than 30. Active commuting to and from work was self-reported and people classified in one of the following groups: car commuters, walking and cycling (active-mixed), cycling-only and walking-only. The health outcomes of interest were death from any cause, death due to heart disease and hospital admission due to non-fatal heart disease.

 

Dr Carlos Celis, from the British Heart Foundation Glasgow Cardiovascular Research Centre at the University of Glasgow and lead investigator of this work, reported that during the follow-up a total of 2,425 participants died and 7,973 developed heart disease. Compared with having a healthy body weight and reported mixed active commuting (walking and cycling to and from work; reference group), being obese combined with car commuting was associated with a 32% higher risk for premature death, a doubling of risk of heart disease mortality and a 59% increase in risk non-fatal heart diseases.

 

In contrast, those people with obesity who reported being active commuters had a risk of death from any cause that was similar to normal weight active commuters, suggesting that cycling or walking to and from work could reduce the detrimental effect of obesity. However, the risk of heart disease was still increased by 82% in active commuters with obesity compared with normal weight active commuters.

 

The authors conclude: "Our findings, if causal, suggest that people with overweight or obesity could potentially decrease the risk of premature mortality if they engage in active commuting."

 

They add: "Regardless of your body weight, being physically active could partly reduce the excess risk associated with obesity. However, compared to other forms of physical activity -- such as gyms and exercises classes -- active commuting can be implemented and fitted within our daily routines, often with no additional cost, but at the same time could increase our overall physical activity levels and therefore help to meet the current physical activity recommendations for health."

https://www.sciencedaily.com/releases/2019/04/190427201946.htm

Obesity and emotional problems appear to develop together from age 7

April 27, 2019

Science Daily/European Association for the Study of Obesity

Obesity and emotional problems, such as feelings of low mood and anxiety, tend to develop hand-in-hand from as young as age 7 years, according to new research being presented at this year's European Congress on Obesity (ECO) in Glasgow, UK (28 April-1 May).

 

The analysis of a large nationally representative sample of over 17,000 children in the UK finds that regardless of their socioeconomic status, girls and boys with obesity at age 7 were at greater risk of emotional problems at age 11, which in turn, predicted high body mass index (BMI) at 14 years of age.

 

While the study did not investigate the reasons why obesity and emotional problems develop together during childhood, the researchers say that a range of factors are likely to be involved.

 

"Children with higher BMI may experience weight-related discrimination and poor self-esteem, which could contribute to increased depressive symptoms over time (as has been shown in adults), while depression may lead to obesity through increased emotional eating of high-calorie comfort foods, poor sleep patterns, and lethargy," explains Dr Charlotte Hardman from the University of Liverpool, UK, who co-led the study. "Our findings highlight the importance of early interventions that target both weight and mental health and minimise negative outcomes later in childhood."

 

Adolescence is a key developmental period for both obesity and emotional problems. But how they relate to each other over time is unclear, and little research has focused on the onset and co-occurrence of these disorders through childhood and adolescence.

 

Lower socioeconomic status is strongly associated with both obesity and poor mental health, but it is unknown whether the association between these two health outcomes is merely a function of shared socioeconomic disadvantage.

 

In this study, researchers used statistical modelling to assess associations between obesity and emotional problems in 17,215 children born in the UK between 2000 and 2002, who are taking part in the Millennium Cohort Study -- a nationally representative, UK birth cohort study of over 19,000 individuals born at the start of the millennium.

 

Information on children's height and weight (BMI) were collected at ages 3, 5, 7, 11 and 14 years, and parents filled in a questionnaire on their children's emotional problems such as feelings of low mood and anxiety. The researchers adjusted for a range of factors known to affect both obesity and mental health including gender, ethnicity, socioeconomic status, and behavioural problems, as well as parents' mental health.

 

Rates of obesity and emotional problems increased gradually throughout childhood and adolescence. Almost 8% (814/10,767 children with available data) of young people were obese by the age of 14, and around twice that number were reported to have had feelings of low mood and anxiety (1369/10,123).

 

By adolescence, around a fifth (137/693) of those with obesity also had high levels of emotional distress.

 

The analysis found that obesity and emotional problems tended to occur together in mid-childhood and adolescence between the 7 and 14 years of age, but not in early childhood (3 to 5 years of age).

 

On average, girls had higher BMIs and emotional symptoms than boys from 7 to 14 years of age, but co-occurrence and development of obesity and emotional problems were similar in both girls and boys.

 

After taking socioeconomic status into account, the association between BMI and emotional problems was reduced slightly, suggesting that socioeconomic disadvantage may partly explain the link between children's obesity and poor mental health.

 

"The shared socioeconomic risk in the development of obesity and poor mental ill-health could be explained by numerous factors. For instance, socioeconomically deprived areas tend to have poorer access to healthy food and green spaces, which may contribute to increased obesity and emotional problems, and compound the effects of family-level socioeconomic disadvantage," says Dr Praveetha Patalay from University College London, UK who co-led the research.

 

"As both rates of obesity and emotional problems in childhood are increasing, understanding their co-occurrence is an important public health concern, as both are linked with poor health in adulthood. The next steps are to understand the implications of their co-occurrence and how to best intervene to promote good health."

 

The authors acknowledge that their findings show observational associations, so conclusions about cause and effect cannot be drawn. They point to several limitations, including unmeasured confounding, parent report, and the attrition rate that may have influenced the results.

https://www.sciencedaily.com/releases/2019/04/190427201943.htm

Nationwide study suggests obesity as an independent risk factor for anxiety and depression in young people

April 27, 2019

Science Daily/European Association for the Study of Obesity

Obesity is linked with an increased risk of developing anxiety and depression in children and adolescents, independent of traditional risk factors such as parental psychiatric illness and socioeconomic status, according to new research being presented at this year's European Congress on Obesity (ECO) in Glasgow, UK (28 April-1 May).

 

The nationwide study comparing over 12,000 Swedish children who had undergone obesity treatment with more than 60,000 matched controls found that girls with obesity were 43% more likely to develop anxiety or depression compared to their peers in the general population. Similarly, boys with obesity faced a 33% increased risk for anxiety and depression compared to their counterparts.

 

"We see a clear increased risk of anxiety and depressive disorders in children and adolescents with obesity compared with a population-based comparison group that cannot be explained by other known risk factors such as socioeconomic status and neuropsychiatric disorders," says Ms. Louise Lindberg from the Karolinska Institutet, Stockholm, Sweden who led the research. "These results suggest that children and adolescents with obesity also have an increased risk of anxiety and depression, something that healthcare professionals need to be vigilant about."

 

Anxiety and depression are reported to be more common in children with obesity than in children of normal weight, but it is unclear whether the association is independent of other known risk factors. Previous studies are hampered by methodological limitations including self-reported assessment of anxiety, depression, and weight.

 

To provide more evidence, researchers from the Karolinska Institutet in Sweden conducted a nationwide population-based study to investigate whether obesity is an independent risk factor for anxiety or depression. 12,507 children aged 6-17 years from the Swedish Childhood Obesity Treatment Register between 2005 and 2015 were compared to 60,063 controls from the general population matched for sex, year of birth, and living area.

 

The research team adjusted for a range of factors known to affect anxiety and depression including migration background, neuropsychiatric disorders, parental psychiatric illness, and socioeconomic status. A total of 4,230 children and adolescents developed anxiety or depression over an average of 4.5 years.

 

Obesity was clearly linked with higher risk of anxiety and depression in childhood and adolescence. Girls (11.6% vs 6.0%) and boys (8.0% vs 4.1%) with obesity were more likely to be diagnosed with anxiety and depression than those in the general population over the study period.

 

In further analyses, excluding children with neuropsychiatric disorders or a family history of anxiety or depression, the risks were even higher. In particular, boys with obesity were twice as likely to experience anxiety or depression as their normal-weight peers -- whilst girls with obesity were 1.5 times more likely.

 

"Given the rise of obesity and impaired mental health in young people, understanding the links between childhood obesity, depression and anxiety is vital," says Ms. Lindberg. "Further studies are needed to explain the mechanisms behind the association between obesity and anxiety/depression."

 

The authors acknowledge that this is an observational study and cannot prove that obesity causes depression or anxiety but only suggests the possibility of such an effect. They point to several limitations including that there is no weight and height data in the comparison group; unmeasured confounding may have influenced results; and that rates of anxiety and depression may be underestimated since a large proportion of individuals suffering from these conditions do not seek medical care.

https://www.sciencedaily.com/releases/2019/04/190427201941.htm

Comfort food leads to more weight gain during stress

April 25, 2019

Science Daily/Garvan Institute of Medical Research

It's no secret that overindulging on high-calorie foods can be detrimental to health, but it turns out that under stress, watching what you eat may be even more important. A team led by Professor Herbert Herzog, Head of the Eating Disorders laboratory at the Garvan Institute of Medical Research, discovered in an animal model that a high-calorie diet when combined with stress resulted in more weight gain than the same diet caused in a stress-free environment. The researchers revealed a molecular pathway in the brain, controlled by insulin, which drives the additional weight gain.

 

They publish their findings in the journal Cell Metabolism on 25 April 2019 (EST).

 

"This study indicates that we have to be much more conscious about what we're eating when we're stressed, to avoid a faster development of obesity," says Professor Herzog.

 

The brain's comfort food 'centre'

Some individuals eat less when they're stressed, but most will increase their food intake -- and crucially, the intake of calorie-dense food high in sugar and fat.

 

To understand what controls this 'stress eating', the Garvan researchers investigated different areas of the brain in mice. While food intake is mainly controlled by a part of the brain called the hypothalamus, another part of the brain -- the amygdala -- processes emotional responses, including anxiety.

 

"Our study showed that when stressed over an extended period and high calorie food was available, mice became obese more quickly than those that consumed the same high fat food in a stress-free environment," explains Dr Kenny Chi Kin Ip, lead author of the study.

 

At the centre of this weight gain, the scientists discovered, was a molecule called NPY, which the brain produces naturally in response to stress to stimulate eating in humans as well as mice.

 

"We discovered that when we switched off the production of NPY in the amygdala weight gain was reduced. Without NPY, the weight gain on a high-fat diet with stress was the same as weight gain in the stress-free environment," says Dr Ip. "This shows a clear link between stress, obesity and NPY."

 

A downward spiral to obesity

To understand what might control the NPY boost under stress, the scientists analysed the nerve cells that produced NPY in the amygdala and found they had receptors, or 'docking stations', for insulin -- one of the hormones which control our food intake.

 

Under normal conditions, the body produces insulin just after a meal, which helps cells absorb glucose from the blood and sends a 'stop eating' signal to the hypothalamus feeding centre of the brain.

 

In the study, the scientists discovered that chronic stress alone raised the blood insulin levels only slightly, but in combination with a high-calorie diet, the insulin levels were 10 times higher than mice that were stress-free and received a normal diet.

 

The study showed that these prolonged, high levels of insulin in the amygdala caused the nerve cells to become desensitised to insulin, which stopped them from detecting insulin altogether. In turn, these desensitised nerve cells boosted their NPY levels, which both promoted eating and reduced the bodies' normal response to burn energy through heat, the study showed.

 

"Our findings revealed a vicious cycle, where chronic, high insulin levels driven by stress and a high-calorie diet promoted more and more eating," explains Professor Herzog. "This really reinforced the idea that while it's bad to eat junk food, eating high-calorie foods under stress is a double whammy that drives obesity."

 

While insulin imbalance is at the centre of a number of diseases, the study indicates that insulin has more wide-spread effects in the brain than previously thought.

 

"We were surprised that insulin had such a significant impact on the amygdala," says Professor Herzog. "It's becoming more and more clear that insulin doesn't only impact peripheral regions of the body, but that it regulates functions in the brain. We're hoping to explore these effects further in future."

https://www.sciencedaily.com/releases/2019/04/190425143610.htm

Obesity linked with differences in form and structure of the brain

Science Daily/April 23, 2019

Radiological Society of North America

Researchers using sophisticated MRI technology have found that higher levels of body fat are associated with differences in the brain's form and structure, including smaller volumes of gray matter, according to a study published in the journal Radiology. The findings add important information to our understanding of the connection between obesity and negative health consequences such as dementia.

 

"MRI has shown to be an irreplaceable tool for understanding the link between neuroanatomical differences of the brain and behavior," said study lead author Ilona A. Dekkers, M.D., from Leiden University Medical Center in Leiden, the Netherlands. "Our study shows that very large data collection of MRI data can lead to improved insight into exactly which brain structures are involved in all sorts of health outcomes, such as obesity."

 

Obesity represents one of the world's most challenging public health problems. The global pandemic has led to a greater incidence of cardiovascular disease and type 2 diabetes. Previous studies have also tied obesity to an increased risk of accelerated cognitive decline and dementia, suggesting that the disease causes changes to the brain.

 

To learn more about these changes, the researchers analyzed brain imaging results from more than 12,000 participants in the UK Biobank study, a major trial begun in 2006 to learn more about the genetic and environmental factors that influence disease. The brain scans used sophisticated MRI techniques that provided information on both the neuron-rich gray matter and the white matter, often referred to as the wiring of the brain.

 

The results show some clear associations in the patients between body fat percentage and brain form and structure, also known as its morphology.

 

"We found that having higher levels of fat distributed over the body is associated with smaller volumes of important structures of the brain, including gray matter structures that are located in the center of the brain," Dr. Dekkers said. "Interestingly, we observed that these associations are different for men and women, suggesting that gender is an important modifier of the link between fat percentage and the size of specific brain structures."

 

Analysis showed that, in men, higher total body fat percentage correlated with lower gray matter volume overall and in specific structures involved in the reward circuitry and the movement system. In women, total body fat only showed a significant negative association with the globus pallidus, a structure involved in voluntary movement. For both men and women, higher total body fat percentage increased the likelihood of microscopic changes to the brain's white matter.

 

The ramifications of these findings, not yet fully clear, could be of significant importance. Smaller gray matter volume suggests loss of neurons, and changes to the white matter could adversely affect the transmission of signals within brain networks. Since the smaller subcortical grey matter volumes are also known to play a role in the food-reward circuitry, these changes may also make it more difficult for obese people to control their weight, Dr. Dekkers said, although more research will be needed to support that connection.

 

The reason for obesity's adverse effects on the brain are not precisely known. Research has shown that the low-grade inflammation characteristic of obesity can have harmful effects on brain tissue. There is evidence that cellular responses produced in the brain due to inflammation may be behind these effects.

 

The study looked at overall body fat percentage and did not distinguish between the different types of fat in the body, which Dr. Dekkers said may be an area for additional research. Of particular interest is the visceral white fat found around the abdominal organs. This type of fat, also known as belly fat, is part of metabolic syndrome, a group of factors that increase the risk of cardiovascular disease and diabetes.

 

"For future research, it would be of great interest whether differences in body fat distribution are related to differences in brain morphological structure, as visceral fat is a known risk factor for metabolic disease and is linked to systemic low-grade inflammation," said the study's senior author, Hildo Lamb, M.D., Ph.D., director of the Cardio Vascular Imaging Group of Leiden University Medical Center.

https://www.sciencedaily.com/releases/2019/04/190423133736.htm

New insight into how obesity, insulin resistance can impair cognition

Science Daily/April 22, 2019

Medical College of Georgia at Augusta University

Obesity can break down our protective blood brain barrier resulting in problems with learning and memory, scientists report.

 

They knew that chronic activation of the receptor Adora2a on the endothelial cells that line this important barrier in our brain can let factors from the blood enter the brain and affect the function of our neurons.

 

Now Medical College of Georgia scientists have shown that when they block Adora2a in a model of diet-induced obesity, this important barrier function is maintained.

 

"We know that obesity and insulin resistance break down the blood brain barrier in humans and animal models, but exactly how has remained a mystery," says Dr. Alexis M. Stranahan, neuroscientist in the MCG Department of Neuroscience and Regenerative Medicine at Augusta University. Stranahan is corresponding author of the study published in The Journal of Neuroscience that provides new insight.

 

In the brain, adenosine is a neurotransmitter that helps us sleep and helps regulate our blood pressure; in the body it's also a component of the cell fuel adenosine triphosphate, or ATP. Adenosine also activates receptors Adora1a and Adora2a on endothelial cells, which normally supports healthy relationships between brain activity and blood flow.

 

Problems arise with chronic activation, particularly in the brain, which is what happens with obesity, says Stranahan.

 

People who have obesity and diabetes have higher rates of cognitive impairment as they age and most of the related structural changes are in the hippocampus, a center of learning and memory and Stranahan's focus of study. Fat is a source of inflammation and there is evidence that reducing chronic inflammation in the brain helps prevent obesity-related memory loss.

 

In a model that mimics what happens to some of us, young mice fed a high-fat diet got fat within two weeks, and by 16 weeks they had increases in fasting glucose and insulin concentrations, all signs that diabetes is in their future.

 

In the minute vasculature of the hippocampus, the investigators saw that obesity first increased permeability of the blood brain barrier to tiny molecules like fluorophore sodium fluorescein, or NaFl. Diet-induced insulin resistance heightened that permeability so that a larger molecule, Evans Blue, which has a high affinity for serum albumin, the most abundant protein in blood, also could get through.

 

When they looked with electron microscopy, they saw a changed landscape. Resulting diabetes promoted shrinkage of the usually tight junctions between endothelial cells and actual holes in those cells. They also saw muscular cells called pericytes that wrap around the exterior of microscopic blood vessels in the brain to give them more strength and help move blood along, start to lose their grip, so blood vessels start to lose their tone and become dysfunctional and inflamed. Pericytes are known to express higher levels of Adora2a than endothelial cells, Stranahan notes. The high-fat diet also promoted swelling of protrusions on astrocytes called end-feet, which also are part of the blood brain barrier. Astrocytes are brain cells that normally nurture neurons, but the pathological state of obesity also altered their form and support.

 

Angiogenesis, the body's natural attempt to make more blood vessels -- albeit usually dysfunctional, leaky ones -- in response to impaired blood and oxygen flow was happening in the hippocampus by 12 weeks, and upon close inspection, blood vessels were inflamed.

 

When they gave a drug to temporarily block Adora2a, it also blocked problems with barrier permeability. Whether that could work in humans and long term as a way to avoid cognitive decline in obese humans, remains to be seen, Stranahan notes.

 

Next they developed a mouse in which they could selectively knock Adora2a out of endothelial cells.

 

In this transgenic mouse, they turned off Adora2a in the endothelial cells at 12 weeks, and at 16 weeks, when mice should have been exhibiting cognitive impairment and a leaky blood brain barrier, they instead had normal cognition and barrier function and no inflammation.

 

When they compared the transgenic mice that were on a high- or low-fat diet, they found evidence that the increased permeability of blood vessels in the brain initiates the cycle of inflammation and cognitive impairment.

 

While it's typically hard to jump from mice to men, the fact that this type of work actually started with human findings likely means that avoiding insulin resistance could potentially halt the increased permeability of the blood brain barrier and decrease in cognitive function, Stranahan says.

 

"If an individual has already progressed to insulin resistance, these studies underscore the importance of controlling blood sugar levels and avoiding progressing to insulin deficiency (diabetes), which opens the blood brain barrier even further."

 

The scientists report that the relative accessibility of blood vessels in the brain may also make them a good avenue for preventing obesity's effects on the brain.

 

It also points to the reality that a variety of drugs given to obese patients may impact their brains to a higher degree, which might be something for patients and their doctors to consider. Stranahan notes that for drugs intended to take action in the brain, such as those for Alzheimer's, that could be a good thing but still needs to be considered. Some commonly prescribed drugs like prednisone, on the other hand, already are really good at getting through and can potentially be bad for the brain, she says.

 

Next steps in her lab include figuring out where the signal arises that chronically activates Adora2 in fat mice. She suspects it's actually a cascade that includes endothelial cells getting stressed, which increases their metabolism, which means they use more ATP, which can activate Adora2a and set in motion a vicious cycle that eventually takes its toll on the blood brain barrier.

 

The concept that obesity could affect the blood brain barrier started with people a dozen years ago when Swedish researchers found obese individuals had higher levels of the major antibody immunoglobulin G in their cerebrospinal fluid, when it should have been in their blood. It was an important finding that suggested that obesity and diabetes could enable things to get from the blood to the brain that should not, Stranahan says. Animal studies confirmed it was happening but, again, few studies have looked at why, Stranahan says.

 

Blood vessels come up from the body and get exceedingly small and fragile as they dive into the brain. While blood vessels that supply areas like our arms and heart are meant to be more porous so they can share plenty of glucose, oxygen and immune cells and other things the body needs, the vasculature in the brain, is supposed to be much more restrictive, letting comparatively little through.

 

"It's more like a gate than a barrier," says Stranahan, and it's a dynamic barrier at that, based on what the brain is up to. "It's got transporters that can move things across and what is happening in the brain and in the blood can change the way it operates."

 

She notes that the brain is a huge consumer, sucking up 70 to 80 percent of our oxygen and glucose, but also more fragile than other tissues, super sensitive even to our own immune cells.

 

"It's like a kid who grows up playing outside in the dirt is going to have a more robust immune system than a kid who grows up staying inside and playing video games," Stranahan says.

 

Cognitive tests on mice in the study included object recognition and maneuvering a water maze. The scientists looked at other normal functions, like simple motor functions, to see if there were other effects and, at least at those early time points, did not identify others.

https://www.sciencedaily.com/releases/2019/04/190422082253.htm

Bigger portions lead to preschoolers eating more over time

April 12, 2019

Science Daily/Penn State

Preschoolers may not be as good at resisting large portions of everyday foods as was previously thought, according to Penn State researchers.

 

In a study, the researchers examined whether children between the ages of three and five were susceptible to the portion size effect -- the tendency of people to eat more when larger portions are served.

 

They found that when served larger portions of typical meals or snacks, the children consumed more food, both by weight and calories.

 

Alissa Smethers, a doctoral student in nutritional sciences, said the findings -- recently published in the American Journal of Clinical Nutrition -- suggest that caregivers should pay close attention to not just the amount of food they serve but also the variety of food.

 

"It's hard to define portions that are appropriate for all preschoolers, since their calorie requirements vary due to differences in height, weight and activity level," Smethers said. "But it's a good idea to look at the proportions of different foods you're serving, with fruits and vegetables filling up half the plate and with smaller portions of more calorie-dense foods, as recommended in the USDA MyPlate nutrition guide."

 

Barbara Rolls, Helen A. Guthrie Chair and director of the Laboratory for the Study of Human Ingestive Behavior at Penn State, added that the results also suggest that the portion-size effect can be used strategically by caregivers to help children eat more fruits and vegetables.

 

"The positive side is that you can use the portion size effect strategically, for example by serving larger portions of fruits and vegetables to increase their consumption," Rolls said. "You can also serve them at the start of the meal or on their own as snacks. When there are no other foods competing with them, kids may be more likely to eat them."

 

Smethers said that while it was known that adults are likely to eat more when served larger portions of food over time, it was thought by some researchers that young children can sense how many calories from food they need and adjust their eating habits accordingly, a process called "self-regulation."

 

Previous studies have tested this theory by looking at children's eating habits at one meal or over a single day. But Smethers said it may take longer -- up to three to four days -- for self-regulation to kick in, and so she and the other researchers wanted to study the portion size effect in children across a full five days.

 

The researchers recruited 46 children between the ages of three and five from childcare centers at the University Park campus for the five-day study. All meals and snacks were provided for the children, who during one five-day period received baseline-sized portions -- based on Child and Adult Care Food Program requirements -- and during another period had portions that were increased in size by 50 percent.

 

"In the larger portion meals, we wanted to serve portion sizes that the children might encounter in their everyday lives," Smethers said. "For example, instead of getting four pieces of chicken nuggets, they would get six, for a 50 percent increase."

 

During both five-day periods, the children were allowed to eat as much or as little of their meals or snacks as they wanted. After the children were done eating, the leftover foods were weighed to measure how much each child consumed.

 

Additionally, each child wore an accelerometer throughout each five-day period to measure their activity levels, and the researchers measured their height and weight.

 

After analyzing the data, the researchers found that serving larger portions led to the children eating 16 percent more food than when served the smaller portions, leading to an extra 18 percent of calories.

 

"If preschoolers did have the ability to self-regulate their calorie intake, they should have sensed that they were getting extra over the five days and started eating less," Rolls said. "But we didn't see any evidence of that."

 

The researchers also found that children with higher BMI percentiles for their age were more likely to be influenced by larger portions. Additionally, the portion size effect seemed stronger in children with overweight or obesity than for children without.

 

"We found that while the portion size effect is powerful overall, some children seemed to be more susceptible to the effect than others," Smethers said. "Children who were rated by their parents as more responsive to food when it's in front of them were also affected more by portion size, while children who were rated as paying attention to whether or not they were actually hungry were less affected by portion size."

https://www.sciencedaily.com/releases/2019/04/190412110333.htm

People with obesity often 'dehumanized

April 3, 2019

Science Daily/University of Liverpool

New research, published in Obesity, has found that people with obesity are not only stigmatised, but are blatantly dehumanised.

 

Obesity is now very common in most of developed countries. Around one third of US adults and one quarter of UK adults are now medically defined as having obesity. However, obesity is a complex medical condition driven by genetic, environmental and social factors.

 

Previous research has suggested that people often hold stigmatising and prejudiced views about obesity.

 

This new research conducted at the University of Liverpool, led by Dr Inge Kersbergen and Dr Eric Robinson examined whether stigmatising views about obesity may be more extreme than previously shown. The research examined whether people believe that individuals with obesity are less evolved and human than those without obesity.

 

Methods used

As part of a recognised research approach employed in a number of other studies, more than 1500 participants, made up of people from the UK, USA and India, completed online surveys to indicate how evolved they consider different groups of people to be on a scale from 0-100.

 

The researchers also recorded the BMI of those completing the survey to find out whether blatant dehumanisation of obesity was more common among thinner people and investigated whether blatant dehumanisation predicted support for health policies that discriminate against people because of their body weight.

 

Results

Participants on average rated people with obesity as 'less evolved' and human than people without obesity. On average, participants placed people with obesity approximately 10 points below people without obesity. Blatant dehumanisation was most common among thinner participants, but was also observed among participants who would be medically classed as being 'overweight' or 'obese'.

 

People who blatantly dehumanised those with obesity were more likely to support health policies that discriminate against people because of their weight.

 

Eric Robinson, a Reader at the University of Liverpool, said: "This is some of the first evidence that people with obesity are blatantly dehumanised. This tendency to consider people with obesity as 'less human' reveals the level of obesity stigma.

 

"It's too common for society to present and talk about obesity in dehumanising ways, using animalistic words to describe problems with food (e.g. 'pigging out') or using images that remove the dignity of people living with obesity. Obesity is a complex problem driven by poverty and with significant genetic, psychological and environmental components. Blatant or subtle dehumanisation of any group is morally wrong and in the context of obesity, what we also know is that the stigma surrounding obesity is actually a barrier to making long-term healthy lifestyle changes."

 

Inge Kersbergen, now a research fellow at the University of Sheffield, said: "Our results expand on previous literature on obesity stigma by showing that people with obesity are not only disliked and stigmatised, but are explicitly considered to be less human than those without obesity. The fact that levels of dehumanisation were predictive of support for policies that discriminate against people with obesity suggests that dehumanisation may be facilitating further prejudice."

https://www.sciencedaily.com/releases/2019/04/190403113933.htm

Depression, obesity, chronic pain could be treated by targeting the same key protein

April 1, 2019

Science Daily/American Chemical Society

Major depression, obesity and chronic pain are all linked to the effects of one protein, called "FK506-binding protein 51," or FKBP51. Until now, efforts to inhibit this target have been hampered by the difficulty of finding something specific enough to do the job and not affect similar proteins. Now a research group has developed a highly selective compound that can effectively block FKBP51 in mice, relieving chronic pain and having positive effects on diet-induced obesity and mood. The new compound also could have applications in alcoholism and brain cancer.

 

The researchers will present their results today at the American Chemical Society (ACS) Spring 2019 National Meeting & Exposition.

 

"The FKBP51 protein plays an important role in depression, obesity, diabetes and chronic pain states," says Felix Hausch, Ph.D., the project's principal investigator. "We developed the first highly potent, highly selective FKBP51 inhibitor, called SAFit2, which is now being tested in mice. Inhibition of FKBP51 could thus be a new therapeutic option to treat all of these conditions."

 

Hausch, who is at the Technical University of Darmstadt, started the project when studies were published linking the protein to depression. "I was intrigued by the peculiar regulatory role it seemed to play in cells," he says. "And there was a known natural product that could serve as a starting point. Collectively, this looked like an interesting protein to work on."

 

FKBP51 is expressed in multiple places throughout the body, such as the brain, skeletal muscle tissue and fat. It also has multiple effects. For example, the protein can restrict the uptake of glucose and the browning of fat, so that the body stores fat instead of burning it. It also affects stress responses. So, Hausch and his colleagues figured that blocking this protein could be the key to developing drugs to treat a variety of conditions.

 

But FKBP51 looks a lot like its closest protein cousin, FKBP52. "These two proteins are very similar in structure, but they are doing opposing things in cells," Hausch says. "We have this yin-yang situation. Selectivity between these two proteins is thought to be crucial, but this is hard to achieve since the two proteins are so similar. We discovered that FKBP51 can change its shape in a way that FKBP52 can't, and this allowed the development of highly selective inhibitors."

 

The researchers have now used nuclear magnetic resonance techniques to detect a previously hidden binding site in FKBP51. The approach could help other researchers identify similar "cryptic" binding sites in challenging drug targets in the future, Hausch says.

 

His team is now testing SAFit2, the lead FKBP51 inhibitor they developed from these studies, in animals. "It indeed helps mice cope better in stressful situations," Hausch says. In mice, SAFit2 reduced stress hormone levels, promoted more active stress coping, was synergistic with antidepressants, protected against weight gain, helped normalize glucose levels and reduced pain in three animal models.

 

According to Hausch, much more needs to be done to get FKBP1 inhibitors to the point where they could be used as a drug molecule in human testing. In the meantime, the team is also exploring FKBP51 inhibitors in other applications. So far, the group has conducted a number of mouse studies on the involvement of FKBP51 in alcoholism, but results are still preliminary. In addition, Hausch points out that certain types of glioblastoma tumors overexpress FKBP51. He hopes that this result indicates FKBP51 inhibitors could be used in cancer treatment, when patients' tumors mutate beyond current drugs' capacity to treat them. "We may be able to resensitize them to different types of chemotherapy using these specific inhibitors," he says.

https://www.sciencedaily.com/releases/2019/04/190401075208.htm

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