Anti-stress brain chemical is related to PTSD resilience after trauma
April 30, 2019
Science Daily/Elsevier
Fewer receptors for the anti-stress brain chemical nociceptin is associated with less severe posttraumatic stress disorder (PTSD) symptoms in college women who have experienced sexual violence, according to a study in Biological Psychiatry, published by Elsevier. The relationship between nociceptin receptor density and PTSD severity was present in women with recent PTSD symptoms but not those with past symptoms, suggesting a role for the receptors in recovery after sexual violence.
Although studies in animal models of PTSD have shown that nociceptin promotes resilience, the receptors had never been studied in people with the disorder. Using positron emission tomography brain imaging, researchers from University of Pittsburgh, Pennsylvania, showed that PTSD symptom severity is associated with fewer receptors in the midbrain and cerebellum -- regions involved in the brain's threat alarm system and that process subconscious triggers of PTSD related to the trauma.
"These results suggest that decreased nociceptin receptor density is a marker of resilience and recovery following trauma. If future studies confirm these results, nociceptin receptor density may become an important resilience biomarker in the evaluation of PTSD," said lead author Rajesh Narendran, MD.
The primary characteristics of PTSD include intrusive memories of the traumatic event and avoidance of anything that reminds one of the trauma. In women with recent PTSD, these primary symptoms were strongly associated with nociception receptor density.
"Alterations in nociceptin receptor regulation in PTSD could point to specific treatments that might target this receptor to treat symptoms of PTSD," said John Krystal, Editor of Biological Psychiatry.
This would be an important advance for the disorder, as currently available medications for PTSD treat secondary symptoms of the disorder, such as negative mood, but do not treat the primary symptoms associated with receptor measures in this study.
This means that the relationship between PTSD symptom severity and nociceptin receptors in the brain of women who have experienced sexual violence not only provides critical insight for understanding the biology of resilience and recovery after trauma, but also opens potential avenues for improving PTSD treatment and prevention.
https://www.sciencedaily.com/releases/2019/04/190430103505.htm
Keeping fit is more than physical: It's a state of mind
April 30, 2019
Science Daily/Elsevier
According to a new study differences in what motivates individuals and how they self-regulate behavior influence how they keep fit. The study appearing in the journal Heliyon, published by Elsevier, associates personal characteristics with whether people are likely to prefer solo or group exercise activities, CrossFit® training, resistance training, or team sports, how frequently they work out, and if they are likely to stick to their routine.
The investigators set out to better understand why individuals adopt and adhere to regular physical activity programs, whether differences exist in personality, participatory motives, and regulation-motivation styles associated with their exercise modes, and to determine the extent to which these factors predict their work-out frequency. Their findings show that individuals selecting CrossFit, sports, or group exercise were more highly motivated by social connectedness (affiliation) than those engaging primarily in aerobic (e.g., long distance running) or resistance training exercise. Although all participants were highly motivated to engage in physical activity for positive health, those who engaged in resistance training and sport were more motivated by a sense of challenge than ill-health avoidance or weight management.
The study also demonstrated that individual differences in exercise motivation and self-control can predict participation frequency. Individuals who were more motivated by intrinsic reasons such as enjoyment, challenge, and stress management, exercised more frequently; CrossFit participants ranked highest in intrinsic motivation. Prior research has shown that people who exercise typically are more extraverted and conscientious, compared to an average population, but this study did not find any significant personality trait variances linked with different forms of exercise.
"Many individuals who initiate exercise programs may actually select activities that conflict with their interests, styles, personalities, and/or reasons for engagement. Our findings support the need for individualized exercise programs, not only from a physical standpoint, but also from a motivational standpoint. Taking these factors into account may impact the amount of physical activity/exercise that individuals actually complete," explained lead investigator Ms. Allyson Box. who began this work as an undergraduate student at Kennesaw State University, Kennesaw, GA, USA.
Data were collected from more than 400 physically active individuals who completed an online survey distributed via social media. Personality factors, motives for participation, and self-control styles were assessed using widely accepted frameworks including the Five Factor Model, revised Exercise Motivation Inventory, Self-determination Continuum, and Behavioral Regulation in Exercise Questionnaire.
Recent evidence suggests physical activity is important to decrease risks associated with metabolic, osteopathic, cardiovascular, and neurovascular diseases, as well as some cancers and mental health disorders. The positive impact of exercise on overall health is widely acknowledged, but most people tend to avoid physical activity and/or not stick with their regimen. Less than 20 percent of the population meets proposed Physical Activity Guidelines for Americans (2018) by engaging in at least 150 minutes of moderate intensity aerobic activity and at least two instances of resistance exercise each week. This lack of physical activity has resulted in an escalation of chronic diseases, such as diabetes or heart disease.
"We encourage individuals to reflect on their personality and reasons for becoming physically active before diving into a physical activity program to ensure they engage in a physical activity that is compatible with their interest, personality, and goals," the authors added.
"Our findings suggest that it may be more than just seeking the latest 'fitness fad' or 'new diet' in order to influence health outcomes; identifying individual characteristics and motivational factors will aid in developing an exercise program that individuals will stick to over a prolonged period of time, not just a few months."
https://www.sciencedaily.com/releases/2019/04/190430103459.htm
Evening exercise will not ruin sleep and might even reduce appetite
February 21, 2019
Science Daily/The Physiological Society
With growing time demands, many middle-aged adults are finding time to engage in exercise increasingly difficult. For many, even the thought of fitting exercise in after a busy day at work can be as tiring as it is unappetizing. The standing belief that high-intensity exercise should be avoided in the early evening due to its effect on sleep only serves to act as another barrier to exercise at this time.
Must cook dinner. Need to pick the kids up from school. Have to catch up on my favourite TV series. Live too far from the gym. Any of these sound familiar? With growing time demands, many middle-aged adults are finding time to engage in exercise increasingly difficult. For many, even the thought of fitting exercise in after a busy day at work can be as tiring as it is unappetising. The standing belief that high-intensity exercise should be avoided in the early evening due to its effect on sleep only serves to act as another barrier to exercise at this time.
However, encouraging new research published in Experimental Physiology has suggested that 30 minutes of high-intensity exercise performed in the early evening does not negatively affect subsequent sleep, and may also reduce feelings of hunger.
Researchers at Charles Sturt University in Australia recruited eleven middle-aged men to complete three experimental trials to investigate sleep and appetite responses to exercise performed in the morning (6 -- 7 am), afternoon (2 -- 4 pm) and evening (7 -- 9 pm). Participants were required to perform high-intensity cycling involving six one-minute, maximal intensity sprints interspersed by four minutes of rest. Blood collections were taken prior to exercise and following exercise to examine appetite-related hormones, and multiple tests were performed during sleep to assess sleep stages.
The results not only showed that evening exercise did not have a detrimental impact on subsequent sleep, but also that afternoon and evening high-intensity exercise were associated with greater reductions of the hunger stimulating hormone, ghrelin. It is important to note that a single bout of exercise was not linked to reduced hunger, but nevertheless, the observations from this study support high-intensity exercise early in the evening as a viable time-of day for exercise.
As this study's sample size was relatively small, the findings extrapolated to other population groups beyond middle-aged men may be limited, given that sleep and appetite regulation are influenced by sex and age.
Penelope Larsen, lead author of the study, commented said:
"In the future, we hope to conduct similar studies recruiting women, to determine whether sleep and appetite responses may be different depending on sex. Also, this study only considered a single bout of exercise; therefore, it would be beneficial to investigate long-term sleep and appetite adaptations to high-intensity exercise training performed either in the morning, afternoon or evening."
Interestingly, power output during the sprint efforts was higher for the afternoon and evening trials compared to the morning trial, indicating that participants were able to perform better during latter parts of the day. Therefore, time-of-day may also need to be considered when planning training schedules."
https://www.sciencedaily.com/releases/2019/02/190221083411.htm
MRI reveals brain damage in obese teens
November 25, 2019
Science Daily/Radiological Society of North America
Researchers using MRI have found signs of damage that may be related to inflammation in the brains of obese adolescents, according to a study being presented next week at the annual meeting of the Radiological Society of North America (RSNA).
Obesity in young people has become a significant public health problem. In the U.S., the percentage of children and adolescents affected by obesity has more than tripled since the 1970s, according to the Centers for Disease Control and Prevention. Data from the World Health Organization indicates that the number of overweight or obese infants and young children ages five years or younger increased from 32 million globally in 1990 to 41 million in 2016.
While obesity is primarily associated with weight gain, recent evidence suggests that the disease triggers inflammation in the nervous system that could damage important regions of the brain. Developments in MRI like diffusion tensor imaging (DTI), a technique that tracks the diffusion of water along the brain's signal-carrying white matter tracts, have enabled researchers to study this damage directly.
For the new study, researchers compared DTI results in 59 obese adolescents and 61 healthy adolescents, ages 12 to 16 years. From DTI, the researchers derived a measure called fractional anisotropy (FA), which correlates with the condition of the brain's white matter. A reduction in FA is indicative of increasing damage in the white matter.
The results showed a reduction of FA values in the obese adolescents in regions located in the corpus callosum, a bundle of nerve fibers that connects the left and right hemispheres of the brain. Decrease of FA was also found in the middle orbitofrontal gyrus, a brain region related to emotional control and the reward circuit. None of the brain regions in obese patients had increased FA.
"Brain changes found in obese adolescents related to important regions responsible for control of appetite, emotions and cognitive functions," said study co-author Pamela Bertolazzi, a biomedical scientist and Ph.D. student from the University of São Paulo in Brazil.
This pattern of damage correlated with some inflammatory markers like leptin, a hormone made by fat cells that helps regulate energy levels and fat stores. In some obese people, the brain does not respond to leptin, causing them to keep eating despite adequate or excessive fat stores. This condition, known as leptin resistance, makes the fat cells produce even more leptin.
Worsening condition of the white matter was also associated with levels of insulin, a hormone produced in the pancreas that helps regulate blood sugar levels. Obese people often suffer from insulin resistance, a state in which the body is resistant to the effects of the hormone.
"Our maps showed a positive correlation between brain changes and hormones such as leptin and insulin," Dr. Bertolazzi said. "Furthermore, we found a positive association with inflammatory markers, which leads us to believe in a process of neuroinflammation besides insulin and leptin resistance."
Dr. Bertolazzi noted that additional studies are needed to determine if this inflammation in young people with obesity is a consequence of the structural changes in the brain.
"In the future, we would like to repeat brain MRI in these adolescents after multi-professional treatment for weight loss to assess if the brain changes are reversible or not," she added.
https://www.sciencedaily.com/releases/2019/11/191125100405.htm
Only-children more likely to be obese than children with siblings
November 6, 2019
Science Daily/`Elsevier
Families with multiple children tend to make more healthy eating decisions than families with a single child.
A new study in the Journal of Nutrition Education and Behavior, published by Elsevier, found that only-children, who researchers refer to as "singletons," had less healthy family eating practices, beverage choices, and total Healthy Eating Index 2010 score, coming in lower on three out of the 12 areas measured. They also had significantly lower total scores across weekdays, weekends, and on average, indicating there are both individual and collective differences in eating patterns between the groups.
"Nutrition professionals must consider the influence of family and siblings to provide appropriate and tailored nutrition education for families of young children," said lead author Chelsea L. Kracht, PhD. Dr. Kracht completed the research during her PhD program alongside Dr. Susan Sisson at the University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. "Efforts to help all children and families establish healthy eating habits and practices must be encouraged."
Data was self-reported in daily food logs kept by mothers over the course of three days -- two weekdays and one weekend day. Teachers kept logs by proxy for any food children ate while at school. Mothers also completed the Family Nutrition and Physical Activity questionnaire to evaluate typical family eating behaviors like food and beverage choice.
Researchers found mothers of singleton children were more likely to be obese themselves. Moreover, maternal BMI had a much stronger connection to child BMI percentile and waist circumference percentile than singleton status. Maternal BMI did not significantly contribute to overall eating patterns but did contribute to empty calories.
The study only looked at mothers and children and so could not speak to the impact of fathers' eating patterns, but the results were independent of marital status.
The study also found that time spent in away-from-home care like school and daycare was not connected to children's eating patterns. This points to the difference coming from inside the household, including a difference in how frequently the family eats in front of the television (family eating practices score) and sugary drinks consumption (beverage choices score), which differed between groups in the study.
"Healthier eating behaviors and patterns may result from household-level changes rather than peer exposure, as peer exposure is also present in away-from-home care," Dr. Kracht said.
Dr. Kracht and her colleagues are continuing their research, looking specifically into household and family dynamics and how they influence children's eating behavior, physical activity, sleep, and other factors contributing to obesity.
https://www.sciencedaily.com/releases/2019/11/191106183102.htm
Glucose wears down circadian clocks in obesity, may drive cardiovascular risk
October 24, 2019
Science Daily/Medical College of Georgia at Augusta University
High glucose in obesity appears to gum up the works of the circadian clocks inside our cells that help regulate the timing of many body functions across the 24-hour day and drive the risk of cardiovascular disease, scientists say.
"We have demonstrated that glucose and cardiovascular problems are intrinsically linked in obesity," says Dr. David Stepp, vascular biologist in the Vascular Biology Center and Leon Henri Charbonnier Endowed Chair in Physiology at the Medical College of Georgia at Augusta University.
"We have also demonstrated that high glucose impairs circadian clock function. Now we want to know if we fix the clock, do we fix the cardiovascular problems," says Stepp.
He and Dr. David Fulton, director of the Vascular Biology Center and Regents professor in the MCG Department of Pharmacology and Toxicology, are principal investigators on a $2.7 million grant from the National Institutes of Health that is enabling the use of intermittent fasting and a developing category of clock repair drugs to find the answer.
Circadian clocks set the rhythm of our bodies so that we eat, sleep and wake at the right time. What is less well recognized is the important role of circadian clocks in anticipating these events and preparing our organs and cells so they function optimally at the right time as well as anticipating when to rest and rejuvenate, says Fulton.
"Every cell in your body has a clock in it that is used to anticipate daily needs," says Fulton, your blood pressure and heart rate drop at nighttime and surge in the morning when your feet hit the ground and blood must fight against gravity.
"Your metabolic needs at night are different than your metabolic needs when you are awake," says Stepp. "Some of them are more; some of them are just different."
Sleep is supposed to be a period of rest and recovery for each of our cells just like it is for us overall. "You are doing regeneration, you are doing restoration, you are doing repair," Stepp says. At daybreak, genes active at night should be turned off, and genes important for daily activities should be turned on and our metabolism should switch from a restorative to active phase.
Blood flow adjusts to match these dynamic metabolic needs, and our circadian clocks are sort of intermediaries between metabolism and our cardiovascular system that coordinate changes in metabolism with changes in cardiovascular gene function.
The MCG scientists have evidence that obesity can break these links between metabolism and cardiovascular regulation. Excessive food consumption, particularly foods that are high in sugar and carbohydrates, some of which our body also breaks down into glucose, dampens clock function and imperils cardiovascular health. "It's certainly an accelerant," Fulton says of high glucose.
They have documented both high glucose levels and significant circadian dysfunction in a mouse model of hyperphagia. These obese mice have tremendous appetites, high glucose and high blood pressure that does not dip at night when it should, and most importantly, dysfunction of the single layer of endothelial cells that line blood vessels. Normally endothelial cells provide a smooth surface for blood to pass over and play a key role in enabling blood vessels to dilate in response to greater blood volume so blood pressure doesn't increase too much.
Endothelial dysfunction, a focus of their cardiovascular studies, is a major initiator of atherosclerosis, and what many of us think of as heart disease. Dysfunctional endothelial cells become inflamed, sticky and produce more damaging reactive oxygen species and less nitric oxide, which impairs blood vessel dilation. The result can be a tortuous passageway for blood, sticky walls where cells pile up and coronary artery disease.
When the MCG scientists disrupt the gears of circadian clocks in mice using genetic approaches or environmental modifications, including jet lag light cycles, both approaches result in loss of clock function and increase the risk of endothelial dysfunction and disease. Now Fulton and Stepp want to know more about how the clocks lose timing and how best to intervene.
They have bred the obese mice with a clock reporter, a gear of the circadian clock linked to a fluorescent protein that lights up when the gear is turned, so they can better track clock activity.
Using these clock reporter mice, they saw huge downturns in circadian rhythms and clock-related genes in obese mice and high levels of glucose in the blood upstream of these events.
"The first thing we want to know is can we understand why the clock is rundown in obesity," says Stepp. "The second thing is what mediates the effects of circadian disruption on cardiovascular disease, and if we fix that disruption, get the amplitude back up, does it fix the cardiovascular problems."
If intermittent fasting, which should help restore the normal peaks and valleys of glucose levels, or the clock-fixer drugs they are using for these studies interfere with progression to cardiovascular problems, they should have some answers.
They and others already have evidence that the small, clock-fixer molecule they are using, nobiletin, enhances the amplitude of and reverses the reduction of clock function in obesity. Whether or not that improves cardiovascular function, is one of the things they want to learn more about now.
That includes checking whether high glucose and resulting clock dysfunction work through the increased expression of galectin-3, a receptor associated with cardiovascular disease that they have seen in their mouse model, to produce expression of the gene NOX1, which converts oxygen to damaging super oxide, in endothelial cells.
They still are not certain which clock(s) are most central to this problem. Everywhere they have looked -- heart, kidney, liver, blood vessels and endothelial cells -- they have seen these rundown clocks. For now they are focusing on clocks in the endothelial cells, where they think a lot of the problems start. They don't expect to identify a specific clock(s) in these studies, but if their findings continue to hold they will start knocking out clocks in other cells in future studies.
They think the problem quite literally is about timing, says Fulton. Proper signaling requires a peak and trough and constant overstimulation by too much glucose has the body instead trying to turn clocks off.
The scientists note that if you have a healthy musculature despite obesity, it mitigates, at least for a time, the impact of high glucose on the vasculature. Muscle is a first and fast user of glucose, quickly pulling it out of the circulation. "If it goes into the muscle, it never comes out again," says Stepp. "It gets used or stored for later." Obese mice, like humans, lose muscle mass. In some of their initial studies, they preserved muscle mass in obese mice, which also prevented cardiovascular damage.
They note that both aging, when muscle naturally loses volume even in individuals who remain active, and spinal cord injuries or other conditions that leave us immobile, have some of the same cardiovascular risks as obesity.
While circadian-related cardiovascular risk also is heightened by lifelike scenarios like shiftwork or chronic jet lag in even a lean mouse, it is way worse for an obese one, Stepp says.
Adult obesity results from factors that include consuming more calories than are expended, medications and other exposures as well as genetics, including gene variants that increase hunger and food intake, according to the Centers for Disease Control and Prevention. It is associated with poorer mental health, reduced quality of life and contributes to the leading causes of death in the United States including diabetes, heart disease, stroke and some types of cancer. Obesity itself is considered a major risk factor for cardiovascular disease, and a major risk as well for diabetes and high blood pressure, which are other top cardiovascular risks.
https://www.sciencedaily.com/releases/2019/10/191024093602.htm
Evidence of behavioral, biological similarities between compulsive overeating and addiction
October 17, 2019
Science Daily/Boston University School of Medicine
Does yo-yo dieting drive compulsive eating? There may be a connection.
According to Boston University School of Medicine (BUSM) researchers the chronic cyclic pattern of overeating followed by undereating, reduces the brain's ability to feel reward and may drive compulsive eating. This finding suggests that future research into treatment of compulsive eating behavior should focus on rebalancing the mesolimbic dopamine system -- the part of the brain responsible for feeling reward or pleasure.
An estimated 15 million people compulsively eat in the U.S. It is a common feature of obesity and eating disorders, most notably, binge eating disorder. People often overeat because it is pleasurable in the short term, but then attempt to compensate by dieting, reducing calorie intake and limiting themselves to "safe," less palatable food. However, diets often fail, causing frequent "relapse" to overeating of foods high in fat and sugar (palatable foods).
"We are just now beginning to understand the addictive-like properties of food and how repeated overconsumption of high sugar -- similar to taking drugs -- may affect our brains and cause compulsive behaviors," said corresponding author Pietro Cottone, PhD, associate professor of pharmacology & experimental therapeutics at BUSM and co-director of the Laboratory of Addictive Disorders.
In order to better understand compulsive and uncontrollable eating, Cottone and his team performed a series of experiments on two experimental models: one group received a high sugar chocolate-flavored diet for two days each week and a standard control diet the remaining days of the week (cycled group), while the other group, received the control diet all of the time (control group).
The group that cycled between the palatable food and the less palatable, spontaneously developed compulsive, binge eating on the sweet food and refused to eat regular food. Both groups were then injected with a psychostimulant amphetamine, a drug that releases dopamine and produces reward, and their behavior in a battery of behavioral tests was then observed.
While the control group predictably became very hyperactive after receiving amphetamine, the cycled group did not. Furthermore, in a test of the conditioning properties of amphetamine, the control group was attracted to environments where they previously received amphetamine, whereas the cycled group were not. Finally, when measuring the effects of amphetamine while directly stimulating the brain reward circuit, the control group was responsive to amphetamine, while the cycled group was not.
After investigating the biochemical and molecular properties of the mesolimbic dopamine system of both groups, the researchers determined that the cycled group had less dopamine overall, released less dopamine in response to amphetamine and had dysfunctional dopamine transporters (protein that carries dopamine back into brain cells) due to deficits in their mesolimbic dopamine system.
"We found that the cycled group display similar behavioral and neurobiological changes observed in drug addiction: specifically, a "crash" in the brain reward system," explained Cottone. "This study adds to our understanding of the neurobiology of compulsive eating behavior. Compulsive eating may derive from the reduced ability to feel reward. These findings also provide support to the theory that compulsive eating has similarities to drug addiction."
"Our data suggest that a chronic cyclic pattern of overeating will reduce the brain's ability to feel reward -- feeling satiated. This results in a vicious circle, where diminished reward sensitivity may in turn be driving further compulsive eating," said lead author Catherine (Cassie) Moore, PhD, former graduate student in the Laboratory of Addictive Disorders at BUSM.
The researchers hope these findings spark new avenues of research into compulsive eating that will lead to more effective treatments for obesity and eating disorders.
https://www.sciencedaily.com/releases/2019/10/191017125240.htm
Bad break-ups may not trigger weight gain from emotional eating
October 17, 2019
Science Daily/Penn State
That pint of ice cream after a nasty breakup may not do as much damage as you think. Despite the emotional turmoil, people on average do not report gaining weight after a relationship dissolution, according to new research.
The study, which included researchers from Penn State, were investigating the German concept of "kummerspeck" -- excess weight gain due to emotional eating -- which literally translates to "grief bacon."
Marissa Harrison, associate professor of psychology at Penn State Harrisburg, said that while hoarding food after a breakup may have made sense for humans thousands of years ago, modern humans may have grown out of the habit.
"Food was much scarcer in the ancestral environment, so if your partner abandoned you, it could have made gathering food much harder," Harrison said. "It may have made sense if our ancestors hoarded food after a breakup. But our research showed that while it's possible people may drown their sorrows in ice cream for a day or two, modern humans do not tend to gain weight after a breakup."
According to the researchers, it has been well documented that people sometimes use food as a way to cope with negative feelings and that emotional eating can lead to unhealthy food choices. Because breakups can be stressful and emotional, it could potentially trigger emotional eating.
Additionally, ancient relationship dynamics may have made packing on the pounds after a breakup evolutionary advantageous.
"Modern women of course have jobs and access to resources now, but back then, it was likely that women were smaller and needed more protection and help with resources," Harrison said. "If their partner left or abandoned them, they would be in trouble. And the same could have gone for men. With food not as plentiful in the ancestral world, it may have made sense for people to gorge to pack on the pounds."
Harrison also noted that the existence of the word "kummerspeck" itself suggested that the phenomenon existed.
The researchers completed two studies to test the theory that people may be more likely to gain weight after a relationship breakup. In the first one, the researchers recruited 581 people to complete an online survey about whether they had recently gone through a breakup and whether they gained or lost weight within a year of that breakup.
Most of the participants -- 62.7 percent -- reported no weight change. According to Harrison, she and the other researchers were surprised by this result and decided to perform an additional study.
For the second study, the researchers recruited 261 new participants to take a different, more extensive survey than the one used in the first study. The new survey asked whether participants had ever experienced the dissolution of a long-term relationship, and whether they gained or lost weight as a result. The survey also asked about participants' attitudes toward their ex-partner, how committed the relationship was, who initiated the breakup, whether the participants tended to eat emotionally, and how much participants enjoy food in general.
While all participants reported experiencing a break up at some point in their lives, the majority of participants -- 65.13 percent -- reported no change in weight after relationship dissolution.
"We were surprised that in both studies, which included large community samples, we found no evidence of kummerspeck," Harrison said. "The only thing we found was in the second study, women who already had a proclivity for emotional eating did gain weight after a relationship breakup. But it wasn't common."
Harrison added that the results -- recently published in the Journal of the Evolutionary Studies Consortium -- may have clinical implications.
"It could be helpful information for clinicians or counselors with patients who tend to eat emotionally," Harrison said. "If your client is going through a breakup and already engages in emotional eating, this may be a time where they need some extra support."
https://www.sciencedaily.com/releases/2019/10/191017121930.htm
Overweight Danes are more likely to have overweight dogs
September 19, 2019
Science Daily/University of Copenhagen
A new study from the University of Copenhagen reports that the prevalence of overweight dogs is markedly larger among overweight owners than among normal weight owners. Part of the explanation lies in whether treats are used as training tools or "hygge-snacks." It is the first major study on canine obesity in Denmark.
There's a bit of truth to the saying "like owner, like dog." This has now been confirmed by researchers. For the first time in Denmark, researchers have systematically investigated the factors related to our four-legged friends being overweight or obese. One of the results demonstrates an unambiguous correlation between the weight status of a dog and its owner.
The study, conducted by researchers at the University of Copenhagen, shows that the prevalence of heavy or obese dogs is more than twice as large among overweight or obese owners than among owners who are slim or of a normal weight.
Part of the explanation rests upon how owners manage dog treats. The research results show a correlation between overweight dog owners and the use of dog treats as "hygge-candy" (cozy-candy).
"Whereas normal weight owners tend to use treats for training purposes, overweight owners prefer to provide treats for the sake of hygge. For example, when a person is relaxing on the couch and shares the last bites of a sandwich or a cookie with their dog," says Charlotte R. Bjørnvad of the University of Copenhagen's Department of Veterinary Clinical Sciences. Bjørnvad, a veterinarian and professor, is the main author of the research article, now published in the journal Preventive Veterinary Medicine.
The researchers studied 268 adult dogs recruited at animal clinics around Zealand and the Capital Region of Denmark. Of the pets recruited, 20% were either heavy or obese.
"Oftentimes, people don't consider their dog's weight status to be a problem. And this might contribute to a dog's being overweight. But being heavy or obese does have a great impact on dog health -- which on average results in a shortened lifespan," according to bioethics professor and article co-author, Peter Sandøe, of the University of Copenhagen's Department of Food and Resource Economics.
Previous studies have shown that on average, heavy dogs live 1.3 years less than dogs on restrictive diets and that part of the explanation may be an earlier development of osteoarthritis with the heavier weight.
Castration triples the risk of being heavy or obese
The researchers also looked into how castration and sterilization can be risk factors in relation to dog weight. The study shows that castrated male dogs have three times as high a risk of being heavy or obese compared to intact dogs. On the other hand, the study demonstrated that sterilization has no impact on weight in female dogs. Whether they are intact or not, female dogs, have an increased risk of being heavy compared with intact males.
"When males are castrated, they face just as high of a risk of becoming overweight as females. Castration seems to decrease the ability to regulate the appetite in male dogs and at the same time, it might also decrease the incentive to exercise which results in an increased risk of becoming overweight. Therefore, an owner should be careful about how they feed their dog after it has been castrated," says Bjørnvad.
Sandøe adds: "They might even want to consider not neutering. As long as there are no runaway females in the area, there are in most cases no reason to neuter."
The researchers hope that this new knowledge raises awareness about canine weight among veterinarians and dog owners, and that it contributes to better obesity prevention and treatment strategies by identifying focus areas for intervention.
https://www.sciencedaily.com/releases/2019/09/190919095230.htm
Deeper understanding of early life experiences can help combat chronic obesity and frequent bingeing
September 17, 2019
Science Daily/Elsevier
According to a new study in the journal Heliyon, published by Elsevier, dysfunctional eating patterns and habits in overweight and obese adults can be triggered by early life experiences that are deeply rooted within patients' personality features. As a result, weight loss interventions like surgery and cognitive-behavior therapy might not be sufficient to guarantee long-term success. Cognitive psychologists used the Schema Therapy (ST) model to gain a deeper understanding of the emotional and psychological functioning of these individuals with a view towards developing more effective treatment options.
"While the biological and environmental causes of obesity are well known, psychological determinants that might indicate chronic predispositions are less clear," explained lead investigator Barbara Basile, PhD, Association of Cognitive Psychology (APC), School of Cognitive Psychotherapy (SPC), Rome, Italy. "The results of our study suggest that dysfunctional eating patterns and habits associated with overweight and obesity are deeply rooted within patients' personality features and current interventions are not enough to guarantee a long-lasting effect."
The key concepts within the ST approach include Early Maladaptive Schemas, Schema Modes and dysfunctional Coping strategies. All of these develop across the life span and originated in early childhood and adolescence, where emotional core needs, such as love and nurturance, safety, acceptance, autonomy, limits setting, etc., might not have been adequately satisfied by caregivers and significant others.
Using an ST framework, investigators assessed early maladaptive schema and coping modes in 75 normal, overweight, and obese patients. Overweight and obese adults reported more maladaptive schemas and dysfunctional coping strategies when compared to normal-weight individuals. Moreover, investigators found that stressors trigger shifts from one coping mode to another, some predictive of frequent binge and bulimic behaviors.
Maladaptive schemas encapsulate dysfunctional thoughts and behaviors and map out patterns of perception, emotion, and physical sensation rooted in early life experiences that subsequently shape individuals' beliefs about themselves and the world. The dysfunctional schemas observed in obesity are linked to coping mechanisms resulting in self-defeating thoughts and emotion-avoidant food attitudes and behaviors.
"Our findings highlight the role of the Insufficient Self-Control schema among overweight and obese individuals, which manifests as difficulties in tolerating distress and restraining impulses. We also documented that overeating and bingeing behaviors serve as self-soothing strategies that help individuals to cut off their feelings and quiet their internalized 'Punitive Parent'," noted Professor Basile.
Among study participants, overeating and bingeing behaviors served as self-soothing strategies when they experienced feelings of abandonment (the belief others will be unavailable or unpredictable in their support or connection); dependence/incompetence (the belief that one has failed, or will fail in important life areas of achievement); and subjugation (the belief that one must surrender control to others), as well as to quiet internalized Punitive Parent voices (inner dialogue that is self-blaming, punishing, and abusive that causes one to detach emotionally and reject help). Frequent bingeing was associated with belief patterns of abandonment, enmeshment (being excessively emotionally involved and connected with others at the expense of full individuation or normal social development); and failure (the belief that one always fails in important life areas of achievement) schemas, as well as by those who react impulsively with anger and frustration (Impulsive/Undisciplined Child) and by those with a Punitive Parent inner dialogue.
Professor Basile and her co-investigators believe that this deeper understanding of the emotional and psychological functioning of obese patients, recognizing the impact of early life experiences, might help clinicians promote the long-term efficacy of psychological interventions in overeating related pathologies.
Identifying each patient's unique maladaptive schema and modes is the first step of ST intervention. To help the patient deal with their future needs and emotions in a healthier way, treatment might also include:
· Addressing and satisfying the frustrated core emotional needs, embedded in the vulnerable child mode, in a safe therapeutic relationship.
· De-potentiating the punitive parental mode and its destructive messages.
· Reducing dysfunctional coping mechanisms, such as the detached protector self-soothing.
· Expanding the healthy adult mode.
"Addressing actual schema modes and the connected early experiences within a caring and solid clinical setting, such as the one used within ST practice, might be of particular value for obese patients," concluded Professor Basile.
https://www.sciencedaily.com/releases/2019/09/190917133050.htm
Negative impacts of food insecurity on children's health
September 9, 2019
Science Daily/American University
Food insecurity -- uncertainty about or a lack of consistent access to food that meets the needs of household members -- is a persistent social problem in the United States that affected roughly 14.3 million households in 2018 and nearly 14% of households with children, according to the U.S. Department of Agriculture. A new paper by researchers at the Boston University School of Social Work (BUSSW) and American University's School of Public Affairs (AU SPA) confirms the negative impact of food insecurity on child health, suggesting the urgent need for policies to combat this problem.
"Previous studies have pointed to a negative impact of food insecurity on child health, but our paper uses rich, nationally representative data to rule out other explanations for this relationship," says study lead author Margaret M.C. Thomas, MSW, doctoral candidate at BUSSW. "By comparing the outcomes of children in food-secure homes to those in food-insecure homes who were alike with respect to a large number of other factors, we have been able to more definitively characterize the serious negative health impacts of food insecurity."
Published in the journal Pediatrics, the research by Thomas and colleagues Associate Professor Daniel P. Miller, PhD (Boston University), and Associate Professor Taryn W. Morrissey, PhD (American University), points to a unique and negative effect of household food insecurity on children's health that is not due to the composition of their homes, the safety of their neighborhoods, or their household's income or receipt of public assistance. Instead, it shows the pervasive negative impacts of household food insecurity on children's health. "Household food insecurity was related to significantly worse general health, some acute and chronic health problems, worse health care access, and heightened emergency department use for children," says Morrissey.
The team of researchers used propensity scoring (PS) methods to investigate the effects of food insecurity on children's health by leveraging the inclusion of a measure of household food insecurity in the nationally representative National Health Interview Survey (NHIS). The NHIS data also include a rich set of background information about families including demographic characteristics, economic information, public program participation, and adult physical and mental health outcomes.
Thomas and her colleagues believe that their analytic approach is an important improvement over previous studies that use traditional regression methods. Using PS methods allowed them to better assess the causal impact of food insecurity on key domains of child health and health care use.
"Propensity scoring, a quasi-experimental family of methods, seeks to mimic the context of an experimental design by comparing outcomes among children who differ with respect to the household's food insecurity but who are alike in all other observable ways," Thomas says. "Because of the highly detailed information in the NHIS data, we were able to create a sample that is balanced with respect to known predictors of food insecurity."
Data on the independent impact of food insecurity on child health helps guide efforts to prevent food insecurity and ameliorate its consequences. The researchers suggest immediate policy responses, such as an increase in federal SNAP (Supplemental Nutrition Assistance Program) benefits for families.
"There are clear and consistent harmful impacts of food insecurity on children's general health, chronic health, acute health, and access to health care," Thomas says. "Without intervention, household food insecurity will continue to detrimentally impact children's health."
https://www.sciencedaily.com/releases/2019/09/190909131110.htm
Sugar alters compounds that impact brain health in fruit flies
September 6, 2019
Science Daily/University of Michigan
When fruit flies are exposed to a high sugar diet, key metabolites associated with brain health become depleted, according to a University of Michigan study.
This finding could tell researchers why behaviors that change with the internal energy state, such as food intake, learning and memory, and sleep, change on high-nutrient diets.
When our bodies metabolize food, that food is broken down into metabolites -- small molecules that perform many functions in the body, including providing fuel to cells and activating or inhibiting enzyme production. The study, published in Nature Communications, examines how metabolites in the brains and bodies of fruit flies change as the flies transition between hunger and satiety.
Through the study, the researchers found that the flies' metabolic profiles change rapidly during the quick transition from hunger to satiety, with the flies' brains showing a larger change than their bodies. In particular, the high sugar diet lowered the levels the brain metabolites N-acetyl aspartate, or NAA, and kynurenine.
The alteration of metabolites could impact how quickly the fly senses satiety, causing it to eat more. In fact, U-M researchers previously found that an increase in a specific metabolite with a high sugar diet caused overeating and weight gain.
Although scientists aren't clear on the role of NAA in the brain, it appears to provide fuel for brain cells and balances osmolarity -- or regulates cell volume -- in the brain. Lower levels of another metabolite, kynurenine, which is produced in high levels during exercise, is associated with depression.
"What we found was a metabolic remodeling," said senior author Monica Dus, U-M assistant professor of molecular, cellular and developmental biology. "It wasn't just a gradual accumulation from an early to longer exposure, but by the seventh day on a high sugar diet, these fruit flies had a completely different metabolic profile."
Cancer cells also undergo this type of metabolic remodeling in order to fuel their growth, which is why diet may play a role in cancer treatment and a reason the Dus lab wanted to examine the shift of metabolites in the brain.
To examine how a high sugar diet affects the brains and bodies of fruit flies, the research team compared a group of fasting flies to a group of fed flies. In the fed flies, the researchers skipped giving them dinner, then fed them a breakfast of moderately sweet glucose jelly the next day.
The researchers mix the sugar jelly with blue or green dye, and after an hour, check the belly of the fly to make sure it's eaten. To make sure the animals have eaten their fill, the researchers put the flies on a lickometer covered with the glucose jelly. A lickometer is exactly what it sounds like: A meter that counts the number of times it has been licked.
Then, inside separate tubes, researchers freeze the sated flies as well as the group of fasting flies. This stops the metabolic process, so that researchers can look at what's going on in the flies' brains at the moment of satiety. The researchers shake the tubes, which shatters the fly. A sieve separates the fly's head, thorax, abdomen and legs. These parts were then sent to a company that uses mass spectrometry to measure the metabolites within the fly.
To help refine the list of metabolites in the flies, Alla Karnovsky, a research associate professor of computational medicine and bioinformatics at Michigan Medicine, created a tool called FlyScape. She based it on a previous tool she created for the analysis of human metabolomics data called MetScape. Like Metscape, Flyscape is open access: any researcher studying metabolites in fruit flies can use the software.
These tools help researchers look for patterns in metabolomics data. A researcher like Daniel Wilinski, a postdoctoral fellow in the Dus lab and first author of the manuscript, can input a list of metabolites found in her fruit fly subjects, as well as a list of genes from fruit flies, into Flyscape. The tool will produce visualizations of the metabolic networks of fruit flies.
"You can view the metabolites and genes that are changing between different conditions," Karnovsky said. "This helps us understand what biological processes are happening."
Co-author Peter Freddolino, assistant professor of biological chemistry and computational medicine and bioinformatics at Michigan Medicine, has worked with Dus on previous papers to study how a high sugar diet dulls the sense of taste in fruit flies.
"We examined what the changes in metabolites are that could be fundamentally perturbing the way that these cells were working," Freddolino said. "What this study tells us is what metabolomic pathways might be involved."
Ultimately, the study found that 20 metabolites, in addition to NAA and kynurenine, were impacted by sugar consumption. Next, says Dus, the research team plans to dial down into how changes in these metabolites impact the brain, altering food intake and affecting other conditions such as sleep, learning and memory.
https://www.sciencedaily.com/releases/2019/09/190906090559.htm
Poor diet can lead to blindness
September 3, 2019
Science Daily/University of Bristol
An extreme case of "fussy" or "picky" eating caused a young patient's blindness, according to a new case report published today in Annals of Internal Medicine.
The University of Bristol researchers who examined the case recommend clinicians consider nutritional optic neuropathy in any patients with unexplained vision symptoms and poor diet, regardless of BMI, to avoid permanent vision loss.
Nutritional optic neuropathy is a dysfunction of the optic nerve which is important for vision. The condition is reversible, if caught early. But, left untreated, it can lead to permanent structural damage to the optic nerve and blindness.
In developed countries like the UK, the most common causes of nutritional optic neuropathy are bowel problems or drugs that interfere with the absorption of various important nutrients from the stomach. Purely dietary causes are less common because food supply is good, but elsewhere in the world, poverty, war and drought are linked to malnutrition and higher rates of nutritional optic neuropathy.
Clinician scientists from Bristol Medical School and the Bristol Eye Hospital examined the case of a teenage patient who first visited his GP complaining of tiredness. The link between his nutritional status and vision was not picked up until much later, and by then, his visual impairment had become permanent.
Aside from being a "fussy eater," the patient had a normal BMI and height and no visible signs of malnutrition and took no medications. Initial tests showed macrocytic anemia and low vitamin B12 levels, which were treated with vitamin B12 injections and dietary advice. When the patient visited the GP a year later, hearing loss and vision symptoms had developed, but no cause was found. By age 17, the patient's vision had progressively worsened, to the point of blindness. Further investigation found the patient had vitamin B12 deficiency, low copper and selenium levels, a high zinc level, and markedly reduced vitamin D level and bone mineral density. Since starting secondary school, the patient had consumed a limited diet of chips, crisps, white bread, and some processed pork. By the time the patient's condition was diagnosed, the patient had permanently impaired vision.
The researchers concluded that the patient's 'junk food' diet and limited intake of nutritional vitamins and minerals resulted in the onset of nutritional optic neuropathy. They suggest the condition could become more prevalent in future, given the widespread consumption of 'junk food' at the expense of more nutritious options, and the rising popularity of veganism if the vegan diet is not supplemented appropriately to prevent vitamin B12 deficiency.
Dr Denize Atan, the study's lead author and Consultant Senior Lecturer in Ophthalmology at Bristol Medical School and Clinical Lead for Neuro-ophthalmology at Bristol Eye Hospital, said: "Our vision has such an impact on quality of life, education, employment, social interactions, and mental health. This case highlights the impact of diet on visual and physical health, and the fact that calorie intake and BMI are not reliable indicators of nutritional status."
The team recommends dietary history should be part of any routine clinical examination like asking about smoking and alcohol intake. This may avoid a diagnosis of nutritional optic neuropathy being missed or delayed as some associated visual loss can fully recover if the nutritional deficiencies are treated early enough.
https://www.sciencedaily.com/releases/2019/09/190903091437.htm
Suggested move to plant-based diets risks worsening brain health nutrient deficiency
Woman with vegetarian meal (stock image). Credit: © sonyakamoz / Adobe Stock
Suggested move to plant-based diets risks worsening brain health nutrient deficiency
And UK failing to recommend or monitor dietary levels of choline, warns nutritionist
August 29, 2019
Science Daily/BMJ
The momentum behind a move to plant-based and vegan diets for the good of the planet is commendable, but risks worsening an already low intake of an essential nutrient involved in brain health, warns a nutritionist in the online journal BMJ Nutrition, Prevention & Health.
To make matters worse, the UK government has failed to recommend or monitor dietary levels of this nutrient -- choline -- found predominantly in animal foods, says Dr Emma Derbyshire, of Nutritional Insight, a consultancy specialising in nutrition and biomedical science.
Choline is an essential dietary nutrient, but the amount produced by the liver is not enough to meet the requirements of the human body.
Choline is critical to brain health, particularly during fetal development. It also influences liver function, with shortfalls linked to irregularities in blood fat metabolism as well as excess free radical cellular damage, writes Dr Derbyshire.
The primary sources of dietary choline are found in beef, eggs, dairy products, fish, and chicken, with much lower levels found in nuts, beans, and cruciferous vegetables, such as broccoli.
In 1998, recognising the importance of choline, the US Institute of Medicine recommended minimum daily intakes. These range from 425 mg/day for women to 550 mg/day for men, and 450 mg/day and 550 mg/day for pregnant and breastfeeding women, respectively, because of the critical role the nutrient has in fetal development.
In 2016, the European Food Safety Authority published similar daily requirements. Yet national dietary surveys in North America, Australia, and Europe show that habitual choline intake, on average, falls short of these recommendations.
"This is....concerning given that current trends appear to be towards meat reduction and plant-based diets," says Dr Derbyshire.
She commends the first report (EAT-Lancet) to compile a healthy food plan based on promoting environmental sustainability, but suggests that the restricted intakes of whole milk, eggs and animal protein it recommends could affect choline intake.
And she is at a loss to understand why choline does not feature in UK dietary guidance or national population monitoring data.
"Given the important physiological roles of choline and authorisation of certain health claims, it is questionable why choline has been overlooked for so long in the UK," she writes. "Choline is presently excluded from UK food composition databases, major dietary surveys, and dietary guidelines," she adds.
It may be time for the UK government's independent Scientific Advisory Committee on Nutrition to reverse this, she suggests, particularly given the mounting evidence on the importance of choline to human health and growing concerns about the sustainability of the planet's food production.
"More needs to be done to educate healthcare professionals and consumers about the importance of a choline-rich diet, and how to achieve this," she writes.
"If choline is not obtained in the levels needed from dietary sources per se then supplementation strategies will be required, especially in relation to key stages of the life cycle, such as pregnancy, when choline intakes are critical to infant development," she concludes.
https://www.sciencedaily.com/releases/2019/08/190829184143.htm
Excess body fat increases the risk of depression
August 27, 2019
Science Daily/Aarhus University
Carrying ten kilograms of excess body fat increases the risk of depression by seventeen per cent. The more fat, the greater the probability of developing depression. This is the main conclusion of a new study carried out by researchers from Aarhus University and Aarhus University Hospital, Denmark.
"Our study also indicated that the location of the fat on the body makes no difference to the risk of depression. This suggests that it is the psychological consequences of being overweight or obese which lead to the increased risk of depression, and not the direct biological effect of the fat. If the opposite was true we would have seen that fat located centrally on the body increased the risk the most, as it has the most damaging effect in biological terms," says the study's last author Dr. Søren Dinesen Østergaard.
He is professor at the Department of Clinical Medicine at Aarhus University and affiliated with the Department of Affective Disorders at Aarhus University Hospital.
Prior studies in the field have predominantly used Body Mass Index (BMI) to measure obesity. BMI is calculated solely on the basis of body weight and height and is therefore a fairly crude measure, that does not, for example, take build and muscle mass into account.
"BMI is an inaccurate way of measuring overweight and obesity. Many elite athletes with a large muscle mass and a low body fat mass will have a BMI above 25, which is classified as overweight according to the common definition. This obviously doesn't make much sense. Therefore, one of the strengths of our study is that we've been able to zoom in and look at the specific relationship between the amount of body fat and the risk of depression," explains Dr. Østergaard.
In the study, which has been published in the journal Translational Psychiatry, the researchers have analysed data from two large genetic data sets: the UK Biobank, which contains data on the correlation between genetic variants and physical measurements (including body fat mass distributed around parts of the body); and the Psychiatric Genomics Consortium, which contains information on the correlation between genetic variants and depression.
Dr. Østergaard also highlights his research group's choice of the 'Mendelian randomization' method as the main reason why the study was successful. He also emphasises that the findings are particularly significant in light of the fact that almost 40 per cent of the world's adult population is overweight.
"In addition to the known physical consequences of obesity such as diabetes and cardiovascular disease, there is also a significant and now well-documented psychological component, which needs to be dealt with as well. This is yet another argument for resolving the obesity epidemic," he says, before emphasising that it is important to have a balanced approach to the issue:
"As it appears to be the psychological consequences of obesity, such as a negative body image and low self-esteem that is the main driving force behind the increased risk of depression, society's efforts to combat obesity must not stigmatise, as this will probably increase the risk of depression even further. It is important to bear this in mind so we can avoid doing more harm than good in the effort to curb the obesity epidemic," says Dr. Østergaard.
FACTS ABOUT MENDELIAN RANDOMIZATION:
Mendelian randomization (named after the Austrian monk Gregor Mendel, who was the father of modern genetics) is a method which in recent years has helped researchers to overcome a major challenge associated with observational studies -- namely that of making causal inference. In observational studies researchers often find correlations between two conditions -- e.g. between obesity and depression -- where it is difficult, or rather impossible, to determine whether there is indeed a causal effect going from obesity to depression -- or vice versa. Mendelian randomization may solve this challenge.
Mendelian randomization can be described as nature's version of the randomised controlled trials that are carried out when testing whether a new drug has the desired (causal) effect in the treatment of a disease. In the clinical trials of drugs, lots are drawn to determine whether individual participants will receive the active drug or a placebo, without them knowing which treatment they have been assigned to. Instead, Mendelian randomization takes advantage of the fact that a completely natural randomization takes place during the formation of the sex cells (egg cells and sperm cells), which represent the origin of all human beings. When sex cells are formed, the parents' genetic variants -- including those that give rise to increased body fat- are randomly distributed. Therefore, some individuals will have received many of these variants and others less. In the study in question, the researchers have utilised this natural and random source of variation to determine whether people who have received many genetic variants for increased body fat have an increased risk of suffering depression.
THE RESEARCH RESULT -- MORE INFORMATION
Genetic epidemiological study utilising data from the UK Biobank (with information on the association between genetic variants and fat mass based on a study of 330,000 people) and the Psychiatric Genomics Consortium (with information on the association between genetic variants and depression based on a study of 135,000 people with depression and 345,000 control subjects).
https://www.sciencedaily.com/releases/2019/08/190827095100.htm
Junk food intake in children reduced by health education that addresses emotional issues
August 23, 2019
Science Daily/European Society of Cardiology
Teacher training followed by classroom education with information, activities, and emotional support improves lifestyles in teachers and students, according to research to be presented at ESC Congress 2019 together with the World Congress of Cardiology.(1) The study suggests that knowledge alone is insufficient to change behaviour.
"Numerous studies have addressed health issues in the school setting, but most have focused on physical activity and nutrition, with little attention to emotional issues such as self-esteem, depression and eating behaviours," said study author Dr Carolinne Santin Dal Ri, a paediatrician at the Institute of Cardiology of Rio Grande do Sul, Porto Alegre, Brazil.
The Happy Life, Healthy Heart programme randomly allocated ten public schools in the city of Frederico Westphalen, Brazil, to the intervention group (five schools) or control group (five schools). The study included 473 students aged 6 to 12 and 32 teachers. Baseline assessments included weight, height, physical activity, food intake, and health knowledge in children; and physical activity and food consumption in teachers. Measurements were repeated after the intervention was completed.
The intervention had two stages: teacher training followed by students in the classroom. Teachers attended four meetings over a four-month period, were given a booklet, and had access to video lessons. The material was in seven chapters:
1) risk factors for cardiovascular diseases in childhood;
2) choice of healthy foods;
3) food labelling;
4) sodium, sugars and fats;
5) emotional health and quality of life;
6) physical activity; and
7) healthy practices and changes in habits.
Each section contained theory plus suggestions for classroom activities based on the theme, age of the children, and intended goals.
In the classroom, teachers covered one theme per week, including at least one activity.(2) Teachers were free to choose or amend the activities and could incorporate them into projects based on the school's syllabus. To encourage teacher participation, a group was created on a social network where they received messages and reminders from the researcher on the topic they were supposed to work on. Teachers also shared their own experiences. The researcher visited the intervention schools to stimulate teachers and offer guidance.
For the control group schools, teachers did not participate in the training course and students attended the school's usual classes about health and healthy eating based on the curriculum.
Both students and teachers benefitted from the intervention. The proportion of students following Brazilian Food Guide advice to avoid pizza/hamburgers and soft drinks increased significantly by 15% and 20%, respectively. In addition, there was a 28% increase in the number of teachers who were physically active.
Dr Santin Dal Ri said: "Children in both the intervention and control groups increased their level of health knowledge during the study. But only those in the intervention group changed their eating behaviours. This suggests that information on its own does not lead to lifestyle improvements. In our study, a programme that combined information with playful activities and emotional support was beneficial for children and teachers."
https://www.sciencedaily.com/releases/2019/08/190823080023.htm
How stress can curb the desire to eat in an animal model
August 16, 2019
Science Daily/University of Texas Health Science Center at Houston
Eating disorder researchers at The University of Texas Health Science Center at Houston (UTHealth) have discovered a neurocircuit in mice that, when activated, increased their stress levels while decreasing their desire to eat. Findings appear in Nature Communications.
The scientists believe their research could aid efforts to develop treatments for a serious eating disorder called anorexia nervosa, which has the highest mortality rate of any mental disorder, according to the National Institute of Mental Health. People with anorexia nervosa avoid food, severely restrict food, or eat very small quantities of only certain foods. Even when they are dangerously underweight, they may see themselves as overweight.
"We have identified a part of the brain in a mouse model that controls the impact of emotions on eating," said Qingchun Tong, PhD, the study's senior author and an associate professor in the Center for Metabolic and Degenerative Disease at McGovern Medical School at UTHealth.
Because mice and humans have similar nervous systems, Tong, the Cullen Chair in Molecular Medicine at UTHealth, believes their findings could shed light on the part of the human brain that regulates hunger.
The investigators believe they are among the first to demonstrate the role of this neurocircuit in the regulation of both stress and hunger.
While previous research has established that stress can both reduce and increase a person's desire to eat, the neural mechanisms that act on the regulation of eating by stress-related responses largely remain a mystery.
Tong's team focused on a neurocircuit connecting two parts of the mouse brain: the paraventricular hypothalamus, an eating-related zone in the brain, and the ventral lateral septum, an emotional zone in the brain. The neurocircuit acts as an on/off switch.
When researchers activated the neurocircuit, there was an increase in anxiety levels and a decrease in appetite. Conversely, when the investigators inhibited the neurocircuit, anxiety levels dropped and hunger increased.
The scientists used a research technique called optogenetics to turn the neurons in question on and off.
https://www.sciencedaily.com/releases/2019/08/190816191450.htm
Gut-brain connection helps explain how overeating leads to obesity
Overeating, junk food concept (stock image). Credit: © motortion / Adobe Stock
August 12, 2019
Science Daily/Baylor College of Medicine
A multi-institutional team reveals a previously unknown gut-brain connection that helps explain how those extra servings lead to weight gain.
Eating extra servings typically shows up on the scale later, but how this happens has not been clear. A new study published today in the Journal of Clinical Investigation by a multi-institutional team led by researchers at Baylor College of Medicine reveals a previously unknown gut-brain connection that helps explain how those extra servings lead to weight gain.
Mice consuming a high-fat diet show increased levels of gastric inhibitory polypeptide (GIP), a hormone produced in the gut that is involved in managing the body's energy balance. The study reports that the excess GIP travels through the blood to the brain where it inhibits the action of leptin, the satiety hormone; consequently, the animals continue eating and gain weight. Blocking the interaction of GIP with the brain restores leptin's ability to inhibit appetite and results in weight loss in mice.
"We have uncovered a new piece of the complex puzzle of how the body manages energy balance and affects weight," said corresponding author Dr. Makoto Fukuda, assistant professor of pediatrics at Baylor and the USDA/ARS Children's Nutrition Research Center at Baylor and Texas Children's Hospital.
Researchers know that leptin, a hormone produced by fat cells, is important in the control of body weight both in humans and mice. Leptin works by triggering in the brain the sensation of feeling full when we have eaten enough, and we stop eating. However, in obesity resulting from consuming a high-fat diet or overeating, the body stops responding to leptin signals -- it does not feel full, and eating continues, leading to weight gain.
"We didn't know how a high-fat diet or overeating leads to leptin resistance," Fukuda said. "My colleagues and I started looking for what causes leptin resistance in the brain when we eat fatty foods. Using cultured brain slices in petri dishes we screened blood circulating factors for their ability to stop leptin actions. After several years of efforts, we discovered a connection between the gut hormone GIP and leptin."
GIP is one of the incretin hormones produced in the gut in response to eating and known for their ability to influence the body's energy management. To determine whether GIP was involved in leptin resistance, Fukuda and his colleagues first confirmed that the GIP receptor, the molecule on cells that binds to GIP and mediates its effects, is expressed in the brain.
Then the researchers evaluated the effect blocking the GIP receptor would have on obesity by infusing directly into the brain a monoclonal antibody developed by Dr. Peter Ravn at AstraZeneca that effectively prevents the GIP-GIP receptor interaction. This significantly reduced the body weight of high-fat-diet-fed obese mice.
"The animals ate less and also reduced their fat mass and blood glucose levels," Fukuda said. "In contrast, normal chow-fed lean mice treated with the monoclonal antibody that blocks GIP-GIP receptor interaction neither reduced their food intake nor lost body weight or fat mass, indicating that the effects are specific to diet-induced obesity."
Further experiments showed that if the animals were genetically engineered to be leptin deficient, then the treatment with the specific monoclonal antibody did not reduce appetite and weight in obese mice, indicating that GIP in the brain acts through leptin signaling. In addition, the researchers identified intracellular mechanisms involved in GIP-mediated modulation of leptin activity.
"In summary, when eating a balanced diet, GIP levels do not increase and leptin works as expected, triggering in the brain the feeling of being full when the animal has eaten enough and the mice stop eating," Fukuda said. "But, when the animals eat a high-fat diet and become obese, the levels of blood GIP increase. GIP flows into the hypothalamus where it inhibits leptin's action. Consequently, the animals do not feel full, overeat and gain weight. Blocking the interaction of GIP with the hypothalamus of obese mice restores leptin's ability to inhibit appetite and reduces body weight."
These data indicate that GIP and its receptor in the hypothalamus, a brain area that regulates appetite, are necessary and sufficient to elicit leptin resistance. This is a previously unrecognized role of GIP on obesity that plays directly into the brain.
Although more research is needed, the researchers speculate that these findings might one day be translated into weight loss strategies that restore the brain's ability to respond to leptin by inhibiting the anti-leptin effect of GIP.
https://www.sciencedaily.com/releases/2019/08/190812160533.htm
Scientists eager to explain brain rhythm boost's broad impact in Alzheimer's models
December 11, 2019
Science Daily/Picower Institute at MIT
Neuroscientists lay out the the few knowns and many unknowns that must be understood to determine why sensory stimuluation of 40Hz brain rhythms have broad effects, particularly in Alzheimer's models.
The sweeping extent to which increasing 40Hz "gamma" rhythm power in the brain can affect the pathology and symptoms of Alzheimer's disease in mouse models has been surprising, even to the MIT neuroscientists who've pioneered the idea. So surprising, in fact, they can't yet explain why it happens.
In three papers, including two this year in Cell and Neuron, they've demonstrated that exposing mice to light flickering or sound buzzing at 40Hz, a method dubbed "GENUS" for Gamma Entrainment Using Sensory stimuli, strengthens the rhythm across the brain and changes the gene expression and activity of multiple brain cell types. Pathological amyloid and tau protein buildups decline, neurons and their circuit connections are protected from degeneration and learning and memory endure significantly better than in disease model mice who do not receive GENUS.
In a new review article in Trends in Neurosciences two researchers leading those efforts lay out the few knowns and many unknowns that must be understood to determine how the widespread effects take place. It's a challenge they relish because the answers could both break new scientific ground and help them improve how GENUS could become a therapeutic or preventative approach for people.
"While we know it affects pathology in mice, we want to understand how because that will help us understand and refine potential treatment," said lead author Chinnakkaruppan Adaikkan, a postdoc in the lab of senior author Li-Huei Tsai, Picower Professor of Neuroscience and director of The Picower Institute for Learning and Memory.
Adaikkan has been interested in understanding how neural activity produces brain rhythms since his doctoral research. At MIT, he is channeling that passion into understanding how sensory stimulation can entrain oscillations.
"That's what drives me to come to the lab every day to study these mechanisms," Adaikkan said. "When we got the data from the first mouse where we recorded from the visual cortex, the hippocampus and the prefrontal cortex we were surprised to see that visual stimulation entrains in these brain regions. That was very exciting but we have a very long way to go to understand how this happens."
The new paper raises that question and many others for the field. What cells underlie the brain's response to GENUS? How do gamma rhythms engage non-neuronal cells such as astrocytes and microglia? How does it propagate beyond the brain regions responsible for perception? How extensively can enhancing gamma affect cognition? Does long-term stimulation affect brain circuit connections and how they change?
Cell roles
Studies of how groups of neurons engage in coherent oscillations of electrical activity have yielded two models to explain gamma rhythms. Both involve an interplay between excitatory and inhibitory neurons but differ on which type leads the interaction, Adaikkan and Tsai wrote. In his work, Adaikkan is attempting to dissect the roles of specific neuron types in GENUS and how closely those patterns mirror other sources of gamma, such as that invoked by cognitive tasks.
GENUS affects more than neurons. Tsai's lab has found that microglia change their gene expression, their physical form, their protein-consuming behavior and their inflammatory response depending on the Alzheimer's model involved. Work from another group showed that blocking vesicle release in astrocytes can hinder gamma power in mice and Tsai's group found that auditory GENUS recruits an increase reactive astrocytes, which are more inclined to consume pathological proteins.
The new paper offers three hypotheses about how such "glial" cells are involved: They might contribute directly to gamma entrainment by regulating the flow of ions that carry electrical charge; even if they don't contribute to rhythms, their ionic sensitivity may still make them responsive to gamma changes; they might instead be affected by changes in levels of neurotransmitters as a result of gamma.
Moreover, different glia may also become involved because of their proximity to electrical couplings between neurons called synapses, or because of how their activity is otherwise governed by neural activity.
The broader brain
That GENUS extends to the hippocampus, which is key for memory, and the prefrontal cortex, which is key for cognition, is likely a factor in how it preserves brain function. But again there are competing models for how increased gamma could facilitate multi-regional communication. In one, the authors write, coherence at the same frequency optimizes communication, while in the other model, one region's gamma activity directly drives activity in regions downstream. New experiments that directly manipulate inter-regional circuits, they argue, could help resolve which model better explains gamma entrainment's effects.
Finally, the effects of GENUS on brain function and behavior also aren't fully explained. The Tsai lab's has shown significant effects on spatial memory and some effects on other forms of memory, depending on the stimulation method. Other studies have shown that stimulating brain rhythms by other means, such as via genetic or optogenetic manipulations in mice, or via transcranial stimulation in humans, can also improve functions such as working memory. Adaikkan is interested in closing a gap between those studies and the Tsai lab's work: Most studies measure cognitive performance during stimulation, while the Tsai lab has done so after the conclusion of repeated stimulation. He said he'd like to also test how mice perform while GENUS is actively underway.
"Our lab is excited to tackle these many hypotheses and to see how the field tackles many more," Tsai said. "GENUS has created many intriguing new questions for neuroscience."
https://www.sciencedaily.com/releases/2019/12/191211115624.htm
How playing the drums changes the brain
Many years of playing the instrument leave clear traces
December 9, 2019
Science Daily/Ruhr-University Bochum
People who play drums regularly for years differ from unmusical people in their brain structure and function. The results of a study by researchers from Bochum suggest that they have fewer, but thicker fibres in the main connecting tract between the two halves of the brain. In addition, their motor brain areas are organised more efficiently. This is the conclusion drawn by a research team headed by Dr. Lara Schlaffke from the Bergmannsheil university clinic in Bochum and Associate Professor Dr. Sebastian Ocklenburg from the biopsychology research unit at Ruhr-Universität Bochum following a study with magnetic resonance imaging (MRI). The results have been published in the journal Brain and Behavior, online on 4 December 2019.
Drummers were never previously studied
"It has long been understood that playing a musical instrument can change the brain via neuroplastic processes," says Sarah Friedrich, who wrote her bachelor's thesis on this project. "But no one had previously looked specifically into drummers," she adds.
The researchers from Bochum were interested in this group because their motor coordination far surpasses that of untrained people. "Most people can only perform fine motor tasks with one hand and have problems playing different rhythms with both hands at the same time," explains Lara Schlaffke. "Drummers can do things that are impossible for untrained people."
Drumming first, then brain scans
The team intended to gain new insights into the organisation of complex motor processes in the brain by identifying the changes in the brain caused by this training. The researchers tested 20 professional drummers who have played their instrument for an average of 17 years and currently practice for more than ten hours per week. They examined them using various MRI imaging techniques that provide insights into the structure and function of the brain. They then compared the data with measurements of 24 unmusical control subjects. In the first step, both groups had to play drums to test their abilities and were then examined in the MRI scanner.
More efficient motor processing
Drummers presented clear differences in the front part of the corpus callosum, a brain structure that connects the two hemispheres and whose front part is responsible for motor planning. The data indicated that the drummers had fewer but thicker fibres in this important connecting tract between the brain hemispheres. This allows musicians to exchange information between the hemispheres more quickly than the controls. The structure of the corpus callosum also predicted the performance in the drum test: the higher the measure of the thickness of the fibres in the corpus callosum, the better the drumming performance.
Moreover, the brain of drummers was less active in motor tasks than that of control subjects. This phenomenon is referred to as sparse sampling: a more efficient brain organisation in the areas leads to less activation in professionals.
Older participants wanted for new study
"We would like to thank our highly motivated participants who took part in the study," says Lara Schlaffke. "It was great fun working with you."
https://www.sciencedaily.com/releases/2019/12/191209110513.htm