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

Scientists find brain mechanism that naturally combats overeating

March 28, 2019

Science Daily/Rockefeller University

Studying a brain region involved in memory, researchers discovered a set of neurons that help mice control their appetite.

Food is, generally speaking, a good thing. In addition to being quite tasty, it is also necessary for survival. That's why animals have evolved robust physiological systems that attract them to food and keep them coming back for more.

Now, research in mice reveals the existence of brain cells that have the opposite effect, curbing an animal's impulse to eat. Published in Neuron, the study shows that these cells also play a role in regulating memory, and are part of a larger brain circuit that promotes balanced eating.

The belly and the brain

Historically, researchers have thought of feeding as a visceral, instinctive process: An animal smells or sees an appealing snack and, without hesitation, proceeds to eat said snack. However, an increasingly detailed picture is now emerging in which mental processes inform animals' decision to either consume or refuse a meal.

A human, for example, may consider, "I'm supposed to be at brunch in 20 minutes, so I better save my appetite." Though other mammals may not have the equivalent internal monologue, there is reason to suspect that their eating habits do involve complex cognition. For example, research has shown that defects in the hippocampus -- a brain area involved in memory -- can alter feeding behavior, suggesting that past experiences influence an animal's attraction to food.

Building on this research, Estefania Azevedo, a postdoctoral associate in the lab of Jeffrey M. Friedman, recently identified a group of hippocampal cells, known as hD2R neurons, that become active whenever a mouse is fed. Collaborating with Paul Greengard, the Vincent Astor Professor, and Jia Cheng, a postdoctoral associate in his lab, the researchers also found that when these neurons were stimulated, mice ate less; and when they were silenced, they ate more. In short, hD2R neurons respond to the presence of food by deterring animals from eating that food.

Interpreting these findings, Azevedo says that, though animals usually benefit from eating the snacks in front of them, in some instances it is useful to exercise restraint. For example, if an animal has recently eaten, then searching for another meal is both unnecessary and risky, as foraging exposes animals to predators. The newly discovered neurons, it seems, help animals stop feeding when it no longer behooves them.

"These cells keep an animal from overeating," says Azevedo. "They appear to make eating less rewarding and, in that sense, are tuning the animal's relationship to food."

Everything in moderation

In the wild, you can't eat unless you know where to find food. Fortunately, brains are quite good at remembering the location of past meals: When an animal encounters sustenance in a particular locale, it makes a mental connection between the place and the food. To test how hD2R cells might affect these connections, Friedman and Azevedo stimulated the neurons as mice wandered around a food-filled environment. This intervention, they found, made mice less likely to return to the area in which food was previously located -- suggesting that hDR2 activation somehow diminishes meal-related memories.

"Mental connections between food and location are important for survival, and the strength of these connections is regulated by how rewarding an experience is," says Azevedo. "Because hD2R neurons affect an animal's relationship with food, it also ends up affecting these connections."

Further experiments showed that hD2R neurons receive input from the entorhinal cortex, which processes sensory information, and send output to the septum, which is involved in feeding. The first to identify this brain circuit, the researchers conclude that the neurons serve as a regulatory checkpoint between sensing food and eating food.

Together with analyses of other neural circuits, this research suggests that the brain has elaborate mechanisms for fine-tuning appetite: While some systems help an animal remember and find food, others restrain food intake.

"Our study shows that brain areas involved in cognitive processing and memory formation affect feeding behavior," says Azevedo. "So it is possible that, with training, people may be able to learn to change their relationship to food."

https://www.sciencedaily.com/releases/2019/03/190328150732.htm

Skinny self-image, heavy workouts in adolescence are warning signs

22 percent of young men, 5 percent of young women engage in 'disordered eating' to bulk up

June 21, 2019

Science Daily/University of California - San Francisco

Adolescents who see themselves as puny and who exercise to gain weight may be at risk of so-called muscularity-oriented disordered eating behaviors, say researchers led by UCSF Benioff Children's Hospitals.

The researchers found that 22 percent of males and 5 percent of females ages 18-to-24 exhibit these disordered eating behaviors, which are defined as including at least one of the following: eating more or differently to gain weight or bulk up, and use of dietary supplements or anabolic steroids to achieve the same goal.

Left unchecked, these behaviors may escalate to muscle dysmorphia, characterized by rigid diet, obsessive over-exercising and extreme preoccupation with physique, say the researchers in their study publishing in the International Journal of Eating Disorders on June 20, 2019.

"Some eating disorders can be challenging to diagnose," said first author Jason Nagata, MD, of the UCSF Division of Adolescent and Young Adult Medicine. "Unlike anorexia nervosa, which may be easily identified by parents or pediatricians, disordered eating to increase bulk may masquerade as healthy habits and because of this, it tends to go unnoticed."

Heart Failure, Depression, Social Isolation in Worst Cases

At its most extreme, it can lead to heart failure due to insufficient calories and overexertion, as well as muscle dysmorphia, which is associated with social withdrawal and depression, Nagata said.

The 14,891 young adults in the study, who came from throughout the United States, had been followed for seven years. The researchers wanted to see if the early data, when the participants' average age was 15, revealed something about their perceptions and habits that may serve as warning signs.

They found that boys who exercised specifically to gain weight had 142 percent higher odds of this type of disordered eating; among girls, the odds were increased by 248 percent. Boys who perceived themselves as being underweight had 56 percent higher odds; in girls the odds were 271 percent higher. Smoking and alcohol use in boys, and smoking in girls, increased odds moderately.

Additionally, being of black race bolstered odds by 66 percent in boys and 181 percent in girls.

Non-heterosexual identity, which the participants had been asked about when they reached adulthood, was not found to be a risk factor, the researchers said.

In young adulthood, 6.9 percent of males reported supplement use to gain weight or build muscle and 2.8 percent said they used anabolic steroids. Use by young women was significantly lower at 0.7 percent and 0.4 percent respectively.

"Supplements are a black box, since they are not regulated," noted Nagata. "In extreme cases, supplements can cause liver and kidney damage. Anabolic steroids can cause both long-term and short-term health issues, including shrunken testicles, stunted growth and heart disease."

Nagata said that clues that indicate behaviors may approach muscle dysmorphia include a highly restrictive diet that omits fats and carbohydrates, compulsive weighing and checking of appearance, and extensive time dedicated to exercise that may cut into social activities.

https://www.sciencedaily.com/releases/2019/06/190621220750.htm

The brain consumes half of a child's energy -- and that could matter for weight gain

New paper proposes that variation in brain energy expenditure during childhood could be linked to obesity risk

June 17, 2019

Science Daily/Northwestern University

Weight gain occurs when an individual's energy intake exceeds their energy expenditure -- in other words, when calories in exceed calories out. What is less well understood is the fact that, on average, nearly half of the body's energy is used by the brain during early childhood.

In a new paper published in the journal Proceedings of the National Academy of Sciences (PNAS), "A hypothesis linking the energy demand of the brain to obesity risk," co-authors Christopher Kuzawa of Northwestern University and Clancy Blair of New York University School of Medicine, propose that variation in the energy needs of brain development across kids -- in terms of the timing, intensity and duration of energy use -- could influence patterns of energy expenditure and weight gain.

"We all know that how much energy our bodies burn is an important influence on weight gain," said Kuzawa, professor of anthropology in the Weinberg College of Arts and Sciences and a faculty fellow with the Institute for Policy Research at Northwestern. "When kids are 5, their brains use almost half of their bodies' energy. And yet, we have no idea how much the brain's energy expenditure varies between kids. This is a huge hole in our understanding of energy expenditure."

"A major aim of our paper is to bring attention to this gap in understanding and to encourage researchers to measure the brain's energy use in future studies of child development, especially those focused on understanding weight gain and obesity risk."

According to the authors, another important unknown is whether programs designed to stimulate brain development through enrichment, such as preschool programs like Head Start, might influence the brain's pattern of energy use.

"We believe it plausible that increased energy expenditure by the brain could be an unanticipated benefit to early child development programs, which, of course, have many other demonstrated benefits," Kuzawa said. "That would be a great win-win."

This new hypothesis was inspired by Kuzawa and his colleagues' 2014 study showing that the brain consumes a lifetime peak of two-thirds of the body's resting energy expenditure, and almost half of total expenditure, when kids are five years old. This study also showed that ages when the brain's energy needs increase during early childhood are also ages of declining weight gain. As the energy needed for brain development declines in older children and adolescents, the rate of weight gain increases in parallel.

"This finding helped confirm a long-standing hypothesis in anthropology that human children evolved a much slower rate of childhood growth compared to other mammals and primates in part because their brains required more energy to develop," Kuzawa said.

https://www.sciencedaily.com/releases/2019/06/190617164629.htm

Even in young children: Higher weight = higher blood pressure

June 13, 2019

Science Daily/European Society of Cardiology

Overweight four-year-olds have a doubled risk of high blood pressure by age six, raising the hazard of future heart attack and stroke. That's the finding of a study published today in the European Journal of Preventive Cardiology, a journal of the European Society of Cardiology (ESC).

"The myth that excess weight in children has no consequences hampers the prevention and control of this health problem," said study author Dr Iñaki Galán, of Carlos III Health Institute, Madrid, Spain. "Parents need to be more physically active with young children and provide a healthy diet. Women should shed extra pounds before becoming pregnant, avoid gaining excess weight during pregnancy, and quit smoking, as these are all established risk factors for childhood obesity."

According to the World Health Organization, childhood obesity is one of the most serious public health challenges of the 21st century. The problem is global and the prevalence has increased at an alarming rate. In 2016, more than 41 million children under the age of five were overweight.

This study, based on the ELOIN cohort, examined the link between excess weight and high blood pressure in 1,796 four-year-olds who were followed up two years later. Blood pressure was measured at both time points, as was body mass index (BMI in kg/m2) and waist circumference.

Compared to children maintaining a healthy weight between ages four and six, those with new or persistent excess weight according to BMI had 2.49 and 2.54 higher risks of high blood pressure, respectively. In those with new or persistent abdominal obesity, the risks for high blood pressure were 2.81 and 3.42 greater, respectively. Children who lost weight did not have an increased risk of high blood pressure. The findings applied to all children regardless of sex or socioeconomic status.

"There is a chain of risk, whereby overweight and obesity lead to high blood pressure, which heightens the chance of cardiovascular disease if allowed to track into adulthood," said Dr Galán. "But the results show that children who return to a normal weight also regain a healthy blood pressure."

The best way to maintain a healthy weight and lose excess kilos is to exercise and eat a healthy diet, said Dr Galán. In addition to the central role of parents, the school curriculum needs to include three to four hours of physical activity every week. Teachers should supervise activities during breaks, while schools can offer games and sports after classes and provide nutritionally balanced meals and snacks.

Doctors should routinely assess BMI and waist circumference at early ages, added Dr Galán. "Some paediatricians think the harms of overweight and obesity begin in adolescence but our study shows they are mistaken," he said. "We need to detect excess weight as soon as possible so the damaging impact on blood pressure can be reversed."

Overweight children should have their blood pressure measured. Three consecutive elevated readings constitute high blood pressure. In young children, the most common cause is excess weight, but doctors will rule out other reasons such as heart defects, kidney disease, genetic conditions, and hormonal disorders. If the cause is overweight, more activity and dietary improvements will be advised. If lifestyle changes don't help, blood pressure lowering medication may be prescribed.

Dr Galán noted that overweight in children is most accurately assessed using both BMI and waist circumference. In the study, using either measurement alone would have missed 15% to 20% of cases.

https://www.sciencedaily.com/releases/2019/06/190613095224.htm

Being teased about weight linked to more weight gain among children

May 30, 2019

Science Daily/NIH/Eunice Kennedy Shriver National Institute of Child Health and Human Development

Youth who said they were teased or ridiculed about their weight increased their body mass by 33 percent more each year, compared to a similar group who had not been teased, according to researchers at the National Institutes of Health. The findings appear to contradict the belief that such teasing might motivate youth to change their behavior and attempt to lose weight. The study was conducted by Natasha A. Schvey, Ph.D., of the Uniformed Services University of the Health Sciences in Bethesda, MD, and colleagues at NIH's Eunice Kennedy Shriver National Institute of Child Health and Human Development and National Institute of Diabetes and Digestive and Kidney Diseases. It appears in Pediatric Obesity.

The study involved 110 youth who were an average of 11.8 years of age when they enrolled. The participants were either overweight (defined as a body mass index above the 85th percentile) when they began the study or had two parents who were overweight or obese. At enrollment, they completed a six-item questionnaire on whether they had been teased about their weight. They then participated in annual followup visits for the next 15 years.

The researchers found that youth experiencing high levels of teasing gained an average of .20 kg (.44 lbs) per year more than those who did not. The authors theorize that weight-associated stigma may have made youths more likely to engage in unhealthy behaviors, such as binge eating and avoiding exercise. Another possible explanation is that the stress of being teased could stimulate the release of the hormone cortisol, which may lead to weight gain.

https://www.sciencedaily.com/releases/2019/05/190530101213.htm

Defining obesity in children should be based on health issues, not just BMI

Mental health issues are consistent across BMI groups

April 2, 2019

Science Daily/McMaster University

A new study aims to identify what influences the success participants achieve in weight management programs and help improve these programs. The study follows participants for three years.

Physicians are told to gauge the severity of a child's problem with obesity using the body mass index (BMI) that measures weight against height. But that doesn't work well to identify health issues, especially those of mental health, in children with obesity seeking care, says a study led by McMaster University.

Other medical issues, including high blood pressure, prediabetes and non-alcoholic fatty liver disease are also common, and are only slightly more frequent in those with the most severe obesity compared to those with less severe obesity, according to the study.

The details of the study called the Canadian Pediatric Weight Management Registry (CANPWR) were published today in The Lancet Child & Adolescent Health. This study found two thirds of children entering weight management programs across Canada have severe obesity based on their BMI.

"We found that social and mechanical health issues were more common in those with the highest body mass index. However, mental health issues, for example, are consistent across the BMI groups," said Katherine Morrison, principal investigator of the CANPWR study, and professor of the Department of Pediatrics at McMaster.

"If you are only using BMI to identify the youth who need the most care, you would be presuming the kids with the lowest BMI class would be the least likely to have mental health issues or metabolic issues, but our findings suggest this is not true. This study suggests that using a clinical staging system, one that evaluates the health of the child and not just the BMI, is likely the best approach."

Morrison is also co-director of the Centre for Metabolism, Obesity and Diabetes Research at McMaster, an investigator of the Population Health Research Institute, and a pediatric endocrinologist at McMaster Children's Hospital. She said the end goal is to improve care of these children.

"There is a lot said about preventing obesity, we also really need to focus on how best to treat children with obesity. This is especially true when we see the burden of health illness that is associated with obesity in children entering weight management programs."

The CANPWR study aims to identify what influences the success participants achieve in weight management programs and help improve these programs. The study follows participants for three years.

The 10 clinics taking part in the study are in Vancouver, Edmonton, Calgary, Toronto, Hamilton, Ottawa and Montreal.

The paper used information from 847 children with obesity and the health issues were determined at their initial visit to one of the multidisciplinary weight management clinics across Canada. Participants were aged five to 17 at the time of enrolment.

In this study, researchers showed that using a clinical staging system called the Edmonton Obesity Staging System for Pediatrics, or EOSS-P, was more useful for understanding the health issues of the children in these clinics than the BMI class system. They suggest that using a clinical staging system will better assist the design of health care interventions for children with obesity.

Obesity-related health issues were common. Mental health concerns were the most common (90 per cent), followed by metabolic (85 per cent), social (65 per cent) and mechanical (62 per cent) health issues. The most common mental health issue identified was anxiety.

The most commonly identified metabolic health complication was dyslipidemia, followed by non-alcoholic fatty liver disease.

Bullying was the most commonly identified social health factor, followed very closely by low household income. More than one-third of children in the highest obesity group came from low income homes, which was significantly higher than those with lower levels of obesity.

Those with the most severe obesity by BMI were more likely to have experienced bullying, and more likely to report difficulties with peer relationships, compared to the less severe obesity groups. 

https://www.sciencedaily.com/releases/2019/04/190402215621.htm

Sleeping with artificial light at night associated with weight gain in women

June 10, 2019

Science Daily/NIH/National Institute of Environmental Health Sciences

Sleeping with a television or light on in the room may be a risk factor for gaining weight or developing obesity, according to scientists at the National Institutes of Health. The research, which was published online June 10 in JAMA Internal Medicine, is the first to find an association between any exposure to artificial light at night while sleeping and weight gain in women. The results suggest that cutting off lights at bedtime could reduce women's chances of becoming obese.

The research team used questionnaire data from 43,722 women in the Sister Study, a cohort study that examines risk factors for breast cancer and other diseases. The participants, aged 35-74 years, had no history of cancer or cardiovascular disease and were not shift workers, daytime sleepers, or pregnant when the study began. The study questionnaire asked whether the women slept with no light, a small nightlight, light outside of the room, or a light or television on in the room.

The scientists used weight, height, waist and hip circumference, and body mass index measurements taken at baseline, as well as self-reported information on weight at baseline and follow-up five years later. Using this information, the scientists were able to study obesity and weight gain in women exposed to artificial light at night with women who reported sleeping in dark rooms.

The results varied with the level of artificial light at night exposure. For example, using a small nightlight was not associated with weight gain, whereas women who slept with a light or television on were 17% more likely to have gained 5 kilograms, approximately 11 pounds, or more over the follow-up period. The association with having light coming from outside the room was more modest.

Also, the scientists wondered if not getting enough rest factored into the findings.

"Although poor sleep by itself was associated with obesity and weight gain, it did not explain the associations between exposure to artificial light while sleeping and weight," said corresponding author Dale Sandler, Ph.D., chief of the Epidemiology Branch at the National Institute of Environmental Health Sciences (NIEHS), part of NIH.

Co-author Chandra Jackson, Ph.D., head of the NIEHS Social and Environmental Determinants of Health Equity Group, is interested in racial disparities in sleep health. She notes that for many who live in urban environments, light at night is more common and should be considered. Streetlights, store front neon signs, and other light sources can suppress the sleep hormone melatonin and the natural 24-hour light-dark cycle of circadian rhythms.

"Humans are genetically adapted to a natural environment consisting of sunlight during the day and darkness at night," Jackson said. "Exposure to artificial light at night may alter hormones and other biological processes in ways that raise the risk of health conditions like obesity."

The authors acknowledge that other confounding factors could explain the associations between artificial light at night and weight gain. However, their findings did not change when analyses controlled for characteristics that may be associated with exposure to light at night. These factors included age, having an older spouse or children in the home, race, socioeconomic status, calories consumed, and physical activity. Also, the study did not include men.

Lead author Yong-Moon (Mark) Park, M.D., Ph.D., is a postdoctoral fellow in Sandler's group. He said the research suggests a viable public health strategy to reduce obesity incidence in women.

"Unhealthy high-calorie diet and sedentary behaviors have been the most commonly cited factors to explain the continuing rise in obesity," Park said. "This study highlights the importance of artificial light at night and gives women who sleep with lights or the television on a way to improve their health."

https://www.sciencedaily.com/releases/2019/06/190610130121.htm

Why you love coffee and beer

May 2, 2019

Science Daily/Northwestern University

Why do you swig bitter, dark roast coffee or hoppy beer while your coworker guzzles sweet cola?

Scientist Marilyn Cornelis searched for variations in our taste genes that could explain our beverage preferences, because understanding those preferences could indicate ways to intervene in people's diets.

To Cornelis' surprise, her new Northwestern Medicine study showed taste preferences for bitter or sweet beverages aren't based on variations in our taste genes, but rather genes related to the psychoactive properties of these beverages.

"The genetics underlying our preferences are related to the psychoactive components of these drinks," said Cornelis, assistant professor of preventive medicine at Northwestern University Feinberg School of Medicine. "People like the way coffee and alcohol make them feel. That's why they drink it. It's not the taste."

The paper will be published May 2 in Human Molecular Genetics.

The study highlights important behavior-reward components to beverage choice and adds to our understanding of the link between genetics and beverage consumption -- and the potential barriers to intervening in people's diets, Cornelis said.

Sugary beverages are linked to many disease and health conditions. Alcohol intake is related to more than 200 diseases and accounts for about 6 percent of deaths globally.

Cornelis did find one variant in a gene, called FTO, linked to sugar-sweetened drinks. People who had a variant in the FTO gene -- the same variant previously related to lower risk of obesity -- surprisingly preferred sugar-sweetened beverages.

"It's counterintuitive," Cornelis said. "FTO has been something of a mystery gene, and we don't know exactly how it's linked to obesity. It likely plays a role in behavior, which would be linked to weight management."

"To our knowledge, this is the first genome-wide association study of beverage consumption based on taste perspective," said Victor Zhong, the study's first author and postdoctoral fellow in preventive medicine at Northwestern. "It's also the most comprehensive genome-wide association study of beverage consumption to date."

How the study worked

Beverages were categorized into a bitter-tasting group and a sweet-tasting group. Bitter included coffee, tea, grapefruit juice, beer, red wine and liquor. Sweet included sugar-sweetened beverages, artificially sweetened beverages and non-grapefruit juices. This taste classification has been previously validated.

Beverage intake was collected using 24-hour dietary recalls or questionnaires. Scientists counted the number of servings of these bitter and sweet beverages consumed by about 336,000 individuals in the UK Biobank. Then they did a genome-wide association study of bitter beverage consumption and of sweet beverage consumption. Lastly, they looked to replicate their key findings in three U.S. cohorts.

https://www.sciencedaily.com/releases/2019/05/190502100814.htm

How eating feeds into the body clock

April 25, 2019

Science Daily/Medical Research Council

New research has found it is not just what you eat, but when you eat that is important -- knowledge which could improve the health of shift workers and people suffering from jet lag.

The Medical Research Council (MRC)-funded study, published today in the journal Cell, is the first to identify insulin as a primary signal that helps communicate the timing of meals to the cellular clocks located across our body, commonly known as the body clock.

The team behind the research believe this improved understanding may lead to new ways to alleviate the ill-health associated with disruption to the body clock. These could include eating at specific times or taking drugs that target insulin signalling.

The body clock -- also known as the circadian rhythm -- is a 24-hour biological cycle that occurs individually in every cell of the body, driving daily rhythms in our physiology, from when we sleep, to hormone levels, to how we respond to medication. Our body clock is synchronised with the surrounding environment by exposure to daylight and the timing of meals. This synchrony is important for long-term health, and it is well known that disrupting your circadian rhythm by shift work or travel across time zones can be detrimental for health. Importantly, it is thought that eating at unusual times, as often occurrs during shift work and jet lag, is a major cause of body clock disruption. However, it has not previously been known exactly how the body clock senses and responds to meal timing, making it difficult to provide medical advice or interventions that might alleviate the problem.

Researchers at the MRC Laboratory of Molecular Biology (LMB) in Cambridge and the University of Manchester have now identified insulin as a primary signal that helps communicate the timing of meals to the cellular clocks across our body, and in doing so strengthen the circadian rhythm. The team's experiments in cultured cells, and replicated in mice, show that insulin, a hormone released when we eat, adjusts circadian rhythms in many different cells and tissues individually, by stimulating production of a protein called PERIOD, an essential cog within every cell's circadian clock.

Dr John O'Neill, a research leader at the MRC LMB who led the Cambridge research team, said: "At the heart of these cellular clocks is a complex set of molecules whose interaction provides precise 24-hour timing. What we have shown here is that the insulin, released when we eat, can act as a timing signal to cells throughout our body."

Working with Dr David Bechtold, a senior lecturer at the University of Manchester, the researchers found that when insulin was provided to mice at the 'wrong' biological time -- when the animals would normally be resting -- it disrupted normal circadian rhythms, causing less distinction between day and night.

Dr Bechtold said: "We already know that modern society poses many challenges to our health and wellbeing -- things that are viewed as commonplace, such as shift-work, sleep deprivation, and jet lag, disrupt our body clock. It is now becoming clear that circadian disruption is increasing the incidence and severity of many diseases, including cardiovascular disease and type 2 diabetes."

Dr Priya Crosby, a researcher at the MRC LMB and lead author on the study, highlighted: "Our data suggests that eating at the wrong times could have a major impact on our circadian rhythms. There is still work to do here, but paying particular attention to meal timing and light exposure is likely the best way to mitigate the adverse effects of shift-work. Even for those who work more traditional hours, being careful about when we eat is an important way to help maintain healthy body clocks, especially as we age."

https://www.sciencedaily.com/releases/2019/04/190425143607.htm

Eating small amounts of red and processed meats may increase risk of early death

March 27, 2019

Science Daily/Loma Linda University Adventist Health Sciences Center

A new study out of Loma Linda University Health suggests that eating red and processed meats -- even in small amounts -- may increase the risk of death from all causes, especially cardiovascular disease.

Saeed Mastour Alshahrani, lead author of the study and a doctoral student at Loma Linda University School of Public Health, said the research fills an important gap left by previous studies that looked at relatively higher levels of red meat intake and compared them with low intakes.

"A question about the effect of lower levels of intakes compared to no-meat eating remained unanswered," Alshahrani said. "We wanted to take a closer look at the association of low intakes of red and processed meat with all-cause, cardiovascular diseases, and cancer mortality compared to those who didn't eat meat at all."

This study, "Red and Processed Meat and Mortality in a Low Meat Intake Population" is part of the Adventist Health Study-2 (AHS-2), a prospective cohort study of approximately 96,000 Seventh-day Adventist men and women in the United States and Canada. The principal investigator of AHS-2 is Gary E. Fraser, MD, PhD, professor of medicine and epidemiology at Loma Linda University Health.

Adventists are a unique population -- approximately 50 percent are vegetarians, and those who consume meat do so at low levels. This allowed researchers to investigate the effect of low levels of red and processed meat intake compared to zero-intake in a large setting such as the Adventist Health Study.

The study evaluated the deaths of over 7,900 individuals over an 11-year period. Diet was assessed by a validated quantitative food frequency questionnaire and mortality outcome data were obtained from the National Death Index. Of those individuals who consumed meat, 90 percent of them only ate about two ounces or less of red meat per day.

Nearly 2,600 of the reported deaths were due to cardiovascular disease, and over 1,800 were cancer deaths. Processed meat -- modified to improve flavor through curing, smoking, or salting (such as ham and salami) -- alone was not significantly associated with risk of mortality possibly due to a very small proportion of the population who consume such meat. However, the total intake of red and processed meat was associated with relatively higher risks of total and cardiovascular disease deaths.

Michael Orlich, MD, PhD, co-director of AHS-2 and co-author of the present study, said these new findings support a significant body of research that affirms the potential ill health effects of red and processed meats.

"Our findings give additional weight to the evidence already suggesting that eating red and processed meat may negatively impact health an

Integrated therapy treating obesity and depression is effective

March 5, 2019

Science Daily/University of Illinois at Chicago

An intervention combining behavioral weight loss treatment and problem-solving therapy with as-needed antidepressant medication for participants with co-occurring obesity and depression improved weight loss and depressive symptoms compared with routine physician care.

Obesity and depression commonly occur together. Approximately 43 percent of adults with depression are obese, and adults with obesity are at increased risk of experiencing depression. To treat both conditions, patients must visit multiple practitioners usually including dietitians, wellness coaches and mental health counselors or psychiatrists. The burden associated with visiting multiple health care providers consistently over the long periods of time required to treat obesity and depression can be significant and lead to dropping out of therapy altogether. Additionally, these health services may not be available due to a lack of trained providers or reimbursement, and the cost of seeing numerous specialists can be prohibitive.

"Treatments exist that are effective at treating obesity and depression separately, but none that address both conditions in concert, which is a critical unmet need because of the high prevalence of obesity and depression together," said Dr. Jun Ma, professor of medicine in the University of Illinois at Chicago College of Medicine and principal investigator on the study. "We have shown that delivering obesity and depression therapy in one integrated program using dually trained health coaches who work within a care team that includes a primary care physician and a psychiatrist, is effective at reducing weight and improving depressive symptoms."

Ma and colleagues analyzed results of the Research Aimed at Improving Both Mood and Weight (RAINBOW) randomized clinical trial, which compared an integrated collaborative care program to treat co-occurring obesity and depression -- delivered by trained health coaches -- with usual care provided by a personal physician in primary care settings.

The RAINBOW weight loss intervention promotes healthy eating and physical activity, while the psychotherapy portion focuses on problem-solving skills. A psychiatrist is able to recommend adding antidepressant medication if needed, which the participant's personal physician would prescribe and manage.

Health coaches trained to deliver this integrated program worked in consultation with a primary care physician and a psychiatrist who jointly reviewed the clinical status of patients and advised on treatment adjustments for patients who were not progressing. The primary care physician and psychiatrist did not have direct contact with patients, nor did they prescribe medications or furnish other treatment to patients in the program directly. Their role was supportive and consultative to the health coaches with whom they worked as a team. This care team communicated and collaborated with patients' personal physicians who oversaw the patients' care, including prescribing medications, providing treatments for medical conditions and making referrals to specialty care when needed.

Participants in the RAINBOW trial included 409 patients with obesity and depression. All participants received usual medical care from their personal physicians and were provided with information on health care services for obesity and depression at their clinic as well as wireless physical activity trackers.

Two hundred and four participants were randomly assigned to receive the integrated collaborative care program and were seen by a health coach for one year. In the first six months, they participated in nine individual counseling sessions and watched 11 videos on healthy lifestyles. In the following six months, participants had monthly telephone calls with their health coach. Two hundred and five participants randomly assigned to the usual care control group did not receive any additional intervention.

Participants in the integrated care program experienced more weight loss and decline in the severity of depressive symptoms over one year compared with control participants receiving usual care. On average, patients in the integrated program experienced a decline in body mass index from 36.7 to 35.9 while participants in the usual care group had no change in BMI. Participants receiving integrated therapy reported a decline in depression severity scores based on responses to a questionnaire from 1.5 to 1.1, compared with a change from 1.5 to 1.4 among those in the control group.

"While the demonstrated improvements in obesity and depression among participants receiving the integrated therapy were modest, the study represents a step forward because it points to an effective, practical way to integrate fragmented obesity and depression care into one combined therapy, with good potential for implementation in primary care settings, in part because the integrated mental health treatment in primary care settings is now also reimbursable by Medicare. For patients, this approach is an attractive alternative to seeing multiple practitioners each charging for their services as is done traditionally," Ma said.

Ma and colleagues are currently investigating ways to tailor the integrated therapy for individual patients by targeting underlying neurobehavioral mechanisms to further improve outcomes.

"We have some preliminary data that suggests if we can tailor therapy based on the patient's engagement and response early in the treatment -- for example by offering motivational interviewing to augment integrated therapy for patients who show early signs of poor engagement or progress -- we may further improve the effectiveness of the therapy," Ma said. "In addition, a better understanding of the mechanisms of brain function and behavior change can guide targeted therapy."

https://www.sciencedaily.com/releases/2019/03/190305124714.htm

Daily intake of nutritional supplements cannot prevent depression

March 6, 2019

Science Daily/European Association for the Study of Obesity

MooDFOOD, the largest randomized clinical trial to study the effects of nutritional strategies on the prevention of major depressive disorder concludes that daily intake of nutritional supplements cannot prevent depression.

Over 1000 participants who were overweight or had obesity and were identified as being at elevated risk for depression but who were not currently depressed, from four European countries -the Netherlands, the United Kingdom, Germany and Spain, took part in the study. Participants were randomized to either take nutritional supplements containing folic acid, vitamin D, zinc, selenium or to a pill placebo, and half of participants also received a behavioural lifestyle intervention intended to change dietary behaviours and patterns.

Researcher Mariska Bot from Amsterdam UMC reported: "Daily intake of nutritional supplements over a year does not effectively prevent the onset of a major depressive episode in this sample. Nutritional supplements were not better than placebo. Therapeutic sessions aimed at making changes towards a healthy dietary behaviour did also not convincingly prevent depression." Dr. Bot is first author of a paper showing these results in today's issue of the Journal of the American Medical Association (JAMA).

Depression is a common disorder

More than 40 million Europeans experience a major depressive disorder. One in ten men and one in five women suffer from clinical depression at least once during their lifetime. Depression is one of the most prevalent and disabling disorders in the EU.

Given the increasing prevalence of depression, more people are actively searching for ways to decrease their risk through lifestyle modification, but are often overwhelmed by confusing and contradictory information. To help European citizens the MooDFOOD project has developed evidence-based nutritional strategies to help prevent depression.

Prevention of depression through a healthy diet

The MooDFOOD prevention trial formed a crucial part of the five year MooDFOOD project, which investigated the relationship between nutrition and depression. MooDFOOD was funded by the European Commission and led by the Vrije Universiteit Amsterdam.

Although the behavioural therapy to encourage a healthy dietary behavior and improve diet was not effective at preventing depression overall, there was some evidence that it prevented depressive episodes in those participants who attended a recommended number of sessions. This may suggest the food behavioural therapy only works if the participants get sufficient exposure and are able to sufficiently improve their diet and dietary behaviour.

MooDFOOD project coordinators professor Marjolein Visser and professor Ingeborg Brouwer of the Vrije Universiteit Amsterdam said:

"Several studies within, and outside the five year MooDFOOD project show that consuming a healthy dietary pattern is important for European citizens, not only for physical health, but it may also help to prevent depressive symptoms. " Based on a large number of studies and careful analysis, MooDFOOD researchers have come to three important conclusions at the end of their project. First, a healthy dietary pattern, typified by a Mediterranean style diet high in fruit, vegetables, whole grains, fish, pulses and olive oil, and low in red meat and full-fat dairy products, may reduce the risk of developing depression. Second, in people with obesity, weight loss can lead to a reduction in depressive symptoms. Third, current evidence does not support the use of nutritional supplements in order to prevent depression.

Practical tools

These recent results have important implications for all Europeans. The MooDFOOD team has translated these findings into tools for the general population, health professionals (GPs, dieticians and psychologists), researchers and policy makers.

https://www.sciencedaily.com/releases/2019/03/190306100545.htm

Insufficient sleep in children is associated with poor diet, obesity and more screen time

New study suggests a relationship between insufficient sleep and an unhealthy lifestyle

November 12, 2018

Science Daily/American Academy of Sleep Medicine

A new study conducted among more than 177,000 students suggests that insufficient sleep duration is associated with an unhealthy lifestyle profile among children and adolescents.

Results show that insufficient sleep duration was associated with unhealthy dietary habits such as skipping breakfast (adjusted odds ratio 1.30), fast-food consumption (OR 1.35) and consuming sweets regularly (OR 1.32). Insufficient sleep duration also was associated with increased screen time (OR 1.26) and being overweight/obese (OR 1.21).

"Approximately 40 percent of schoolchildren in the study slept less than recommended," said senior author Labros Sidossis, PhD, distinguished professor and chair of the Department of Kinesiology and Health at Rutgers University in New Brunswick, New Jersey. "Insufficient sleeping levels were associated with poor dietary habits, increased screen time and obesity in both genders."

The study results are published in the Oct. 15 issue of the Journal of Clinical Sleep Medicine.

The American Academy of Sleep Medicine recommends that children 6 to 12 years of age should sleep nine to 12 hours on a regular basis to promote optimal health. Teenagers 13 to 18 years of age should sleep eight to 10 hours.

Population data were derived from a school-based health survey completed in Greece by 177,091 children (51 percent male) between the ages of 8 and 17 years. Dietary habits, usual weekday and weekend sleeping hours, physical activity status, and sedentary activities were assessed through electronic questionnaires completed at school. Children who reported that they usually sleep fewer than nine hours per day, and adolescents sleeping fewer than eight hours per day, were classified as having insufficient sleep. Anthropometric and physical fitness measurements were obtained by physical education teachers.

A greater proportion of males than females (42.3 percent versus 37.3 percent) and of children compared with adolescents (42.1 percent versus 32.8 percent) reported insufficient sleep duration. Adolescents with an insufficient sleep duration also had lower aerobic fitness and physical activity.

"The most surprising finding was that aerobic fitness was associated with sleep habits," said Sidossis. "In other words, better sleep habits were associated with better levels of aerobic fitness. We can speculate that adequate sleep results in higher energy levels during the day. Therefore, children who sleep well are maybe more physically active during the day and hence have higher aerobic capacity."

The authors noted that the results support the development of interventions to help students improve sleep duration.

"Insufficient sleep duration among children constitutes an understated health problem in Westernized societies," Sidossis said. "Taking into consideration these epidemiologic findings, parents, teachers and health professionals should promote strategies emphasizing healthy sleeping patterns for school-aged children in terms of quality and duration."

https://www.sciencedaily.com/releases/2018/11/181112191814.htm