new research shows that overeating

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New research shows that a ‘cheat day’ might not be that bad

Photo by Arturo Holmes/Getty Images

• A new study at the University of Bath found that binge eating on occasion doesn’t have major metabolic consequences.
• 14 healthy young men were instructed to eat pizza until full or to keep going until they couldn’t eat another bite.
• Their blood sugar levels were similar to having eaten normally and blood lipids levels were only slightly higher than normal.

The eternal diet dilemma: to have a cheat day or to never indulge?

Researchers at the Centre for Nutrition, Exercise and Metabolism at the University of Bath wanted to understand the effects of overeating, given the prevalence of obesity in the Western world. They asked 14 men to eat pizza—or, as they wonderfully phrased it, a “homogenous mixed-macronutrient meal.” Some of the volunteers ate a lot of pizza.

That was the point. The men, all between the ages of 22 and 37, were either told to eat until full or to keep going until they couldn’t possibly eat another bite. The results of this study were published in the British Journal of Nutrition.

Despite some men eating up to two-and-a-half pizzas in one sitting (roughly 5,000 calories), their metabolism didn’t change much. Their blood sugar levels were similar to having eaten a normal meal; their blood lipids levels were only slightly higher. All of this was a surprise to the researchers.

Not that all went swimmingly. Blood insulin was 50 percent higher and the signaling hormones that scream “hey, stop eating,” were altered. Waist circumference and sagittal abdominal diameter increased in the overeating group, though for how long is not known.

The researchers noticed that, despite the prevalence of obesity, “no study has ever examined the metabolic response to eating beyond feeling comfortably full in a single eating occasion.” They pulled from a few studies that detail the effects of overeating, yet those focus on weight gain, not metabolic changes.

Marion Nestle: Why Do We Overeat? www.youtube.com

Lead researcher Aaron Hengist says the results showed the resilience of our body during times of excess.

“Our findings show that the body actually copes remarkably well when faced with a massive and sudden calorie excess. Healthy humans can eat twice as much as ‘full’ and deal effectively with this huge initial energy surplus.”

Of course, these were all young, healthy men, which will skew the outcome. Still, they expected more of a metabolic impact.

The researchers also focused on mood. Four hours after eating maximally, overeaters had no desire to eat sweet foods. This contradicts previous research that shows the brain’s reward centers are food-specific—pizza shouldn’t change cravings for sweets. The overeating groups also felt lethargic after their binge, which is to be expected.

The researchers are not giving a pass for overeating. Caloric intake remains the main driver of obesity. Signaling hormones are altered with continued overeating, making it difficult for the obese to know when to stop. Regular overeating changes body composition, metabolic rates, and mood.

In the past, humans had to stock up on food when they found it while hunting and foraging. We are equipped to handle the occasional caloric overload. James Betts, who was also involved in the study, says that an occasional binge for healthy people is not necessarily a bad thing.

“This study shows that if an otherwise healthy person overindulges occasionally, for example eating a large buffet meal or Christmas lunch, then there are no immediate negative consequences in terms of losing metabolic control.”

Acknowledging the study’s limitations of age, health, and gender of participants, the researchers are planning on investigating the metabolic and mood effects of operating on women, obese volunteers, and the elderly.

Stay in touch with Derek on Twitter , Facebook and Substack . His next book is “ Hero’s Dose: The Case For Psychedelics in Ritual and Therapy.”

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Thursday, May 16, 2019

NIH study finds heavily processed foods cause overeating and weight gain

Small-scale trial is the first randomized, controlled research of its kind.

People eating ultra-processed foods ate more calories and gained more weight than when they ate a minimally processed diet, according to results from a National Institutes of Health study. The difference occurred even though meals provided to the volunteers in both the ultra-processed and minimally processed diets had the same number of calories and macronutrients. The results were published in Cell Metabolism .

This small-scale study of 20 adult volunteers, conducted by researchers at the NIH’s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), is the first randomized controlled trial examining the effects of ultra-processed foods as defined by the NOVA classification system . This system considers foods “ultra-processed” if they have ingredients predominantly found in industrial food manufacturing, such as hydrogenated oils, high-fructose corn syrup, flavoring agents, and emulsifiers.

Previous observational studies looking at large groups of people had shown associations between diets high in processed foods and health problems. But, because none of the past studies randomly assigned people to eat specific foods and then measured the results, scientists could not say for sure whether the processed foods were a problem on their own, or whether people eating them had health problems for other reasons, such as a lack of access to fresh foods.

“Though we examined a small group, results from this tightly controlled experiment showed a clear and consistent difference between the two diets,” said Kevin D. Hall, Ph.D., an NIDDK senior investigator and the study’s lead author. “This is the first study to demonstrate causality — that ultra-processed foods cause people to eat too many calories and gain weight.”

For the study, researchers admitted 20 healthy adult volunteers, 10 male and 10 female, to the NIH Clinical Center for one continuous month and, in random order for two weeks on each diet, provided them with meals made up of ultra-processed foods or meals of minimally processed foods. For example, an ultra-processed breakfast might consist of a bagel with cream cheese and turkey bacon, while the unprocessed breakfast was oatmeal with bananas, walnuts, and skim milk.

The ultra-processed and unprocessed meals had the same amounts of calories, sugars, fiber, fat, and carbohydrates, and participants could eat as much or as little as they wanted.

On the ultra-processed diet, people ate about 500 calories more per day than they did on the unprocessed diet. They also ate faster on the ultra-processed diet and gained weight, whereas they lost weight on the unprocessed diet. Participants, on average, gained 0.9 kilograms, or 2 pounds, while they were on the ultra-processed diet and lost an equivalent amount on the unprocessed diet.

“We need to figure out what specific aspect of the ultra-processed foods affected people’s eating behavior and led them to gain weight,” Hall said. “The next step is to design similar studies with a reformulated ultra-processed diet to see if the changes can make the diet effect on calorie intake and body weight disappear.”

For example, slight differences in protein levels between the ultra-processed and unprocessed diets in this study could potentially explain as much as half the difference in calorie intake.

“Over time, extra calories add up, and that extra weight can lead to serious health conditions,” said NIDDK Director Griffin P. Rodgers, M.D. “Research like this is an important part of understanding the role of nutrition in health and may also help people identify foods that are both nutritious and accessible — helping people stay healthy for the long term.”

While the study reinforces the benefits of unprocessed foods, researchers note that ultra-processed foods can be difficult to restrict. “We have to be mindful that it takes more time and more money to prepare less-processed foods,” Hall said. “Just telling people to eat healthier may not be effective for some people without improved access to healthy foods.”

Support for the study primarily came from the NIDDK Division of Intramural Research.

About the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK): The NIDDK, a component of the National Institutes of Health (NIH), conducts and supports research on diabetes and other endocrine and metabolic diseases; digestive diseases, nutrition and obesity; and kidney, urologic and hematologic diseases. Spanning the full spectrum of medicine and afflicting people of all ages and ethnic groups, these diseases encompass some of the most common, severe, and disabling conditions affecting Americans. For more information about the NIDDK and its programs, see https://www.niddk.nih.gov .

About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov .

NIH…Turning Discovery Into Health ®

Hall KD, et al. Ultra-processed diets cause excess calorie intake and weight gain: A one-month inpatient randomized controlled trial of ad libitum food intake. Cell Metabolism . May 16, 2019.

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Overeating now bigger global problem than lack of food

By Jessica Hamzelou

13 December 2012

Not good for global health

(Image: Peter Reali/Plainpicture)

The largest ever study into the state of the world’s health has revealed that, for the first time, the number of years of healthy living lost as a result of people eating too much outweigh the number lost by people eating too little.

The Global Burden of Disease report – a massive research effort involving almost 500 scientists in 50 countries – also concludes that we have finally got a handle on some common infectious diseases, helping to save millions of children from early deaths. But collectively we are spending more of our lives living in poor health and with disability.

“The Global Burden of Disease 2010 is the most comprehensive assessment of human health in the history of medicine,” says Richard Horton , editor of The Lancet , in which the report will be published. “It provides insights into human health that are comparable in scope and depth to the sequencing of the human genome.”

The report assessed the prevalence of diseases and causes of death across the globe in 2010, and compared these to data collected in 1990 to identify any trends.

For the first time on a global scale, being overweight has become more of a health problem than lack of nutrition. In 1990, undernutrition was the leading cause of disease burden, measured as the number of years of healthy life an average person could expect to lose as a result of illness or early death. Back then, a high body-mass index, or BMI, was ranked tenth. Now, undernutrition has dropped to eighth place, while BMI has risen to become the sixth leading cause of disease burden.

Too much to eat

“A greater amount of disease burden has occurred because people are fat and have too much to eat, as opposed to having too little to eat,” says Alan Lopez at the University of Queensland in Brisbane, Australia, who worked on the study.

Being overweight can hike a person’s blood pressure and cause stroke and heart disease; together, these two conditions are responsible for a quarter of all deaths. And the problem isn’t limited to the west – the Middle East is one region that is seeing significant increases in BMI.

But while more of us may be overweight, we are also living longer. In some countries, the change has been huge – the Maldives, for example, has seen an increase in life expectancy of almost 30 years since the 1970s. Rural health programmes have also contributed to big improvements in countries including Bangladesh and Iran.

“There has been a lot of progress,” says Majid Ezzati at Imperial College London, who led part of the study investigating the risk factors of disease. “These are countries that have implemented programmes in large regions and nationwide to get interventions to the people that really need them.”

Progress in eliminating the causes of early childhood death – mainly infections, diarrhoea and birth problems – has been astounding. The rate of death in the under-5s has dropped by 60 per cent since 1990.

High mortality

Sub-Saharan Africa is still experiencing high levels of mortality from infectious diseases such as HIV and malaria, yet globally deaths from infectious diseases have dropped. In fact, we are more likely to die from non-infectious diseases – especially those caused by being overweight.

Looking forward, obesity and the use of tobacco and alcohol are obvious targets for health policy change. But it is also important to focus on healthy ageing.

“The large burden [of disease] related to disability was a surprise,” says Christopher Murray at the University of Washington in Seattle. “There’s been a focus on mortality, but there’s a huge volume [of disease burden] related to things that don’t really kill you.”

Musculoskeletal disorders – such as neck and back pain – dominate this category, as do mental disorders and substance abuse.

There’s a need to improve awareness of these chronic conditions in the developing world, says Irene Agyepong at the University of Ghana in Accra, who was not involved in the study. “The kind of awareness we have in the western world is not there in the south,” she says. “We have to focus on it now rather than wait until it is upon us, like the HIV AIDS epidemic is on us.”

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Why Do You Overeat?

Knowing why is the start to making the lifelong changes you truly want..

Posted January 5, 2021 | Reviewed by Abigail Fagan

Knowing why we overeat can direct us to ultimately change our overeating behavior. Overeating is habitual and behavioral which is known to be directly impacted by our thoughts and feelings. Understanding why we overeat and how our thoughts and feelings can thwart or positively contribute to our self-belief , motivation , and commitment to the process can lead to lifelong sustained changes.

The Why and How of Making Real Changes

Our propensity, unfortunately, is to deny, avoid or disregard our uncomfortable thoughts and feelings. There can be great discomfort sitting with a craving or urge or facing that we have the impulse to eat much more than we wanted or intended to. When change requires an inquiry and discovery of our thoughts and feelings, the “why” and “how” is the start of the journey. Barriers such as reluctance, fear and/or hopelessness need to be unearthed, processed and worked on if we are looking to achieve long-term changes.

If it were so easy, we would all have effective behavioral change nailed down. As imperfect human beings, we all relate to having personal challenges that make behavioral change feel arduous, disappointing, frustrating, and at times, downright impossible. It’s the very behaviors we can identify as having a hard time working on, committing to and sticking with.

We fall into a cycle of making change, and then periodically or for the long haul, slipping back into old patterns of behavior which are all too familiar and unnerving. This cycle typically trails along with deep personal regret, shame and disappointment. Overeating most definitely fits into the category of behaviors that prove challenging for us.

Why Do We Overeat?

So let’s tackle the question of why we overeat. In his informative TED talk on simple ways to break a bad habit, neuroscientist and fellow Psychology Today blogger Judson Brewer explains that overeating is learned and becomes a habit. The nuance behind it is that we are triggered (see the enticing food), engage in eating behavior, and then get immediately rewarded by the behavior (experience pleasure because it tastes so incredibly good which satiates our appetite, and we feel better emotionally because it helps to meet an emotional need).

We commit to memory the reward process and continually chase that pleasure (the first delicious bite, the immediate joyfulness, etc.). This is why it is so difficult to change the behavior — because it’s what we have learned, what’s become engrained in our memory and the associations we then naturally make when we eat.

To expand on the above, overeating might have been learned and utilized as a coping mechanism to deal with emotions (i.e., emotional eating ). It could have been the way we learned to cope with sadness, disappointment, frustration, joy, or some other emotion . It serves as a good distraction and can be an effective, yet maladaptive way to keep emotions at bay.

Food and eating are also part of the fabric in our society and can be a sign of status. It’s part of the way we celebrate holidays, religious celebrations and rituals, birthday parties, and special occasions. The inclusion of food is a major part of the way we socialize in general.

Whether we are going to a Super Bowl party, a 4th of July BBQ or our friend’s milestone birthday party, food is usually plentiful. It’s what we arrange for and what we expect to have available to us.

Second, snacking can be addicting . Because snacking on something sweet, salty, or crunchy is pleasurable, it stimulates the brain’s reward centers through the neurotransmitter dopamine , exactly like other addictive drugs, and releases the body’s own opioids in the brain, sending signals that it needs more.

Studies have proven that certain foods can be addictive. That is why people tend to binge on potato chips, chocolate, or cupcakes rather than on carrot sticks and apple slices. Brain imaging using PET scans showed that high sugar and high fat foods work just like drugs such as heroin, opium, or morphine. People also develop a tolerance of sugar; they will need more and more to be satisfied.

Research shows that when given a choice, rats were more attracted to sweetened water than to cocaine or heroin.[i] In order to understand biochemistry, when a person consumes glucose, a type of sugar, it spikes the blood sugar and creates a high insulin reaction. High insulin then blocks leptin, the appetite hormone , so our brain does not get the “I’m full” signal and instead thinks that we’re starving. Our pleasure-based reward center becomes activated, which drives us to consume more sugar. This explains why individuals may have difficulty controlling the consumption of foods high in sugar when they are continuously exposed to foods containing sugar.

Lastly, our minds trip us up. Because food can be so incredibly satisfying and addicting, we gain mastery over rationalizing our behavior which keeps us enrolled in this cycle. From speaking to adults and children, I came up with 40 rationalizations for why individuals justify their overeating. They include “watching what I eat is too hard,” “it’s low-fat/fat-free,” “I will make up for it later,” “I’ll burn it off later,” “I don’t usually eat this,” “it’s free,” “everyone else is eating it,” “I am anxious /tired/sad/upset/ bored ,” “I will just eat these few nibbles,” “it’s a special occasion,” “I’m treating myself,” “I can start eating more healthfully again tomorrow,” “I really want it,” “no one will know,” “I’ll end up eating it eventually,” “healthy food doesn’t taste as good,” and “it’s freshly baked/cooked.” I expect these rationalizations and others sound all too familiar, for good reason, because we all utilize them.

Understanding the Psychological and Emotional Factors

So now that we can say that we know the main reasons why we overeat, why is it still so fundamentally difficult for us to change our behavior? As I started out saying, this is a journey. A quick fix, like just focusing on diet and exercise, as we previously were led to believe would do the trick, we now know, falls short. The psychological and emotional factors that directly create and impact our barriers and keep us in this perpetual cycle need to be addressed as well.

For real incremental sustaining change to occur, we need to be open to discovering, processing and working through these barriers. My book, Free Your Child From Overeating: 53 Mind-Body Strategies For Lifelong Health , uses psychological treatments such as Cognitive-Behavioral Therapy (CBT), Acceptance and Commitment Therapy (ACT), and Mindfulness to tackle the psychological and emotional barriers that keep us stuck. Although it is geared toward parents and practitioners, I use the strategies widely with adults, teens, and adolescents.

The four step model, utilizing the 4P's — predict , plan , put into action , and practice — emphasizes making change in a lasting way. It's predicated on better understanding how your mind works, connecting with your fundamental values, doing a thorough assessment of your thinking and behavior, and implementing effective strategies to restructure and work toward a growth mindset . Each of the 4P's has systematic strategies that reinforce insight and behavior change.

We are constantly implementing strategies in regard to our health and wellness that help in the short-term but do not lead to sustaining changes. It's what feels like an endless cycle of getting on and off the roller coaster. You have spent enough money, time, and energy, with no real results. Understanding the emotional and psychological barriers is the missing link. Now is the time to live the life you are proud of and which truly empowers you.

Here is a "Self-Love Guided Meditation " that I led.

[i] Lenoir, M., Serre, F., Cantin, L., and Ahmed, S.H. (2007). “Intense Sweetness Surpasses Cocaine Reward.” PLOS ONE , 2(8), e698.

Ahmed, S.H., Guillem, K., and Vandaele, Y. (2013). “Sugar Addiction: Pushing the Drug-Sugar Analogy to the Limit.” Current Opinion in Clinical Nutrition and Metabolic Care , 16(4), 434–39.

Madsen, H.B., and Ahmed, S.H. (2014). “Drug Versus Sweet Reward: Greater Attraction to and Preference for Sweet Versus Drug Cues.” Addiction Biology , published online March 7, 2014.

Michelle P. Maidenberg, Ph.D., MPH, LCSW-R, CGP maintains a private practice in Harrison, NY. She is an adjunct graduate professor of Mindfulness Practice at New York University and the president and clinical director of the Thru My Eyes Foundation. My new book is ACE Your Life: Unleash Your Best Self and Live the Life You Want.

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New Treatment Leads to Much Less Overeating

Summary: A new treatment system that focuses on the link between eating and mental health helps people with obesity make healthier decisions when it comes to eating.

Source: NUST

The current advice and treatment given to patients with obesity mostly involves eating less and healthier food and exercising more. In some of the most severe cases, patients undergo obesity surgery.

“We see a strong need for interdisciplinary treatment that considers the psychological aspects of morbid obesity much more than is happening now,” says Trine Tetlie Eik-Nes. “The treatment we’ve been using is based on teaching patients to make them aware of the reasons for their overeating, followed by exercises and group discussions.”

Eik-Nes is an associate professor at NTNU’s Department of Neuromedicine and Movement Science and has led the project.

Patients who wanted help

Overeating is defined as repeated episodes where a person eats far more than normal. The 42 adults who participated in the study were people who had visited the Obesity Outpatient Clinic at St. Olav’s Hospital to ask for help.

All the participants had third-degree obesity, meaning a body mass index (BMI) of 40 or more, or second-degree obesity with additional problems. The majority of the group were women. Six people had undergone obesity surgery.

Compound causes

Eik-Nes believes that the understanding and treatment of obesity and overeating has been too narrow.

“The explanation is more complicated than simply having a big appetite, genetic susceptibility and “laziness.” International research indicates that 30 to 50 percent of people with a high degree of overeating who seek treatment for obesity have psychological challenges around loss of control, such as overeating that lasts a whole day,” she says.

Eating to numb the pain

According to the researcher, overeating is often related to internal and external stressors. The causes can be many and complex: for example, childhood trauma, negative thoughts about oneself, contempt for the body, problematic relationships with parents and social difficulties.

A lot of people feel stigmatized because of their large body—in their family, at school, at work and elsewhere in society. Food acts to numb and help cope with everyday life.

“If you have security, good support, decent finances and a manageable everyday life, you don’t need to regulate your emotions so much with food, alcohol or other stimuli,” says Eik-Nes.

Lack of treatment

She believes that the health service offers patients with morbid obesity lifestyle changes, when they really need a comprehensive assessment and treatment that combines mental health care and somatics.

“This approach will give people with eating disorders a chance to succeed. Psychological treatment isn’t used enough for morbid obesity, and the methods are too limited for such a heterogeneous group,” Eik-Nes says.

The treatment method used in the study was developed by Eik-Nes and Kjersti Hognes Berg. An interdisciplinary team conducted the assessments and treatment, which emphasized emotional safety and openness.

The participants came together for 30 hours over ten weeks. After each teaching session, the patients broke into small groups for training in “dissecting” their own everyday lives. All 42 stayed with the study to the end.

“We wanted to teach and make the patients aware of the connection between weight and mental health. During the ten weeks, the goal was for them to become more aware of the challenges they faced in everyday life and what strategies could help. Every individual was able to receive customized goals and measures this way,” says Eik-Nes.

Carryover to own life

During treatment, patients became more aware of what causes them to react and triggers their overeating. For example, overeating or grazing (constant snacking) can calm the experience of being outside one’s comfort zone.

Many participants felt that their negative body image and shame posed a barrier to physical activity and a social life. Eik-Nes believes this might explain why it is so difficult for this group to put lifestyle measures into practice.

Less eating and restlessness, more social life

A clear improvement was measured at the end of the ten weeks.

“The patients experienced a nearly 30 percent reduction in the number of overeating episodes and a significant improvement in their emotional issues, like inner turmoil, anxiety, depression and irritability. In addition, the patients reported that they felt far less restricted in their social activities,” says Eik-Nes.

The study did not measure weight loss, but the impression was that a good number of the participants had experienced some weight loss.

According to the researcher, an important point of the study was to investigate how treatment that spans both physical and mental health can work.

“Our interdisciplinary approach worked well. Just the fact that everyone completed the study is a very good result,” says Eik-Nes.

“We can’t say anything about the long-term effect of the treatment yet. We hope this study can lay the foundation for a larger project on morbid obesity and psychological disorders. Then we’d like to investigate change over time,” says Eik-Nes.

About this obesity and psychology research news

Author: Press Office Source: NUST Contact: Press Office – NUST Image: The image is in the public domain

Original Research: Open access. “ A Group Intervention for Individuals With Obesity and Comorbid Binge Eating Disorder: Results From a Feasibility Study ” by Trine T. Eik-Nes et al. Frontiers in Endocrinology

A Group Intervention for Individuals With Obesity and Comorbid Binge Eating Disorder: Results From a Feasibility Study

Purpose:  A common challenge among a subgroup of individuals with obesity is binge eating, that exists on a continuum from mild binge eating episodes to severe binge eating disorder (BED). BED is common among bariatric patients and the prevalence of disordered eating and ED in bariatric surgery populations is well known. Conventional treatments and assessment of obesity seldom address the underlying psychological mechanisms of binge eating and subsequent obesity. This study, titled PnP (People need People) is a psychoeducational group pilot intervention for individuals with BED and obesity including patients with previous bariatric surgery. Design, feasibility, and a broad description of the study population is reported.

Material and Methods:  A total of 42 patients were from an obesity clinic referred to assessment and treatment with PnP in a psychoeducational group setting (3-hour weekly meetings for 10 weeks). Of these, 6 (14.3%) patients had a previous history of bariatric surgery. Feasibility was assessed by tracking attendance, potentially adverse effects and outcome measures including body mass index (BMI), eating disorder pathology, overvaluation of shape and weight, impairment, self-reported childhood difficulties, alexithymia, internalized shame as well as health related quality of life (HRQoL).

Results:  All 42 patients completed the intervention, with no adverse effects and a high attendance rate with a median attendance of 10 sessions, 95% CI (8.9,9.6) and 0% attrition. Extent of psychosocial impairment due to eating disorder pathology, body dissatisfaction and severity of ED symptoms were high among the patients at baseline. Additionally, self-reported childhood difficulties, alexithymia, and internalized shame were high among the patients and indicate a need to address underlying psychological mechanisms in individuals with BED and comorbid obesity. Improvement of HRQoL and reduction of binge eating between baseline and the end of the intervention was observed with a medium effect

Conclusion:  This feasibility study supports PnP as a potential group psychoeducational intervention for patients living with BED and comorbid obesity. Assessments of BED and delivery of this intervention may optimize selection of candidates and bariatric outcomes. These preliminary results warrant further investigation  via  a randomized control trial (RCT) to examine the efficacy and effectiveness of PnP.

This is what I’ve been looking for with my BED. I have been unable to follow through with any program as all doctors want to do is give me a pill and a diet. Counselors don’t have the science to cover the daily/hourly mental fight.

I am a former life long over eater / later in life bulimic .. Food Addicts in Recovery Anonymous has helped me more than anything else I have ever done …13 years in recovery and going strong despite the pandemic ..the support is exactly what an addict like me needs 24/7 ..greatest thing in my life today is this program

Try researching overeaters anonymous

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Articles on Overeating

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Our sense of taste helps pace our eating – understanding how may lead to new avenues for weight loss

Zachary Knight , University of California, San Francisco

Overeating at Christmas can cause weight gain – but that doesn’t necessarily mean it’s permanent

Duane Mellor , Aston University

Festive bulge: scientists offer advice on how to beat overeating

Thomas C. Erren , University of Cologne ; Philip Lewis , University of Cologne , and Ursula Wild , University of Cologne

Your tendency to overindulge these holidays could relate to your ‘eating personality’. Which type are you?

Georgie Russell , Deakin University and Alan Russell , Flinders University

Step away from the table – why you keep eating when you’re full

Amanda Salis , The University of Western Australia

COVID kilos: why now is the best time to shed them

Hoi Lun Cheng , University of Sydney and Amanda Salis , The University of Western Australia

Preparing your own food or watching it being made could lead to overeating – new research

Jane Ogden , University of Surrey

Food variety is important for our health – but the definition of a ‘balanced diet’ is often murky

Rochelle Embling , Swansea University ; Aimee Pink , Swansea University ; Laura Wilkinson , Swansea University , and Menna Price , Swansea University

A doctor’s open apology to those fighting overweight and obesity

J. David Prologo , Emory University

Here’s how the body reacts to one-off overeating – new research

Aaron Hengist , University of Bath ; James Betts , University of Bath , and Rob Edinburgh , University of Bath

How to use habit science to help you keep your New Year’s resolution

Wendy Wood , USC Dornsife College of Letters, Arts and Sciences

How to lose weight and keep it off – according to science

Kevin Deighton , Leeds Beckett University

Memories of eating influence your next meal – new research pinpoints brain cells involved

Marise Parent , Georgia State University

Why some people overeat when they’re upset

Laura Wilkinson , Swansea University ; Angela Rowe , University of Bristol , and Charlotte Hardman , University of Liverpool

One in three women binge eat during pregnancy

Nadia Micali , UCL

How a better understanding of the seven ages of appetite could help us stay healthy

Alex Johnstone , University of Aberdeen

Five reasons why we overeat

Jenny Morris , University of Sussex

For restaurants looking to boost profits, it’s often about everything but the food

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Christmas stuffing: here’s what happens to your body when you overeat

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Stress, overeating, and obesity: insights from human studies and preclinical models

Maria razzoli.

1 Department of Integrative Biology and Physiology University of Minnesota, 2231 6th Street SE, Minneapolis, MN 55455, Phone: + 612-626-7006, Fax: + 612-625-51492

Carolyn Pearson

2 Department of Psychiatry, University of Minnesota, 2450 Riverside Avenue, Minneapolis, MN 55454, Phone: + 612-273-9800, Fax: + 612-273-9779

3 The Emily Program, 2265 Como Avenue, St. Paul, MN 55108, Phone: + 651-645-5325

Alessandro Bartolomucci

Eating disorders and obesity have become predominant in human society. Their association to modern lifestyle, encompassing calorie-rich diets, psychological stress, and comorbidity with major diseases are well documented. Unfortunately the biological basis remains elusive and the pharmacological treatment inadequate, in part due to the limited availability of valid animal models. Human research on binge eating disorder (BED) proves a strong link between stress exposure and bingeing: state-levels of stress and negative affect are linked to binge eating in individuals with BED both in laboratory settings and the natural environment. Similarly, classical animal models of BED reveal an association between acute exposure to stressors and binging but they are often associated with unchanged or decreased body weight, thus reflecting a negative energy balance, which is uncommon in humans where most commonly BED is associated with excessive or unstable body weight gain. Recent mouse models of subordination stress induce spontaneous binging and hyperphagia, altogether more closely mimicking the behavioral and metabolic features of human BED. Therefore the translational relevance of subordination stress models could facilitate the identification of the neurobiological basis of BED and obesity-associated disease and inform on the development of innovative therapies.

Graphical abstract

Introduction

The etiology and therapy of eating disorders have been receiving increasing scientific attention in light of the current epidemic of metabolic diseases, for which Western diet, sedentary life style and environmental stress are considered predisposing factors ( GBD 2013 Risk Factors Collaborators, 2015 ; Polivy and Herman, 2002 ). Food overconsumption can be conducive to the excessive body weight and adiposity that define obesity, a condition that is pervasively damaging of health and is now included among the high-burden chronic conditions such as diabetes, hypercholesterolemia, and hypertension ( Bauer et al. 2014 ; National Task Force on the Prevention and Treatment of Obesity, 2000 ; O’Connor et al. 2008 ; Whiteford et al. 2013 ; Wilfley et al. 2003 ).

Obesity is fundamentally dependent on the disruption of complex neuromolecular mechanisms receiving inputs from brain regions codifying autonomic responses, memory, arousal, cognition, reward processing, and emotional reactivity. The physiologic regulation of metabolism indeed relies on the communication between brain, gut, and adipose tissue (reviewed in Berthoud and Morrison, 2008 ; Cummings and Overduin, 2007 ; Lee and Abizaid, 2014 ) and its complexity embodies its essentiality for metabolic disease. Malfunctioning at the central pathways level can result in abnormal elevation of sympathetic outflow or, in case of defective or weakened signal feedback by the brain in response to satiety and nutrients from the gut, can cause overfeeding and disinhibition of liver glucose production, and thereby promote metabolic disease ( Berthoud, 2002 ). The inherent complexity of metabolic regulation is further magnified in the interaction with stress. Stress imposes on metabolic responses the influence of higher levels of glucocorticoids as well as many other stress-related pathways, including the sympathetic nervous system / sympatho-adreno-medullary axis ( Cacho et al. 2003 ; Pankevich et al. 2010 ; Razzoli and Bartolomucci, 2016 ).

Stress and negative affect are increasingly recognized as risk factors for obesity and binge eating disorder (BED; Goldschmidt et al. 2008 ; O’Connor et al. 2008 ; Stein et al. 2007 ; Striegel-Moore et al. 2007 ). BED is the most common eating disorder and is currently included in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5, 5th ed.; American Psychiatric Association, 2013 ). BED is characterized by recurrent binge-eating episodes, which are defined as ingestion of large amounts of food in discrete periods of time accompanied by feelings of loss of control and marked distress. This occurs in the absence of compensatory behaviors such as purging, fasting, or excessive exercise. BED has been shown to impact quality of life, to be associated with other psychopathologies, and to confer an increased risk for components of the metabolic syndrome (MetS), in particular for glucose dysregulation and diabetes, as seen in BED patients compared to BMI matched controls (see Mitchell, 2016 for a review). Not all BED patients present obesity. Nevertheless, excessive or unstable body weights are consequences of significant binging and have been associated to BED since its first description ( Spitzer et al., 1992 , 1993 ), making BED the eating disorder with the higher prevalence of obesity ( Villarejo et al. 2012 ).

Overall, the parallel increase in incidence of seemingly independent psychiatric and metabolic diseases has long been suspected to be due to common predispositions. The difficulty to identify their causal factors and underlying molecular mechanisms in humans makes animal models very valuable and needed to address mechanistic questions. Nevertheless, current animal models present several limitations. Data from human clinical studies as well as from classical and recently developed animal models of BED will be reviewed hereafter to highlight possible mechanisms of a stress-bingeing-obesity pathway for obesity and obesity-associated metabolic disease.

Binge Eating and Obesity

Binge eating is one of the most commonly reported disordered eating behaviors among individuals with obesity, and similarly full-syndrome BED, which is one of the most commonly occurring eating disorders ( American Psychiatric Association, 2013 ; Hudson, et al., 2007 ; Swanson et al., 2011 ). BED has been identified among children and adolescents in epidemiologic samples such as the National Comorbidity Survey – Adolescent Supplements ( Swanson et al., 2011 ); however, diagnosing binge eating in this age group can be complex, and thus “loss of control eating” is often studied instead ( Matherne, et al., 2015 ; Matheson, et al., 2012 ; Tanofsky-Kraff, et al., 2011 ). Further complicating the diagnosis of BED, many obese individuals who initially deny binge eating during face-to-face interviews later endorse this behavior during real-time, naturalistic assessments (i.e., ecological momentary assessment [EMA]), suggesting the utility and significance of studying binge eating in individuals with obesity ( Greeno et al., 2000 ; Le Grange et al., 2001 ). Binge eating is considerably more common among adults with obesity than in the general population, and individuals who binge eat are more likely to become obese than individuals without disordered eating ( Hudson et al., 2007 ). This is particularly concerning because the co-occurrence of binge eating and obesity is linked to more problematic eating-, activity-, and weight-related patterns, poorer quality of life, and more severe psychopathology ( de Zwaan et al., 1994 ; Goldschmidt et al., 2011 ; Hsu et al., 2002 ; Perez and Warren, 2012 ; Striegel-Moore et al., 1998 ; Wadden et al., 1992 ; Yanovski et al., 1992 ). In order to improve existing treatments and develop more effective interventions, it is necessary to understand the complex interplay of precipitating factors that promote binge eating among individuals with obesity.

Stress and binge-eating in the clinical population

Research in humans examining stress and binge-eating has proceeded along three main lines. First, brief manipulations of stress or inductions of negative affect have been used to study the stress and binge-eating relationship. Second, the relationship of stress occurring in the natural daily environment and its link to binge eating have been examined using ecological momentary assessment, a technique ideally suited to this purpose. Last, a very small literature has examined biochemical or physiologic correlates of binge eating and stress. Each of these areas will be examined in turn.

Experimental Stress Manipulations and Binge-Eating

Existing theories (e.g., affect regulation model: Polivy and Herman, 1993 ; escape theory: Heatherton and Baumeister, 1991 ) suggest that individuals may binge eat in the presence of stress or negative affect, perhaps in an effort to alleviate or distract from that state ( Dallman et al. 2003 ). Indeed, research to date supports this notion that negative affect and stress are important state-level risk factors for binge eating in BED (e.g., Cardi et al. 2015 ; Haedt-Matt and Keel, 2011 ; Leehr et al. 2015 ; Nicholls et al. 2016 ). Two types of methodologies have been employed to enhance our understanding of the link between state-levels of stress and binge eating in BED: (a) laboratory studies in which negative mood or stress is induced followed by a test meal of some kind and (b) ecological momentary assessment (EMA) in which negative affect and stress are measured in one’s natural environment in the hours leading up to a binge eating episode.

Laboratory Mood Induction Studies

Although the affect-focused theories of binge eating have existed for some time, researchers have only begun to study the link between BED and stress in the laboratory. These studies tend to employ various valid procedures, ranging from watching sad videos (e.g., Svaldi et al. 2014 ) to undergoing a stressful performance task (e.g., tier social stress test, TSST: Kirschbaum et al. 1993 ; Laessle and Schultz 2009 ), to elicit a negative mood which is supposed to produce a stress-response. The overall objective of these studies is to create a negative mood state in a controlled environment and to then assess the impact of that state on food consumption, thus directly assessing the link between negative mood and binge eating in BED. Overall, five studies using this design with adult BED samples found that when individuals with BED are in a negative mood or stressed, they display a higher amount of food intake compared (a) to when they are in a relaxed state and (b) to non-BED individuals in a negative mood state ( Rosenberg et al. 2013 ; Schultz and Laessle, 2010 , 2012 ; Svaldi et al. 2014 ; Zeeck et al. 2011 ). Furthermore, two of these studies also identified a higher loss of control in the BED samples following the mood induction compared to both the relaxed state and to non-BED controls following the mood induction ( Rosenberg et al. 2013 ; Schultz and Laessle, 2012 ). Individuals with BED appear to not only eat more when stressed, but may also eat at greater rates of speed when stressed compared to not-stressed and controls ( Schultz and Laessle, 2012 ), suggesting that they are perhaps eating in such a way to distract from that stressful state. That is, the rapid eating may be “consuming” their thoughts and behaviors, thereby allowing them to “forget” about their stress and negative affect. Moreover, it appears that when the specific feelings of sadness, guilt, and disappointment are induced in the laboratory, individuals with BED show an increased urge to binge ( Zeeck et al. 2011 ). Therefore, it may be the case that these feelings in particular are ones that link general negative affect and stress to binge eating.

Overall, laboratory studies have enhanced our understanding of the relationship between stress and binge eating behavior in BED. In particular, the controlled environment is incredibly beneficial for directly investigating this link; however, one downfall of this is the potential lack of ecological validity. That is, it is difficult to know if these laboratory findings generalize to the daily lives of individuals with BED.

Ecological Momentary Assessment Studies and Binge-Eating

Ecological Momentary Assessment (EMA) is an important technique that has been used to examine the relationship of stress to disordered eating. EMA involves the use of palm computers or smartphones to collect data about behaviors of interest and their correlates in the natural environment. Participants provide self-report data in response to device prompts, at the time of behaviors of interest (such as binge eating), and at the end of the day. The typical recording window is the one to two weeks. There are clear advantages to EMA, as compared to typical retrospective recall techniques. First, the data are collected in, more or less, real time (that is, they are “momentary”). Furthermore, the behaviors are assessed in the natural living environment, as compared to the laboratory (that is, the data are “ecological”).

Although less controlled than a laboratory study of mood induction, EMA studies have the advantage of gathering data as individuals go about their days in their natural environment. Thus, considering the findings from both methodologies is important for understanding the relationship between stress and binge eating in BED. EMA findings suggest that binge eating episodes tend to occur on days when negative affect is high ( Berg et al. 2014 ). Unlike healthy controls, individuals with BED report significantly worse moods prior to binge eating episodes compared to normal eating episodes ( Hilbert and Tuschen Caffier, 2007 ). Furthermore, negative affect and tension tend to increase in the hours leading up to a binge eating episode while positive affect tends to decrease ( Berg et al. 2015 ; Munsch et al. 2012 ). In fact, EMA findings mimic that of laboratory mood induction studies in that the specific emotion of guilt tends to increase prior to binge eating episodes ( Berg et al. 2015 ) ( Figure 1 ). It also seems to be the case that momentary distress is linked to not only binge eating episodes in BED, but loss of control episodes as well ( Goldschmidt et al. 2012 ). Thus, it appears that findings from both laboratory and EMA studies suggest that state-levels of stress and negative affect, and particularly guilt, are significantly linked to binge eating in individuals with BED.

The figure shows the momentary levels and trajectories of the facets of negative affect associated with binge eating episodes. The pre- and post-event trajectories of each negative affect subscale were modeled separately using piecewise linear, quadratic, and cubic functions centered on the time at which each of the eating episodes occurred. Momentary observations (Level 1) were nested within subjects (Level 2). With regard to Guilt, there were significant findings for both the pre- and post-event linear components of the binge eating model. The scaling of the y-axis ranged from 1.0 to 5.0. **p<.01. Modified from [ Berg et al., 2015 ].

Biologic Markers, Stress, and Binge-Eating

Very limited work has investigated changes in biological markers of stress in the context of binge eating. The results have been quite mixed in terms of identifying biological stress markers.

First, Radin et al. (2015) described a sample of 178 adolescents with or without loss-of-control eating who underwent a mood induction and subsequently consumed a test meal. Throughout, salivary cortisol was measured. The results of the study showed that depressive symptoms correlated with cortisol levels, but loss-of-control eating was not correlated in any way with cortisol results ( Radin et al. 2015 ). Second, Klatzkin et al. (2015) reported the results of a small study examining obese individuals with BED (n=9), obese, non-BED individuals (n=15), and 15 normal-weight, non-binge-eating participants (n=15). After baseline assessment, a mental stress task was used. In the BED group, increases in blood pressure in response to the mental health stressor were greater than those seen in the other two samples. However, while heart rate response was blunted in the BED group, the BED group did not differ from the other two groups after controlling for depression. Finally, Gluck and colleagues ( Gluck et al. 2014 , 2004 ) have reported in two studies on findings of biochemical markers after a cold pressor test in 10 non-BED and 11 individuals with BED. In this study, baseline ghrelin was equivalent in the two groups and they also did not differ significantly after a cold pressor test. In a second analysis, the BED group had higher basal cortisol levels than the non-BED group, and the area under curve after the cold pressor test was greater in the BED group.

Overall these studies provide a mixed picture, with inconsistent support for biological stress marker elevations in BED.

Classical rodent models of BED

Available animal models of eating disorders have been classified to evaluate their relevance to human disease and are ranked according to four criteria: etiologic, isomorphic, mechanistic, and predictive (Smith 1989) ( Table 1 ). These criteria closely resemble the ones established for models of psychiatric disorders ( McKinney 1974 ) in that they capture their causal, symptomatic, mechanistic, and therapeutic valence.

Rodent models associated with the development of binge-eating like behaviors.

The sham feeding model is achieved by equipping the animals with chronic fistulas to drain liquid food before entering the gastrointestinal tract therefore producing a defect in satiation. This allows to separate positive oro-sensory feedback, stimulating feeding, from negative intestinal feedback, inhibiting feeding ( Corwin and Buda-Levin, 2004 ; Smith, 2004 ). While this model allows for the exploration of basic mechanisms relevant for binging, it presents limitations for most validity criteria, not reproducing the voluntary elements of food restriction and since animals maintain weight by being fed outside the sham-feeding tests.

Several models have been based upon cycles of dieting and overeating. Restriction/refeeding cycles consist of several days of limited food access followed by a few days of ad libitum access ( Corwin and Buda-Levin, 2004 ; Virts et al. 1992 ). Most commonly body weight diminishes during these protocols, and the increased food intake accomplished with this procedure does not seem to be greater than the amount of food than most animals would eat during a similar time, due to compensatory eating. Nevertheless, some of these studies highlight neural and biological changes that might have importance to binging related disorders ( Colantuoni et al. 2002 , 2001 ; Rada et al. 2005 ).

Another common methodology is based on limited access to fatty food, in particular to an optional source of dietary fat under non-food-deprived conditions over extended period of time. As access to the fat decreases, consumption of the fat increases when it is provided ( Avena et al. 2009 ; Czyzyk et al. 2010 ). Nevertheless, a compensatory eating pattern emerges, as animals overeat on binge days and under eat on non-binge days. This response is very robust as it does not seem to habituate however doesn’t lead to excess body weight or adiposity ( Czyzyk et al. 2010 ). With these limitations in mind, this model presents the advantage of voluntary behaviors that are reliably expressed and of good isomorphic validity, although the binging and non-binging phases seem to correspond to different neurobiological substrates.

Stress and binge eating disorders

Stress ( Koolhaas et al. 2011 ; Harris 2015 for a review) has been often applied in developing eating disorder models. During chronic stress and the corresponding hyperactivation of the hypothalamus-pituitary-adrenal (HPA) axis, glucocorticoids and insulin increase craving for calorie-reach meals, a phenomenon explained by the “comfort food” hypothesis ( Dallman et al. 2003 ; Dallman, 2010 ). According to this hypothesis, the preference for palatable food ingestion reduces the negative effects of stress via downregulation of corticotropin releasing factor (CRF) in the amygdala as well as through stimulation the anterior part of the pleasure-associated anterior nucleus accumbens shell that outweighs the contribution of the stress-stimulated posterior, defensive part of this nucleus ( Dallman 2004 , 2003 ; La-Fleur, 2004; Pecoraro, 2004 ; Rebuffe'-Scrive, 1992 ). Additionally, the consumption of palatable foods downregulates the stress response by activating reward pathways through reward-based structural plasticity ( Avena and Bocarsly, 2012 ; Teegarden and Bale, 2008 ). Insulin level, elevated by food overconsumption, are thought to contribute to dampening adrenocorticotropic hormone (ACTH) and glucocorticoid responses to stress, as supported by the negative correlation between the hypothalamic para ventricular nucleus (PVN) CRF mRNA expression and plasma insulin levels ( Dallman et al. 2007 ). As a result, the stress-induced increase in consumption of palatable foods is also associated with reduced behavioral stress indices, such as anxiety-related behaviors, stress-induced learned helplessness, and reactions of pain and distress ( Ulrich-Lai et al. 2015 ).

A variety of stress models have been used to stimulate food intake, differing in nature (physical or psychological), severity, and time of application.

The tail-pinch model has been used to induce hyperphagia, but the effect is short lived and does not set the stage for an increased body weight ( Rowland and Antelman, 1977 ). Furthermore, results from the application of several pharmacological compounds have provided conflicting results, limiting the predictive validity of the model ( Morley et al. 1983 ).

While a similar case can be made for the application of shock stress per se, when combined with food restricting/refeeding protocols shock stress induces binge eating of palatable food ( Hagan et al. 2002 ). Although again the model doesn’t facilitate the development of obesity and has been used to induce bingeing during short durations only, it seems to possess good construct validity and to prove useful for identifying mechanistic predispositions to bingeing. The ability of chronic psychological stress to increase food preferences towards highly palatable food has been related to the intensity of the stress experienced. A milder version of the traditional chronic variable stress in terms of severity and duration/frequency of stress application, resulted in a more modest and short-lived increased preference for palatable foods than in rats stressed in the traditional chronic variable stress ( Thompson et al. 2015 ). These data would suggest that higher intensity paradigms correspond to more pronounced and sustained preference for high palatable foods ( Thompson et al. 2015 ). While the stress relief properties of the consumption of high palatable food may be transitory/temporary during continuous stress exposure, the unresolved hyperactivation of the HPA axis over time can continue to sustain food overconsumption and facilitate obesity, due for example to the permissive effect of glucocorticoids on lipogenesis and fat deposition ( de Guia and Herzig, 2015 ). Nevertheless, palatable food intake blunts acute stress responses both in human and rodent studies, although the mechanisms involved still remain elusive ( Ulrich-Lai et al. 2015 ).

Validity of classical models of binge eating disorders

Most binge eating in humans seems not to be driven by hunger or metabolic demands and most patients are overweight or obese (DSM5; Mathes et al. 2009 ; Mussell et al. 1995 ; Waters et al. 2001 ). Therefore the fact that experimental animals from classical BED models as highlighted above do not show significant increases in body weight/adiposity ( Cao et al. 2014 ; Czyzyk et al. 2010 ) limits their isomorphic validity. Similarly, most stress encountered by human and corresponding with the development of BED are of psychological nature ( Heatherton et al. 1991 ; O’Connor et al., 2008 ), with onset of binge eating being preceded by elevated perceived stress and increased incidence of life stressors ( Pike et al. 2006 ; Striegel-Moore et al. 2007 ).

This again limits the construct validity of some of the traditional models of human BED, particularly if based upon a physical stressor and may only partially target the interested physiology (mechanistic and predictive validity) (Rospond, 2016; add here some of the cits of Rev #3).

Aside from these traditional models of BED recent experimental evidences reviewed below strongly suggest that rodent models of chronic social stress elicit robust changes in eating behavior with high degree of face validity for BED and translational relevance for the human condition ( Table 1 ).

Binge eating, hyperphagia and metabolic disorders in rodent models of social stress

Metabolic disorders due to psychosocial stress have now been well documented in humans ( Bose, 2009 ; Dallman, 2006 ), non-human primates ( Shively, 2009 ), and rodents ( Bartolomucci et al. 2009 , 2004 ; Coccurello et al. 2009 ; Finger, 2011 ; Kuo et al. 2007 ). Social subordination stress has long been considered ideal to mimic the impact of psychosocial stress on human pathologies ( Bartolomucci et al. 2005 ; Koolhaas et al. 2011 ; Sapolsky, 2005 ; Scott, 2012 ; Razzoli and Bartolomucci, 2016 ) and has been recently presented as a major risk factor for insulin resistance and T2D ( Kelly and Ismail, 2015 ).

Nevertheless limited work addresses the role of subordination stress on meal pattern. In the visible burrow system (VBS) laboratory rats are housed together in a mixed-sex colony for several weeks during which males form a dominance hierarchy through agonistic interactions. Subordinate males present reproducible behavioral, endocrine, physiological, and neurochemical changes consistent with a severe stress phenotype, that is also associated to a profound weight loss due to reduced food intake ( Blanchard et al. 1995 ; Nguyen et al., 2007 ). During recovery from the VBS, subordinate rats immediately become hyperphagic and quickly regain the lost weight primarily as fat, resulting in greater overall and visceral adiposity than dominant and control rats. This effect is further enhanced in rats exposed to a second cycle of VBS stress and recovery. Consistent with increased adiposity, subordinates have elevated plasma leptin and insulin levels ( Tamashiro et al. 2011 , 2006 ). Meal pattern alterations have been observed during VBS housing and correspond to reduced meal size and frequency amounting to a hypophagic response that reflects the behavioral and neuroethological adaptations to the VBS environment. On the other hand, the hyperphagia observed during the VBS recovery is the outcome of larger and longer meals with longer inter-meal intervals ( Melhorn et al. 2010 ).

Similarly to subordinate rats recovering from the VBS, a hyperphagic response has been observed in mice recovering from the chronic sensory contact or social defeat stress (CSD) model ( Kumar et al. 2013 ). In this paradigm a link has been demonstrated between increased hypothalamic expression of the orexigenic neuropeptides NPY and AgRP in subordinate mice. This activation of NPY/AgRP neurons can contribute to the observed increased food intake and body weight and promote the use of carbohydrates as fuel while sparing fat ( Chuang et al. 2010a , 2010b ; Kumar et al. 2013 ). At the endocrine level, leptin production remains suppressed, and ghrelin secretion is increased to induce a potent feeding response that increases available energy stores ( Lutter et al. 2008 ; Chuang et al. 2011 ). Similar to the behavior shown by subordinate in the VBS, in the CSD model hyperphagia results from larger but less frequent meals, considered indicative of a deficit in satiation.

In the chronic psychosocial stress model, subordinate mice develop a hyperphagia-dependent insulin resistance which, associated to high fat diet feeding, leads to MetS and obesity ( Bartolomucci et al. 2009 , 2005 ; Dadomo et al. 2011 ; Razzoli et al. 2015a ; Sanghez et al. 2016 , 2013 ). Similarly to the CSD, the chronic psychosocial stress model is also based on the exploitation of a naturalistic valid construct of social disparity, the difference between the two being the instability (the former) versus the stability (the latter) of the social hierarchy ( Razzoli and Bartolomucci, 2016 ). In the chronic psychosocial stress model, the subordinate animals exhibit a complex behavioral and metabolic syndrome characterized by up-regulated HPA axis functioning, behavioral depression-like disorders and autonomic and immune-endocrine changes ( Bartolomucci, 2007 ; Bartolomucci et al. 2010 , 2005 ; Dadomo et al. 2011 ). Hyperphagia arises and persists spontaneously in subordinate mice ( Bartolomucci et al., 2010 , 2009 , 2004 ; Dadomo et al. 2011 ; Patterson et al. 2013 ; Sanghez et al. 2013 ). Furthermore, hyperphagia is not a compensatory response since, in mice housed at room temperature, it develops in absence of increased energy expenditure ( Moles et al. 2006 ; Sanghez et al. 2013 ) and in presence of depression of locomotor activity ( Bartolomucci et al. 2010 , 2009 ; Dadomo et al. 2011 ; Razzoli et al. 2014 ). The overstimulation of food intake that leads to obesity occurs in concert with stress induced elevations of circulating corticosterone, glucose, and ghrelin, and hypothalamic expression of AGRP and NPY mRNA ( Bartolomucci 2007 ; Bartolomucci et al. 2010 , 2005 ; Dadomo et al. 2011 ; Razzoli et al. 2015, 2014 ; Patterson et al. 2013 ). In the subordinate mouse, the presence of an altered inhibitory feedback of the HPA axis suggested by elevated corticosterone levels, downregulated expression of hippocampal GR and dexametasone resistance ( Bartolomucci et al. 2004 , 2003 ; Razzoli et al. 2014 ) could contribute over time to sustain hyperphagia, while it is known that interruption of ghrelin signaling can blunt hyperphagia and its anabolic consequences ( Patterson et al. 2013 ). On the other hand, lower levels of ghrelin receptors in the hypothalamic PVN have been associated with increased consumption of fat rich foods ( Patterson and Abizaid, 2013 ).

An in depth analysis of subordinate meal pattern assigned a strong validity for modeling human BED associated with obesity (Razzoli et al. 2015): subordinate mice ingest more food at higher rate and with reduced satiety ratio than control mice, suggesting an impaired satiety ( Strubbe and Woods, 2004 ), and a heightened stress reactivity ( Harb et al. 1985 ; Krebs et al. 1997 ). Interestingly, this phenomenon does not reach a ceiling effect, since hyperphagia can increase further in response to an acute stress (Razzoli et al. 2015). The microstructure of subordinate hyperphagia changes over time, evolving from longer and more frequent meals to a paroxystic eating, consisting of an exaggerated amount of food consumed over much shorter meal times. Altogether, these features make the case for considering chronic subordination stress a valid model of BED since the majority of the diagnostic criteria are captured ( Corwin and Buda-Levin, 2004 ) ( Table 1 ): 1) The behavior occurs repeatedly over an extended period of time; 2) Bingeing animals consume more food in brief, discrete, periods of time than controls do under similar circumstances. 3) If compensatory behavior is present, it should be initiated by the animal rather than imposed by the investigator.

The association of subordination induced bingeing with the propensity to obesity and MetS as part of the subordinate metabolic phenotype is also very remarkable ( Sanghez et al. 2016 , 2013 ). When subordinate mice are fed standard diet, their hyperphagia is associated with dyslipidemia but normal glucose tolerance in presence of increased body weight ( Sanghez et al. 2013 ). Conversely, glucose intolerance, insulin resistance, and obesity develop due to the synergistic effect of high fat diet and subordination stress induced hyperphagia ( Bartolomucci et al. 2009 ; Dadomo et al. 2011 ; Sanghez et al. 2013 ). Among the endocrine and metabolic changes induced in subordinate mice, increased glucocorticoid and free fatty acid levels might be considered crucial contributors for the development of insulin resistance through the downregulation of the insulin signaling pathway ( Kahn, 1994 ; Sanghez et al. 2013 ; Shpilberg et al. 2012 ; Stumvoll, 2005 ; Taniguchi et al. 2006 ). Subordination stress is able to induce a molecular signature of insulin resistance in skeletal muscle and liver which is larger in magnitude to the effect of high fat diet per se ( Sanghez et al. 2016 ). Decreased IRS1/2 appears to be the key molecular node critically downregulated in the signaling pathway of subordinate mice. Interestingly, the adipose tissue is found to remain insulin sensitive possibly to help repartitioning of nutrients to the fat organ ( Sanghez et al. 2016 ).

Because obesity is a major risk factor for the development of the MetS and type 2 diabetes ( Björntorp and Rosmond, 2000 ; Després and Lemieux, 2006 ; Eckel et al. 2005 ; Haslam and James, 2005 ; Zimmet et al. 2001 ) a food restriction regimen promoting weight loss should normalize the MetS as well ( Aude et al. 2004 ; Kastorini et al. 2011 ). Preventing hyperphagia using a pair feeding protocol in subordinate mice abrogated body weight gain and visceral adiposity compared to subordinate mice that were fed ad libitum, without normalizing glucose homeostasis, potentially due to an exaggerated hunger stress sensitivity as demonstrated by the exacerbated hypercorticosteronemia induced by fasting (Razzoli et al. 2015). Additional studies are warranted to evaluate if the limited food availability in pair fed animals could have the potential to stimulate food intake as suggested by increased craving induced by deprivation protocols in humans as well as bingeing as a consequence of limited access models in rodents ( Berner et al., 2008 ; Polivy et al. 2005 ). Still, the prevention of subordination-induced obesity by precluding hyperphagia maintains clear translational implications for therapeutic interventions ( McElroy et al. 2004 ) offering the potential of treating obesity with non-pharmacological interventions effective for binge eating and acting in a faster way (drugs are often effective after several weeks of treatment).

Concluding Remarks and Future Perspectives

The treatment of eating and metabolic disorders has proven challenging. While obesity, T2D, and metabolic disorders have become pandemic, there are still unmet needs in spite of the available pharmacological, surgical, and behavioral therapeutic strategies. One critical issue is that obesity is typically viewed as a homogenous condition, but there may be important and discrete etiopathologies – including, for example, binge-eating. This indirectly underscores the role played by external factors such as low socio-economic status and psychosocial stress as predispositions for the development of a broad spectrum of eating and obesity-associated conditions. So far, an increasing scientific scrutiny has contributed to identify several endocrine players in the dynamic regulation of metabolic function in response to stress, both at the central and peripheral level. A strong need remains to develop valid preclinical models of stress-related metabolic disorders. Evidences reviewed here suggest that the development and validation of a preclinical model in which binge-eating is associated with obesity is critical to disentangling underlying molecular mechanisms, generating testable predictions of innovative drug candidates, and translating preclinical observations into clinical settings. This is particularly poignant since the available classical models of BED do not recapitulate most of the diagnostic criteria and lacki construct validity. Conversely, chronic subordination stress models offer several advantages in linking stress to binging and obesity to ultimately facilitate the identification of the neurobiological basis of BED-related obesity.

• Eating disorders and obesity are prevalent and can associate with psychological stress.
• Human studies link bingeing and stress exposure.
• Most classic preclinical models of binge eating involve food deprivation and acute stress.
• Mouse subordination stress causes bingeing and metabolic disorder similarly to humans.

Acknowledgments

AB is supported by NIH/NIDDK R01DK102496, NIH/NIA R01AG043972. SC is supported by NIDDK/NIH P30DK50456, and CP is supported by NIMH/NIHT32082761

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Late-night eating and weight gain

Kira Sampson

Brigham and Women’s Communications

Researchers find eating time affects how the body stores fat and regulates appetite hormones

Obesity afflicts approximately 42 percent of the U.S. adult population and contributes to the onset of chronic diseases, including diabetes, cancer, and other conditions.

While popular healthy diet mantras advise against midnight snacking, few studies have comprehensively investigated the simultaneous effects of late eating on the three main players in weight regulation and thus obesity risk: regulation of calorie intake, the number of calories you burn, and molecular changes in fat tissue.

A new study by Harvard Medical School investigators at Brigham and Women’s Hospital found that when we eat significantly impacts our energy expenditure, appetite, and molecular pathways in adipose tissue. Their results are published in  Cell Metabolism .

“We wanted to test the mechanisms that may explain why late eating increases obesity risk,” explained senior author  Frank Scheer , HMS professor of medicine and director of the Medical Chronobiology Program in the Division of Sleep and Circadian Disorders at Brigham and Women’s.

“Previous research by us and others had shown that late eating is associated with increased obesity risk, increased body fat, and impaired weight loss success. We wanted to understand why,” he said.

“In this study, we asked does the time that we eat matter when everything else is kept consistent,” said first author Nina Vujović , a researcher in the Medical Chronobiology Program.

Vujović, Scheer, and their team studied 16 patients with a body mass index in the overweight or obese range. Each participant completed two laboratory protocols: one with a strictly scheduled early meal schedule, and the other with the same meals, each scheduled about four hours later in the day.

In the last two to three weeks before starting each of the in-laboratory protocols, participants maintained fixed sleep and wake schedules, and in the final three days before entering the laboratory, they strictly followed identical diets and meal schedules at home.

“We found that eating four hours later makes a significant difference for our hunger levels, the way we burn calories after we eat, and the way we store fat.” Nina Vujović

In the lab, participants regularly documented their hunger and appetite, provided frequent small blood samples throughout the day, and had their body temperature and energy expenditure measured.

To measure how eating time affected molecular pathways involved in adipogenesis, or how the body stores fat, investigators collected biopsies of adipose tissue from a subset of participants during laboratory testing in both the early and late eating protocols, to enable comparison of gene expression patterns/levels between these two eating conditions.

Results revealed that eating later had profound effects on hunger and the appetite-regulating hormones leptin and ghrelin, which influence our drive to eat. Specifically, levels of the hormone leptin, which signals satiety, were decreased across the 24 hours in the late eating conditions compared to the early eating conditions.

When participants ate later, they also burned calories at a slower rate and exhibited adipose tissue gene expression toward increased adipogenesis and decreased lipolysis, which promote fat growth.

Notably, these findings convey converging physiological and molecular mechanisms underlying the correlation between late eating and increased obesity risk.

Vujović explained that these findings are not only consistent with a large body of research suggesting that eating later may increase one’s likelihood of developing obesity, but they shed new light on how this might occur.

By using a randomized crossover study, and tightly controlling for behavioral and environmental factors such as physical activity, posture, sleep, and light exposure, investigators were able to detect changes in the different control systems involved in energy balance, a marker of how our bodies use the food we consume.

In future studies, Scheer’s team aims to recruit more women to increase the generalizability of their findings to a broader population. While this study cohort included only five female participants, the study was set up to control for menstrual phase, reducing confounding but making recruiting women more difficult.

Going forward, Scheer and Vujović are also interested in better understanding the effects of the relationship between mealtime and bedtime on energy balance.

“This study shows the impact of late versus early eating. Here, we isolated these effects by controlling for confounding variables like caloric intake, physical activity, sleep, and light exposure, but in real life, many of these factors may themselves be influenced by meal timing,” said Scheer.

“In larger scale studies, where tight control of all these factors is not feasible, we must at least consider how other behavioral and environmental variables alter these biological pathways underlying obesity risk, ” he said.

This study was funded by R01DK099512, UL1TR001102 and UL1TR002541. F.A.J.L.S. was supported by NIH grants R01DK099512, R01HL118601, R01DK102696, and R01DK105072 and R01HL140574. M.J.P. and M.J.B. were supported by DK020595. M.G. was supported by the Spanish Government of Investigation, Development and Innovation (SAF2017-84135-R), including FEDER co-funding; the Autonomous Community of the Region of Murcia through the Seneca Foundation (20795/PI/18), and NIDDK R01DK099512. S.L.C. was supported by the Alexander von Humboldt Foundation. J.Q. was supported by the American Diabetes Association (Award 1-17-PDF-103) and by the NIH (Grant K99HL148500 and R01DK10269 6).

Disclosures:  During the execution of this project, Scheer received lecture fees from Bayer HealthCare, Sentara Healthcare, Philips, Vanda Pharmaceuticals, and Pfizer Pharmaceuticals; received consulting fees from the University of Alabama at Birmingham; and served on the board of directors for the Sleep Research Society. Scheer’s interests were reviewed and managed by Brigham and Women’s Hospital and Partners HealthCare in accordance with their conflict of interest policies. None of these are related to the current work. Vujović has been compensated for consulting services provided to the Novartis Institutes of BioMedical Research, also unrelated to the current work.

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New study shows friends can shield us from stress-induced eating

(Photo credit: Adobe Stock)

New research published in the journal Nutrients sheds light a fascinating facet of human behavior: the role of social support in mitigating stress-induced overeating. The study found that participants who received support from friends reported feeling less stressed, chose smaller food portions, and consumed fewer snacks during periods of acute stress.

Stress-induced overeating, commonly referred to as comfort eating, is a behavioral response where individuals consume food in excess, particularly high-calorie, fat, or sugar-laden foods, as a way to cope with emotional stress or discomfort. This behavior is thought to provide a temporary escape from stress, offering a sense of relief and satisfaction through the pleasurable experience of eating. However, while this may seem like a harmless coping mechanism, it carries significant long-term health risks, including obesity, diabetes, and cardiovascular diseases.

The researchers sought to identify potential strategies to mitigate these unhealthy eating habits, focusing on preventive measures that can be integrated into daily life. In particularly, they sought to better understand the role of social support as a potential buffer against the compulsion to overeat in response to stress. To this end, they conducted two experiments.

In their first study, the researchers recruited 138 participants through campus advertisements and a digital research platform. These participants were predominantly young adults, with a higher proportion of females, reflecting a college-aged demographic.

Participants were randomly assigned to one of four groups: those receiving support from a best friend, support from a stranger, a group instructed to self-regulate without specific guidelines (decrease group), and a control group that received no specific regulation instructions (look group). The friend group was unique in that participants were asked to bring along their best friend, who was not romantically involved with them, to provide support.

The procedure for Experiment 1 unfolded in several stages, starting with baseline measurements of stress, hunger, and emotional state. Following this, participants were subjected to a stress induction task, designed to elevate stress levels uniformly across the board. This was achieved through a simulated public speaking task, a well-documented method for inducing stress in laboratory settings. After the stress induction, the support manipulation was introduced, varying according to group assignment. The session concluded with participants selecting portions from an array of high- and low-calorie foods.

The researchers found that participants who received support from their friends reported significantly lower levels of perceived stress and chose smaller portions of both high- and low-calorie foods compared to their counterparts in the other three groups.

Experiment 2, which included 136 participants, aimed to extend the investigation to actual food consumption following stress induction and support manipulation. The setup was similar, with participants divided into the same four groups. However, this experiment introduced a Food Incentive Delay (FID) task and a bogus tasting task to measure not just the preference but the actual intake of high- versus low-calorie foods under stress conditions.

The results were consistent with the hypothesis that social support, particularly from friends, can lead to a reduction in stress-induced overeating. Participants in the friend group consumed fewer calories from both high- and low-calorie foods than those in the other groups.

Notably, the reduction in calorie intake was not just a result of eating less high-calorie food; participants also showed a moderated intake of low-calorie foods, indicating a general reduction in the need to eat as a stress response, rather than a simple shift in food preference.

The findings that the emotional and cognitive support provided by friends plays a critical role in reducing the appeal of comfort foods as a coping mechanism for stress. The mechanism appears to involve an improvement in emotional state and self-efficacy, with participants feeling more capable of handling their stress in a healthy manner and less driven to seek solace in food.

But there are some limitations to consider. The participant pool, mainly young adults from a college setting, suggests a need for broader demographic research to confirm these findings across different age groups and possibly in clinical settings. Additionally, the study’s gender dynamics, predominantly female, point towards a gap in understanding how social support might differentially affect men and women in the context of stress-induced eating.

Looking ahead, the researchers advocate for further exploration into the neural mechanisms underlying the relationship between social support and eating behavior. This future direction could illuminate how the brain processes social and food-related rewards, offering deeper insights into the psychological and neurobiological foundations of comfort eating.

“Overall, the present study elucidated the mechanisms by which social support influences stress-induced overeating behaviors. It also suggests a referential protective factor for people’s physical and mental health in the current unpredictable social environment, as well as providing ideas for therapeutic interventions for clinical eating disorders,” the researchers concluded.

The study, “ Support from a Best Friend Makes People Eat Less under Stress: Evidence from Two Experiments ,” was authored by by Mingyue Xiao, Yijun Luo, Weiyu Zeng, and Hong Chen.

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Press Release

Overeating and starving both damage the liver: Cavefish provide new insight into fatty liver disease

Stowers scientists’ collaboration reveals a genetic basis for starvation-induced fatty liver with a potential therapeutic avenue

14 March 2024

KANSAS CITY, MO—March 14, 2024— Fatty liver, which can lead to liver damage and disease, can occur from both overeating and starvation. Now, new research shows how naturally starvation-resistant cavefish, unlike other animals, are able to protect their liver and remain healthy. The findings have implications for understanding and potentially addressing liver conditions in humans.

Researchers from the Stowers Institute for Medical Research in collaboration with Université Libre de Bruxelles in Belgium and Iowa State University compared cavefish to other animals more susceptible to starvation, and identified a gene responsible for the development of starvation-induced fatty liver. The study , published in Life Science Alliance on March 11, 2024, led by co-first authors Ansa Cobham, Ph.D., in the lab of Associate Investigator Nicolas Rohner, Ph.D. , and Macarena Pozo-Morales, Ph.D., in the lab of Assistant Professor Sumeet Pal Singh, Ph.D. , also showed that this evolutionarily conserved gene can be targeted by an existing drug candidate to protect against liver damage.

“This same approach can be applied to what we see in overconsumption,” Rohner said. “In Western societies where, often, too many calories and not enough exercise is a problem, this new understanding may lead to prevention or potential treatment of fatty liver disease.”

“We have discovered for the first time an organism – cavefish—that can avoid fatty liver under starvation conditions,” said Cobham. “Fatty liver can result in complications like liver cirrhosis and liver failure. This study helps us understand more about the biology underlying these diseases in humans.”

Cavefish are cousins of the Mexican tetra river fish that flooded into underground caves over 100,000 years ago. The researchers show that in the absence of food, cavefish at early developmental stages not only survive much longer than their river fish counterparts, but also do not accumulate liver fat.

“This was the first time we clearly showed that the mechanism for this resistance is accomplished by not accumulating excess fat in the liver,” said Rohner.

The accumulation of fat in liver cells leads to organ damage and atrophy or wasting away. The researchers compared gene expression levels between cavefish, river fish, zebrafish, and even fruit flies, identifying a gene that is activated during prolonged periods of starvation in all but cavefish.

“Expression levels of this gene are reduced in cavefish, which is a good indicator that if we are able to target this gene in humans, we may be able to treat or manage human metabolic diseases such as Type 2 diabetes and obesity,” said Cobham.

The team’s findings indicate that the starvation-induced gene not only regulates fatty liver disease, but its mechanism has also been conserved from fruit flies to fish to humans, or approximately 400 million years of animal evolution.

Inhibiting this gene’s protein in zebrafish and river fish larvae and deleting the gene in fruit flies resulted in less liver fat and larger livers indicating this protects the liver from damage and atrophy.

“The collaboration between Dr. Sumeet Singh’s team in Belgium, our team at Stowers, and scientists from Iowa State University combined our collective expertise in zebrafish, cavefish, and fruit flies to uncover the mechanism for starvation-induced fatty liver,” said Rohner.

Additional authors include Cielo Centola, Mary McKinney, Ph.D., Peiduo Liu, Camille Perazzolo, Anne Lefort, Ph.D., Frédérick Libert, Ph.D., and Hua Bai, Ph.D.

This work was funded by Fonds de la Recherche Scientifique (FNRS) (awards: 40005588, 40013427), the National Institutes of Health (NIH) (awards: 1DP2AG071466-01, R24OD030214, R01AG058741, R01AG075156), the National Science Foundation (NSF) (award: 2046984), and institutional support from the Stowers Institute for Medical Research. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

About the Stowers Institute for Medical Research

Founded in 1994 through the generosity of Jim Stowers, founder of American Century Investments, and his wife, Virginia, the Stowers Institute for Medical Research is a non-profit, biomedical research organization with a focus on foundational research. Its mission is to expand our understanding of the secrets of life and improve life’s quality through innovative approaches to the causes, treatment, and prevention of diseases.

The Institute consists of 21 independent research programs. Of the more than 500 members, over 370 are scientific staff that include principal investigators, technology center directors, postdoctoral scientists, graduate students, and technical support staff. Learn more about the Institute at www.stowers.org and about its graduate program at www.stowers.org/gradschool .

Media Contact:

Joe Chiodo, Head of Media Relations 724.462.8529 [email protected]

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Overeating and starving both damage the liver: Cavefish provide new insight into fatty liver disease

Stowers scientists' collaboration reveals a genetic basis for starvation-induced fatty liver with a potential therapeutic avenue.

Fatty liver, which can lead to liver damage and disease, can occur from both overeating and starvation. Now, new research shows how naturally starvation-resistant cavefish, unlike other animals, are able to protect their liver and remain healthy. The findings have implications for understanding and potentially addressing liver conditions in humans.

Researchers from the Stowers Institute for Medical Research in collaboration with Universite Libre de Bruxelles in Belgium and Iowa State University compared cavefish to other animals more susceptible to starvation, and identified a gene responsible for the development of starvation-induced fatty liver. The study, published in Life Science Alliance on March 11, 2024, led by co-first authors Ansa Cobham, Ph.D., in the lab of Associate Investigator Nicolas Rohner, Ph.D., and Macarena Pozo-Morales, Ph.D., in the lab of Assistant Professor Sumeet Pal Singh, Ph.D., also showed that this evolutionarily conserved gene can be targeted by an existing drug candidate to protect against liver damage.

"This same approach can be applied to what we see in overconsumption," Rohner said. "In Western societies where, often, too many calories and not enough exercise is a problem, this new understanding may lead to prevention or potential treatment of fatty liver disease."

"We have discovered for the first time an organism -- cavefish -- that can avoid fatty liver under starvation conditions," said Cobham. "Fatty liver can result in complications like liver cirrhosis and liver failure. This study helps us understand more about the biology underlying these diseases in humans."

Cavefish are cousins of the Mexican tetra river fish that flooded into underground caves over 100,000 years ago. The researchers show that in the absence of food, cavefish at early developmental stages not only survive much longer than their river fish counterparts, but also do not accumulate liver fat.

"This was the first time we clearly showed that the mechanism for this resistance is accomplished by not accumulating excess fat in the liver," said Rohner.

The accumulation of fat in liver cells leads to organ damage and atrophy or wasting away. The researchers compared gene expression levels between cavefish, river fish, zebrafish, and even fruit flies, identifying a gene that is activated during prolonged periods of starvation in all but cavefish.

"Expression levels of this gene are reduced in cavefish, which is a good indicator that if we are able to target this gene in humans, we may be able to treat or manage human metabolic diseases such as Type 2 diabetes and obesity," said Cobham.

The team's findings indicate that the starvation-induced gene not only regulates fatty liver disease, but its mechanism has also been conserved from fruit flies to fish to humans, or approximately 400 million years of animal evolution.

Inhibiting this gene's protein in zebrafish and river fish larvae and deleting the gene in fruit flies resulted in less liver fat and larger livers indicating this protects the liver from damage and atrophy.

"The collaboration between Dr. Sumeet Singh's team in Belgium, our team at Stowers, and scientists from Iowa State University combined our collective expertise in zebrafish, cavefish, and fruit flies to uncover the mechanism for starvation-induced fatty liver," said Rohner.

• Liver Disease
• Chronic Illness
• Diseases and Conditions
• Cholesterol
• Gene Therapy
• Today's Healthcare
• Liver transplantation
• Hepatitis C
• Hepatocellular carcinoma
• High density lipoprotein

Story Source:

Materials provided by Stowers Institute for Medical Research . Note: Content may be edited for style and length.

Journal Reference :

• Macarena Pozo-Morales, Ansa E Cobham, Cielo Centola, Mary Cathleen McKinney, Peiduo Liu, Camille Perazzolo, Anne Lefort, Frédérick Libert, Hua Bai, Nicolas Rohner, Sumeet Pal Singh. Starvation-resistant cavefish reveal conserved mechanisms of starvation-induced hepatic lipotoxicity . Life Science Alliance , 2024; 7 (5): e202302458 DOI: 10.26508/lsa.202302458

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‘You Don’t Look Anorexic’

New research shows that our assumptions about eating disorders are often wrong — and that many larger-bodied people are starving themselves.

Sharon Maxwell is recovering from atypical anorexia. She suffered from disordered eating for 19 years before receiving a diagnosis. Credit... Ryan Pfluger for The New York Times

Supported by

By Kate Siber

• Published Oct. 18, 2022 Updated Nov. 10, 2022

Listen to This Article

To hear more audio stories from publications like The New York Times, download Audm for iPhone or Android .

Sharon Maxwell spent much of her life trying to make herself small. Her family put her on her first diet when she was 10. Early on Saturday mornings, she and her mother would drive through the empty suburban streets of Hammond, Ind., to attend Weight Watchers meetings. Maxwell did her best at that age to track her meals and log her points, but the scale wasn’t going down fast enough. So she decided to barely eat anything on Fridays and take laxatives that she found in the medicine cabinet.

Food had long been a fraught subject in the Maxwell household. Her parents were also bigger-bodied and dieted frequently. They belonged to a fundamentalist Baptist megachurch where gluttony was seen as a sin. To eat at home was to navigate a labyrinth of rules and restrictions. Maxwell watched one time as her mother lost 74 pounds in six months by consuming little more than carrot juice (her skin temporarily turned orange). Sometimes her father, seized with a new diet idea, abruptly ransacked shelves in the kitchen, sweeping newly forbidden foods into the trash. Maxwell was constantly worried about eating too much. She started to eat alone and in secret. She took to chewing morsels and spitting them out. She hid food behind books, in her pockets, under mattresses and between clothes folded neatly in drawers.

Through Maxwell’s teenage years and early 20s, eating became even more stressful. Her thoughts constantly orbited around food: what she was eating or not eating, the calories she was burning or not burning, the size of her body and, especially, what people thought of it. Her appearance was often a topic of public interest. When she went grocery shopping for her family, other customers commented on the items in her cart. “Honey, are you sure you want to eat that?” one person said. Other shoppers offered unsolicited advice about diets. Strangers congratulated her when her cart was filled with vegetables.

As she grew older, people at the gym clapped and cheered for her while she worked out. “People would say: ‘Go! You can lose the weight!’” she says. While eating in public, other diners offered feedback — and still do to this day — on her choices, a few even asking if she wanted to join their gym. Some would call her names: Pig, Fatty. Sometimes people told her she was brave for wearing shorts, while others said she should cover up. She was always aware, whether she wanted to be or not, of how others viewed her body.

Maxwell tried just about every diet she could find: juice cleanses, Atkins, SlimFast, South Beach, Mediterranean, Whole30 and Ezekiel, a regimen based on biblical references. She tried being vegetarian and vegan and paleo. She tried consuming less than 500 calories a day and taking HCG, a fertility hormone rumored to suppress appetite but flagged by the F.D.A. as risky and unproven for weight loss. During periods of religious fasting at her church, she would take the practice to an extreme, consuming nothing but water for days (and on one occasion, two weeks). “I passed out a few times, but I did it,” she says. Sometimes she exercised more than three hours a day in high-intensity interval-training sessions and kickboxing classes. Eventually, she started vomiting up her food.

Every day, Maxwell stepped on the scale and internalized the number as a reflection of her self-worth. Often, the number on the scale went down. But if she let up on her rigid food rules even briefly, the number shot back up like a coiled spring. “I just cycled through that,” she says, “but it became harder and harder each time to get the weight off.”

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Pizza study finds the body's metabolism to be good at coping with over-indulgence

• Download PDF Copy

A new study, which involved participants eating pizza well after feeling 'full' in order to test what immediate effects this had on the body, finds that our metabolism is surprisingly good at coping with over-indulgence.

Researchers with the Centre for Nutrition, Exercise and Metabolism at the University of Bath compared the effects of normal eating (i.e. 'eat until you are comfortably full') with maximal eating (i.e. 'eat until you cannot manage another bite').

They found that the young, healthy men (aged 22 - 37) who volunteered for the trial consumed almost twice as much pizza when pushing beyond their usual limits, doubling their calorie intake, yet, remarkably, managed to keep the amount of nutrients in the bloodstream within normal range.

This, say the researchers, shows that if an otherwise healthy person overindulges occasionally there are no immediate, negative consequences in terms of losing metabolic control. However, they caution of the risks of prolonged over-eating.

We all know the long-term risks of over-indulgence with food when it comes to obesity, type II diabetes and cardiovascular disease, but we know much less about some of the immediate effects 'all you can eat' places on the body. Our findings show that the body actually copes remarkably well when faced with a massive and sudden calorie excess. Healthy humans can eat twice as much as 'full' and deal effectively with this huge initial energy surplus." Aaron Hengist, Lead Researcher

In the study, the average calorie intake in the all-you-can-eat trial was over 3000 kcal, roughly one and half large pizzas. However, this varied a lot, with some individuals able to consume up to two and half large pizzas in one go.

This is well beyond standard adult guidelines for calorie intake in one day (let alone one meal) - and is even more calories than US Olympic swimmer Michael Phelps famously reported eating for breakfast.

Results show that after eating maximally:

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• Blood sugar (glucose) levels were no higher than after a normal meal.
• The amount of insulin in the blood was 50% higher than normal (this hormone is released by the body to control blood sugar levels).
• Blood lipids (triglycerides and non-esterified fatty acids) were only slightly higher despite having consumed over twice as much fat. This is interesting because previous research had shown that blood lipids increase proportionally when low-to-moderate amounts of fat are consumed.
• Hormones that are released by the gut to stimulate insulin secretion and increase feelings of fullness were changed the most by overeating (e.g. GLP-1 and peptide YY).

The study also looked at appetite and mood throughout the trials:

- Four hours after eating maximally, the participants felt sleepy/lethargic and reported no desire to eat anything else, including sweet foods. This was surprising because reward centres in the brain are usually food specific, so eating pizza might not be expected to change the desire for sweet food - which may be why you always have room for dessert.

Professor James Betts, who oversaw the work, added: "We know that people often eat beyond their needs, which is why so many of us struggle to manage our body weight. It is therefore surprising that no previous research had measured the maximal capacity for eating at a single meal in order to understand how the human body responds to that challenge.

"This study reveals that humans are capable of eating twice as much food as is needed to make us feel 'full', but that our bodies are well adapted to an excessive delivery of dietary nutrients at one huge meal. Specifically, those tested in this study were able to efficiently use or store the nutrients they ingested during the pizza-eating challenge, such that the levels of sugar and fats in their blood were not much higher than when they ate half as much food.

"The main problem with overeating is that it adds more stored energy to our bodies (in the form of fat), which can culminate in obesity if you overeat day after day. However, this study shows that if an otherwise healthy person overindulges occasionally, for example eating a large buffet meal or Christmas lunch, then there are no immediate negative consequences in terms of losing metabolic control."

The researchers acknowledge that their study involved healthy young men, so they plan to investigate whether similar effects are apparent in women, and for overweight and older populations.

University of Bath

Hengist, A., et al. (2020) Physiological responses to maximal eating in men. British Journal of Nutrition. doi.org/10.1017/S0007114520001270 .

Posted in: Medical Science News | Medical Research News | Healthcare News

Tags: Blood , Blood Sugar , Brain , Breakfast , Cardiology , Cardiovascular Disease , Diabetes , Endocrinology , Exercise , Fatty Acids , Food , GLP-1 , Glucose , Hormone , Insulin , Lipids , Metabolism , Nutrients , Nutrition , Obesity , Research

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Lack of exercise, not diet, linked to rise in obesity, Stanford research shows

An examination of national health survey results suggests that inactivity, rather than higher calorie intake, could be driving the surge in obesity.

July 7, 2014 - By Becky Bach

An examination of national health survey records shows Americans are exercising less, which could be driving the rising obesity rates.  Shutterstock

Inactivity rather than overeating could be driving the surge in Americans’ obesity, according to a study by a team of Stanford University School of Medicine researchers.

Examining national health survey results from 1988 through 2010, the researchers found huge increases in both obesity and inactivity, but not in the overall number of calories consumed.

“What struck us the most was just how dramatic the change in leisure-time physical activity was,” said Uri Ladabaum , MD, associate professor of gastroenterology and lead author of the study. “Although we cannot draw conclusions about cause and effect from our study, our findings support the notion that exercise and physical activity are important determinants of the trends in obesity.”

The study will appear in the August issue of The American Journal of Medicine . It’s also available online now in a draft form.

The researchers analyzed data from the National Health and Nutrition Examination Survey, a long-term project of the Centers for Disease Control and Prevention that collects information from surveys and from physical examinations to assess Americans’ health. The researchers considered survey results from 17,430 participants from 1988 through 1994 and from approximately 5,000 participants each year from 1995 through 2010.

Survey participants recorded the frequency, duration and intensity of their exercise within the previous month. The team defined “ideal” exercise as more than 150 minutes a week of moderate exercise or more than 75 minutes a week of vigorous exercise.

Correlation, not causation

The research highlights the correlation between obesity and sedentary lifestyles, but because it is an observational study, it does not address the possible causal link between inactivity and weight gain.

Uri Ladabaum

The percentage of women reporting no physical activity jumped from 19 percent to 52 percent between 1988 and 2010; the percentage of inactive men rose from 11 percent to 43 percent over the same period.

Obesity also increased, climbing from 25 to 35 percent in women and from 20 to 35 percent in men.

Surprisingly, however, the number of calories consumed per day did not change significantly. Nonetheless, diet remains a proven and important component of health, and participants may have been tempted to under-report how much they ate, Ladabaum said.

He added that, although the reported average caloric intake did not change substantially during those periods, it didn’t mean that the number of calories consumed were optimal. “We simply did not detect a substantial increase over time,” he said, noting that caloric intake and physical activity are both important determinants of weight.

Both obesity and abdominal girth, which the team analyzed independently, contribute to a variety of well-documented conditions, such as cancer and cardiovascular disease, as well as increased mortality.

In 2010, 61 percent of women and 42 percent of men had too much belly fat, up from 46 percent and 29 percent in 1988. In addition, the waists of even normal-weight women swelled between 1988 and 2010, the study showed.

Ladabaum noted that the study did not follow one group of participants over that 22-year span; instead, the data came from different samples in each survey cycle. But the samples are constructed to be representative of the population.

Clarion call

In an accompanying editorial, the journal’s managing editor, Pamela Powers Hannley, MPH, called the study “a clarion call.”

Obesity is a complex, multifaceted problem linked to a variety of societal factors, Hannley said in an interview. “There are societal and economic forces at work that we must address,” she said. “Take, for example, the struggle of single mothers who are trying to balance work and child care. They may lack the time or resources to exercise. We shouldn’t assume that people are just lazy. Their lives might be overwhelming to them.”

Recommendations to exercise 30 minutes a day aren’t enough, Hannley added.

“It’s going to take widespread change,” she said. “We shouldn’t just tell patients they need to work out. We need to work with communities, employers and local governments to enable healthy lifestyles by ensuring that there are safe spaces to exercise that are cheap or free.”

Other Stanford co-authors of the study are Ajitha Mannalithara, PhD, social science research associate; Parvathi Myer, MD, a former postdoctoral scholar who is now at Kaiser Permanente, and Gurkirpal Singh, MD, adjunct professor of gastroenterology.

The study was funded by the National Institutes of Health (grant T32DK007056).

Stanford’s Department of Medicine  also supported the research.

About Stanford Medicine

Stanford Medicine is an integrated academic health system comprising the Stanford School of Medicine and adult and pediatric health care delivery systems. Together, they harness the full potential of biomedicine through collaborative research, education and clinical care for patients. For more information, please visit med.stanford.edu .

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What Is Emotional Eating?

There’s a connection between what we eat and how we feel

In a perfect world, you’d decide to have a snack or dinner in response to hunger pangs rumbling from your stomach. However, reality is far different. How many times have you absentmindedly noshed on too many chips during a stressful football game, or reached for an extra piece of chocolate because you’re feeling sad or bored?

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While an occasional overindulgence is perfectly OK, both of these scenarios can be an example of emotional eating .

First off, emotional eating is a very normal coping mechanism in response to strong feelings. “The technical definition of emotional eating is eating to escape, numb, change, or amplify our feelings,” says psychologist  Susan Albers, PsyD . As you might expect, emotional eating is also incredibly common. “Research shows that about 75% of all of our eating is emotionally driven,” Dr. Albers notes. “We eat not because we’re hungry, but because we’re bored, stressed or anxious.”

There’s a biological connection between emotional eating and stress — namely that your body starts producing a hormone called cortisol when you start feeling alarmed or upset.

“Cortisol makes us crave sugary, fatty or salty foods,” says Dr. Albers. “Back in ancient times during times of stress, you needed all the calories you could get because you were involved in fight-or-flight situations. When you’re feeling stressed, you’re dealing with your ancient biology telling you, ‘Go get some food.’”

Society and culture also portrays food as something ideal if you need a mood boost or pick-me-up. “If you look at commercials or ads, they often encourage people to turn to food as something that’s soothing,” says Dr. Albers. “Food is also something that’s available 24/7. We can reach for it any time of the day. So when we’re feeling stressed, it is very easy to make a beeline for food.”

What causes emotional eating?

Emotional eating has many root causes.

Difficulty distinguishing between physical and emotional hunger

Growing up, you probably leaned on external cues to let you know you were done eating. “For example, if I’m eating a plate of food, one of the external cues is when my plate is finished, I’m done,” says Dr. Albers. “Or if a parent says to me, ‘You need to finish your plate,’ then you’re done, instead of those internal cues of paying attention to the stop and start that our body gives us.” With emotional eating, you often have trouble telling the difference between these internal cues — which signify physical hunger, or the signs your body send to let you know it’s time for nourishment — and emotional hunger.

Dieting often leads to emotional eating, because trying to cut back on unhealthy things often means you’re limiting how much you eat and are eliminating certain foods. “Restrictive eating is one of the biggest triggers of emotional eating,” says Dr. Albers.

Anxiety is another “significant trigger” for emotional eating, she adds. But while many people eat more when they’re feeling anxious, others go in the opposite direction. “They don’t eat because they lose their appetite,” says Dr. Albers. “Their emotions are so great and so intense that it pushes away or supersedes that feeling of hunger, and they no longer tune into it. This can be problematic because we need food to help us to deal with stress and emotions.”

Situational stresses

Emotional eating can also arise from situational stresses . For example, the COVID-19 pandemic disrupted routines and led to isolation and boredom, creating an ideal environment for emotional eating. “We do a lot of boredom eating because eating feels purposeful,” says Dr. Albers. “It fills up our time, it gives us some entertainment. During the pandemic, a lot of anxiety, stress and boredom eating happened.”

Seasonal stressors

Seasonal stressors like colder temperatures and earlier sunsets, as well as the holidays, can also lead to episodes of emotional eating. “Holidays can bring up a lot of busyness, stress, contact with family members, and availability of all kinds of great holiday treats ,” says Dr. Albers. “Sometimes it’s the perfect storm for emotional eating.”

What are the signs of emotional eating?

There are several signs that you might be someone prone to emotional eating.

Sudden, urgent cravings. Physical hunger develops slowly over time. “After you eat, you may be satisfied for a while and then your hunger is going to grow,” says Dr. Albers. “You desire a variety of different foods, you feel the sensation of fullness and you can track feeling more satisfied or full as you’re eating.” Emotional eating, in contrast, comes on suddenly and might have urgency, she notes. “You say, ‘I need to eat something. I need some chocolate.’

Craving only certain foods. Not only do your cravings come on suddenly, but you might only want to eat certain foods. “If you’re saying to yourself, ‘I don’t want to just eat something because I’m hungry. I want chocolate, and that’s all that’s going to satisfy me,’ it’s a red flag of emotional eating,” says Dr. Albers.

Overeating. Overeating is another hallmark of emotional eating. “The sensation that a lot of my clients talk about is wanting that food to make them feel better or satisfied. No matter how much they eat, it never really brings them to that feeling until they feel sick or overly full and then they stop eating,” says Dr. Albers. “But they’re hoping that as they’re eating, it’s going to change their sensation in some way.”

Shame or guilt. Feeling emotional distress, like shame or guilt, over your eating habits is another sign.

When does emotional eating become a problem?

Occasionally having too much unhealthy food isn’t harmful. “Sometimes you just need some chocolate to feel better, and that’s okay,” says Dr. Albers. However, this indulgence can be an issue when it happens a lot — or turns into your main coping mechanism. “It’s when you’re feeling stressed, and your first or only way of coping is turning to food. That’s often when emotional eating becomes more of a problem or an issue.”

How to stop emotional eating

There are many strategies to stop emotional eating . And while there’s no one-size-fits-all approach, good rules to follow include:

• Change your diet to be healthier. Vitamin D-rich foods can improve your mood, so stock up on fortified milk and cereals, eggs, mushrooms, and fish like salmon.
• Eat mandarin oranges. Not only are mandarin oranges portable, and easy to peel and eat, but they’re rich in vitamin C, which can help boost your immunity. Plus, citrus smells so good, it’s a stress reliever.
• Be mindful about what you’re eating . Be mindful of the kind of snacks you are buying. Certain foods are more likely to trigger emotional eating. Know exactly which snacks you tend to reach for when feeling stressed.
• Don’t let yourself get too hungry. You’ve probably heard the term “ hangry ,” a portmanteau of “hungry” and “angry” used to describe someone who gets irritable when they’re past time to eat. Making sure you stave off this mood — for example, eating proteins can help you stay full for longer — is a good bet.

Where to turn to for help

If you’re dealing with emotional eating, it’s best to see a physician or a therapist and have an assessment to determine if you have an underlying medical issue or something else going on. For example, chronic pain can turn to emotional eating as a way to feel better, while depression can cause appetite changes.

“One of the things that we really talk about when someone comes in is, ‘Is this the primary issue, or is there another issue that’s making your emotional eating worse?’” says Dr. Albers. “So if you’re feeling depressed, is it the depression that needs to be treated to help the emotional eating? Or is it the other way around: Is emotional eating causing or exacerbating the depression? It’s a chicken and egg approach sometimes.”

However, you also have the power to change your eating habits, by just slowing down and being mindful.

“Before you take a bite, tune into yourself and ask yourself just that question, ‘Am I eating because I’m physically hungry, or because I’m emotionally feeling something?’” says Dr. Albers. “You would be surprised that when you pause and take that mindful moment, how often you discover, ‘You know what? Maybe I’m feeling bored right now’ or ‘Maybe I’m really not that hungry. I’m feeling anxious.’” Having that awareness can really shift your coping in a very different direction.” Hear more on this topic from Dr. Susan Albers on the  Health Essentials Podcast .

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Overeating and starving both damage the liver: Cavefish provide new insight into fatty liver disease

Stowers scientists’ collaboration reveals a genetic basis for starvation-induced fatty liver with a potential therapeutic avenue

Stowers Institute for Medical Research

Stowers scientists discuss their findings related to research surrounding cavefish and fatty liver disease, revealing implications for understanding and potentially addressing liver conditions in humans. 

Credit: Stowers Institute for Medical Research

KANSAS CITY, MO—March 18, 2024—Fatty liver, which can lead to liver damage and disease, can occur from both overeating and starvation. Now, new research shows how naturally starvation-resistant cavefish, unlike other animals, are able to protect their liver and remain healthy. The findings have implications for understanding and potentially addressing liver conditions in humans.

Researchers from the Stowers Institute for Medical Research in collaboration with Université Libre de Bruxelles in Belgium and Iowa State University compared cavefish to other animals more susceptible to starvation, and identified a gene responsible for the development of starvation-induced fatty liver. The  study , published in  Life Science Alliance  on March 11, 2024, led by co-first authors Ansa Cobham, Ph.D., in the lab of Associate Investigator Nicolas Rohner, Ph.D. , and Macarena Pozo-Morales, Ph.D., in the lab of Assistant Professor Sumeet Pal Singh, Ph.D. , also showed that this evolutionarily conserved gene can be targeted by an existing drug candidate to protect against liver damage.

“This same approach can be applied to what we see in overconsumption,” Rohner said. “In Western societies where, often, too many calories and not enough exercise is a problem, this new understanding may lead to prevention or potential treatment of fatty liver disease.”

“We have discovered for the first time an organism – cavefish—that can avoid fatty liver under starvation conditions,” said Cobham. “Fatty liver can result in complications like liver cirrhosis and liver failure. This study helps us understand more about the biology underlying these diseases in humans.” 

Cavefish are cousins of the Mexican tetra river fish that flooded into underground caves over 100,000 years ago. The researchers show that in the absence of food, cavefish at early developmental stages not only survive much longer than their river fish counterparts, but also do not accumulate liver fat.

“This was the first time we clearly showed that the mechanism for this resistance is accomplished by not accumulating excess fat in the liver,” said Rohner.

The accumulation of fat in liver cells leads to organ damage and atrophy or wasting away. The researchers compared gene expression levels between cavefish, river fish, zebrafish, and even fruit flies, identifying a gene that is activated during prolonged periods of starvation in all but cavefish.

“Expression levels of this gene are reduced in cavefish, which is a good indicator that if we are able to target this gene in humans, we may be able to treat or manage human metabolic diseases such as Type 2 diabetes and obesity,” said Cobham.

The team’s findings indicate that the starvation-induced gene not only regulates fatty liver disease, but its mechanism has also been conserved from fruit flies to fish to humans, or approximately 400 million years of animal evolution.    

Inhibiting this gene’s protein in zebrafish and river fish larvae and deleting the gene in fruit flies resulted in less liver fat and larger livers indicating this protects the liver from damage and atrophy.

“The collaboration between Dr. Sumeet Singh’s team in Belgium, our team at Stowers, and scientists from Iowa State University combined our collective expertise in zebrafish, cavefish, and fruit flies to uncover the mechanism for starvation-induced fatty liver,” said Rohner. 

Additional authors include Cielo Centola, Mary McKinney, Ph.D., Peiduo Liu, Camille Perazzolo, Anne Lefort, Ph.D., Frédérick Libert, Ph.D., and Hua Bai, Ph.D. 

This work was funded by Fonds de la Recherche Scientifique (FNRS) (awards: 40005588, 40013427), the National Institutes of Health (NIH) (awards: 1DP2AG071466-01, R24OD030214, R01AG058741, R01AG075156), the National Science Foundation (NSF) (award: 2046984), and institutional support from the Stowers Institute for Medical Research. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

About the Stowers Institute for Medical Research

Founded in 1994 through the generosity of Jim Stowers, founder of American Century Investments, and his wife, Virginia, the Stowers Institute for Medical Research is a non-profit, biomedical research organization with a focus on foundational research. Its mission is to expand our understanding of the secrets of life and improve life’s quality through innovative approaches to the causes, treatment, and prevention of diseases.

The Institute consists of 21 independent research programs. Of the more than 500 members, over 370 are scientific staff that include principal investigators, technology center directors, postdoctoral scientists, graduate students, and technical support staff. Learn more about the Institute at  www.stowers.org  and about its graduate program at www.stowers.org/gradschool .

Media Contact:

Joe Chiodo, Head of Media Relations 724.462.8529 [email protected]

Life Science Alliance

10.26508/lsa.202302458

Method of Research

Experimental study

Subject of Research

Article title.

Starvation-resistant cavefish reveal conserved mechanisms of starvation-induced hepatic lipotoxicity

Article Publication Date

11-Mar-2024

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

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UK researchers find Alzheimer’s-like brain changes in long COVID patients

LEXINGTON, Ky (Aug. 30, 2024)  — New research from the University of Kentucky’s  Sanders-Brown Center on Aging  shows compelling evidence that the cognitive impairments observed in long COVID patients share striking similarities with those seen in Alzheimer’s disease and related dementias. 

The study, published in  Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association , highlights a potential commonality in brain disorders across these conditions that could pave the way for new avenues in research and treatment.

The study was a global effort, funded by a multitude of grants from the U.S. National Institutes of Health, the Alzheimer’s Association and international organizations. The project also brought together experts from various fields of neuroscience. 

Researchers at the UK College of Medicine led the study, including Yang Jiang, Ph.D., professor in the Department of Behavioral Science; Chris Norris, Ph.D., professor in the Department of Pharmacology and Nutritional Sciences; and Bob Sompol, Ph.D., assistant professor in the Department of Pharmacology and Nutritional Sciences. Their work focuses on electrophysiology, neuroinflammation, astrocytes and synaptic functions.

“This project benefited greatly from interdisciplinary collaboration,” Jiang said. “We had input from experts, associated with the Alzheimer’s Association International Society to Advance Alzheimer's Research and Treatment (ISTAART), across six countries, including the U.S., Turkey, Ireland, Italy, Argentina and Chile.”

Jiang and the collaborative team focused their work on understanding the “brain fog” that many COVID-19 survivors experience, even months after recovering from the virus. This fog includes memory problems, confusion and difficulty concentrating. According to Jiang, “the slowing and abnormality of intrinsic brain activity in COVID-19 patients resemble those seen in Alzheimer’s and related dementias.”

This research sheds light on the connection between the two conditions, suggesting that they may share underlying biological mechanisms. Both long COVID and Alzheimer’s disease involve neuroinflammation, the activation of brain support cells known as astrocytes and abnormal brain activity. These factors can lead to significant cognitive impairments, making it difficult for patients to think clearly or remember information.

The idea that COVID-19 could lead to Alzheimer’s-like brain changes is a significant development.

“People don’t usually connect COVID-19 with Alzheimer’s disease,” Jiang said, “but our review of emerging evidence suggests otherwise.”

The publication in  Alzheimer’s & Dementia  reveals that the cognitive issues caused by COVID-19 reflect similar underlying brain changes as those in dementia.

The study’s insights emphasize the importance of regular brain function check-ups for these populations, particularly through the use of affordable and accessible tools like electroencephalography (EEG).

The study not only highlights the shared traits between long COVID and Alzheimer’s, but also points to the importance of further research.

“The new insight opens avenues for future research and clinical practice, particularly in studying brain oscillations related to neural biomarkers of mild cognitive impairment in people with long COVID,” said Jiang.

One of the key findings is the role of astrocytes — support cells in the brain that have not been as thoroughly studied as neurons. The research suggests that damage or activation of these cells by COVID-19 can cause synaptic dysfunctions, leading to the abnormal brain activity observed in both conditions. This discovery is significant because it may help explain why EEG patterns in COVID-19 patients resemble those seen in the early stages of neurodegenerative diseases like Alzheimer’s.

Researchers believe this work could have a direct impact on patient care. They are advocating for routine EEG exams to detect early brain changes in both COVID-19 survivors and those at risk for cognitive decline.

“EEG patterns in COVID-19 patients resemble those seen in early neurodegenerative diseases,” said Norris.

“These similarities may be due to shared issues such as brain inflammation, astrocyte activity, low oxygen levels and blood vessel damage,” said Sompol.

By detecting these changes early, health care providers could potentially identify at-risk individuals sooner and implement interventions to prevent or slow the progression of cognitive decline.

As research continues, the team is particularly interested in how EEG monitoring can predict long-term outcomes in COVID-19 patients and assess the effectiveness of treatments aimed at preventing cognitive decline.

Research reported in this publication was supported by the National Institute on Aging of the National Institutes of Health under Award Numbers P30AG072946, P01AG078116 and R56AG060608. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

UK HealthCare is the hospitals and clinics of the University of Kentucky. But it is so much more. It is more than 10,000 dedicated health care professionals committed to providing advanced subspecialty care for the most critically injured and ill patients from the Commonwealth and beyond. It also is the home of the state’s only National Cancer Institute (NCI)-designated Comprehensive Cancer Center, a Level IV Neonatal Intensive Care Unit that cares for the tiniest and sickest newborns, the region’s only Level 1 trauma center and Kentucky’s top hospital ranked by U.S. News & World Report.

As an academic research institution, we are continuously pursuing the next generation of cures, treatments, protocols and policies. Our discoveries have the potential to change what’s medically possible within our lifetimes. Our educators and thought leaders are transforming the health care landscape as our six health professions colleges teach the next generation of doctors, nurses, pharmacists and other health care professionals, spreading the highest standards of care. UK HealthCare is the power of advanced medicine committed to creating a healthier Kentucky, now and for generations to come. 

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• Aug 30 2024

UK researchers find Alzheimer’s-like brain changes in long COVID patients

New research from the University of Kentucky’s  Sanders-Brown Center on Aging  shows compelling evidence that the cognitive impairments observed in long COVID patients share striking similarities with those seen in Alzheimer’s disease and related dementias. 

The study, published in  Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association , highlights a potential commonality in brain disorders across these conditions that could pave the way for new avenues in research and treatment.

The study was a global effort, funded by a multitude of grants from the U.S. National Institutes of Health, the Alzheimer’s Association and international organizations. The project also brought together experts from various fields of neuroscience. 

Researchers at the UK College of Medicine led the study, including Yang Jiang, Ph.D., professor in the Department of Behavioral Science; Chris Norris, Ph.D., professor in the Department of Pharmacology and Nutritional Sciences; and Bob Sompol, Ph.D., assistant professor in the Department of Pharmacology and Nutritional Sciences. Their work focuses on electrophysiology, neuroinflammation, astrocytes and synaptic functions.

“This project benefited greatly from interdisciplinary collaboration,” Jiang said. “We had input from experts, associated with the Alzheimer’s Association International Society to Advance Alzheimer's Research and Treatment (ISTAART), across six countries, including the U.S., Turkey, Ireland, Italy, Argentina and Chile.”

Jiang and the collaborative team focused their work on understanding the “brain fog” that many COVID-19 survivors experience, even months after recovering from the virus. This fog includes memory problems, confusion and difficulty concentrating. According to Jiang, “the slowing and abnormality of intrinsic brain activity in COVID-19 patients resemble those seen in Alzheimer’s and related dementias.”

This research sheds light on the connection between the two conditions, suggesting that they may share underlying biological mechanisms. Both long COVID and Alzheimer’s disease involve neuroinflammation, the activation of brain support cells known as astrocytes and abnormal brain activity. These factors can lead to significant cognitive impairments, making it difficult for patients to think clearly or remember information.

The idea that COVID-19 could lead to Alzheimer’s-like brain changes is a significant development.

“People don’t usually connect COVID-19 with Alzheimer’s disease,” Jiang said, “but our review of emerging evidence suggests otherwise.”

The publication in  Alzheimer’s & Dementia  reveals that the cognitive issues caused by COVID-19 reflect similar underlying brain changes as those in dementia.

The study’s insights emphasize the importance of regular brain function check-ups for these populations, particularly through the use of affordable and accessible tools like electroencephalography (EEG).

The study not only highlights the shared traits between long COVID and Alzheimer’s, but also points to the importance of further research.

“The new insight opens avenues for future research and clinical practice, particularly in studying brain oscillations related to neural biomarkers of mild cognitive impairment in people with long COVID,” said Jiang.

One of the key findings is the role of astrocytes — support cells in the brain that have not been as thoroughly studied as neurons. The research suggests that damage or activation of these cells by COVID-19 can cause synaptic dysfunctions, leading to the abnormal brain activity observed in both conditions. This discovery is significant because it may help explain why EEG patterns in COVID-19 patients resemble those seen in the early stages of neurodegenerative diseases like Alzheimer’s.

Researchers believe this work could have a direct impact on patient care. They are advocating for routine EEG exams to detect early brain changes in both COVID-19 survivors and those at risk for cognitive decline.

“EEG patterns in COVID-19 patients resemble those seen in early neurodegenerative diseases,” said Norris.

“These similarities may be due to shared issues such as brain inflammation, astrocyte activity, low oxygen levels and blood vessel damage,” said Sompol.

By detecting these changes early, health care providers could potentially identify at-risk individuals sooner and implement interventions to prevent or slow the progression of cognitive decline.

As research continues, the team is particularly interested in how EEG monitoring can predict long-term outcomes in COVID-19 patients and assess the effectiveness of treatments aimed at preventing cognitive decline.

Research reported in this publication was supported by the National Institute on Aging of the National Institutes of Health under Award Numbers P30AG072946, P01AG078116 and R56AG060608. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

Words: Hillary Smith (Public Relations and Strategic Communications) Research illustration by Tom Dolan.

• Alzheimer's Disease
• Neuroscience

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Watch CBS News

Hormone therapy for women in menopause can slow aging and benefit health, study shows

By Sara Moniuszko

Edited By Allison Elyse Gualtieri

August 30, 2024 / 10:48 AM EDT / CBS News

Hormone therapy can benefit women's health during  menopause , according to new research.

In the study, published Thursday in JAMA Network Open , researchers looked at more than 100,000 women in the U.K. and found being on hormone replacement therapy seems to slow biological aging.

"In this study, postmenopausal women with historical (hormone therapy) use were biologically younger than those not receiving (hormone therapy), with a more evident association observed in those with low (socioeconomic status)," the authors wrote. "Promoting (hormone therapy) in postmenopausal women could be important for healthy aging."

Dr. Céline Gounder, CBS News medical contributor and editor-at-large for public health at KFF Health News, said Friday on  "CBS Mornings"  the study is "really significant."

"It wasn't just about how you look, it was about your risk of death, in particular from cardiovascular disease," she said, adding the study looked at both chronological age (the age based on your date of birth) as well as biological age, which is "not just about how you look, but it's really about your health."

Gounder said the association might have been stronger with those of a lower socioeconomic status because aging is "also a reflection of your day-to-day stress ." 

"When we talk about somebody having lived a hard life, it's not just a question of smoking or heavy drinking or using drugs. It's also the day-to-day stress of financial stress, worried about keeping a roof over your head, food on the table, your children's futures — and that stress also ages you," she said. "So of course, women of lower socioeconomic status are experiencing that more. Education is also a important factor here, being able to better access healthcare."

The study comes after longtime public misunderstanding around horomone therapy, stemming partly, Gounder said, from studies done about 20 years ago that have since been show to be problematic in terms of how they were designed.

"Unfortunately, a lot of women were discouraged from taking hormone replacement therapy as a result of those studies," she said. 

Still, for some women, hormone therapy isn't an option, so it's important to talk to your doctor.

"There are some women who cannot take hormone replacement therapy. For example, if you have a history of breast cancer or blood clots," said Gounder. "And so this really depends on who we're talking about, the timing of when to start and how long to be on them." 

• Women's Health

Sara Moniuszko is a health and lifestyle reporter at CBSNews.com. Previously, she wrote for USA Today, where she was selected to help launch the newspaper's wellness vertical. She now covers breaking and trending news for CBS News' HealthWatch.

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New study says Shroud of Turin bloodstains are ‘consistent with Jesus Christ’s tortures’

A study published in July revealed that a new analysis of the Shroud of Turin, including the composition and a microscopic analysis of bloodstains, shows that the marks are consistent with the tortures endured by Christ as described in the Gospels.

The study, titled “New Insights on Blood Evidence from the Turin Shroud Consistent with Jesus Christ’s Tortures,” stated that the presence of creatinine particles with ferritin, which are often a by-product of muscle contractions, “confirms, at a microscopic level, the very heavy torture suffered by Jesus of the HST,” or Holy Shroud of Turin.

Furthermore, “numerous bloodstains scattered throughout the double body image of the HST show evidence that Jesus of the HST was tortured,” it stated.

“Bloodstained marks all over the body image which are consistent with pre-crucifixion flagellation, bloodstained marks on the head that are consistent with a ‘crown’ of thorns, blood marks on the hand and feet that are consistent with crucifixion and the bloodstain on the chest that evidences a post-mortem wound that corresponds with the post-mortem spear wound that Christ received as is described in the Bible,” the report said.

The new study was written by Giulio Fanti, associate professor of Mechanical and Thermal Measurements at the Department of Industrial Engineering of the University of Padua. According to his personal website, Fanti has studied and written about the famed burial cloth since 2004.

The funding for the study, the report said, “was partially supported by a religious group that requested anonymity” and that the group entrusted Fanti with “the analysis of the so-called ‘Padre Pio handkerchief,’ a fabric on which two images considered miraculous are imprinted on the front and back of (a Shroud of Turin-like) Jesus Christ and Saint Pio of Pietrelcina, respectively.”

According to the report, a preliminary study conducted by Fanti, along with Christian Privitera, an engineer, revealed the presence “of an almost transparent substance” between the bloodstained threads of the shroud.

“This substance, given its origin and in agreement with other scholars who have analyzed the Shroud of Oviedo, could be the semi-transparent fluid produced by pulmonary edema,” the report said, referring to the excessive accumulation of fluid in the lungs that Jesus was believed to have suffered from while on the cross.

The Shroud of Oviedo, Spain, is what both tradition and scientific studies claim was the cloth used to cover and clean the face of Jesus after the crucifixion.

Fanti’s study on the Shroud of Turin stated that aside from confirming the Gospel accounts of Jesus’ torture, including the flagellation, the right eye of the man of the shroud, given that it was “more sunken” with a vertical mark over the “apparently furrowed” eyelid,” indicate that he “could have been blinded by another blow of the scourge on the head.”

“As an alternative to the scourge mark on the right eye, one can think of a wound produced by a thorn from the crown placed on Jesus’ head,” the report stated.

The 14-foot-by-4-foot shroud features a full-length photonegative image of a man, front and back, bearing signs of wounds that correspond to the Gospel accounts of the torture Jesus endured in his passion and death.

The Catholic Church has never officially ruled on the shroud’s authenticity, saying judgments about its age and origin belonged to scientific investigation. Scientists have debated its authenticity for decades, and studies have led to conflicting results.

A 1988 carbon testing dated the cloth to the 12th century, leading many to conclude that the shroud is a medieval forgery. However, scientists have challenged that claim by noting that the methodology of the testing was erroneous and that the sample used in the carbon dating process was a piece used to mend the cloth in the Middle Ages.

A 2014 study published in the 2018 Journal of Forensic Sciences by Matteo Borrini, an Italian forensic scientist, and Luigi Garlaschelli, an Italian chemist, stated that blood patterns on the shroud were not consistent with those left by a crucified person.

Garlaschelli also posted a YouTube video of his experiment in 2015 using a live person to study the blood patterns in various positions as well as pressing a sponge against a plastic mannequin to examine the way the fake blood flowed.

However, several experts and researchers criticized the 2014 study, stating that their findings lacked the accuracy of past studies, some of which involved cadavers of men who died of hemopericardium, the pooling of blood in the heart, which is believed to be what ultimately caused Jesus’ death on the cross.

In his report, Fanti questioned the results of the 1988 study, stating that certain factors, including the presence of neutron radiation, transformed elements in the shroud, “thus heavily skewing the results of the radiocarbon dating of the HST performed in 1988 by many centuries.”

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Living in tree-filled neighborhoods may reduce risk of heart disease, study shows

Living in a tree-filled neighborhood may be as beneficial to the heart as regular exercise, new research shows. 

Researchers at the University of Louisville designed a clinical trial that followed hundreds of people living in six low- to middle-income neighborhoods in South Louisville, Kentucky. They used blood and other samples to better understand how their heart risks changed before and after the team planted thousands of mature trees near their homes. 

Results from the Green Heart Louisville Project ’s HEAL Study , released Tuesday, showed that people living in neighborhoods with twice as many trees and shrubs had lower levels of a blood marker associated with heart disease, diabetes and some types of cancer compared with those who lived in more tree-bare neighborhoods. 

“We are trying to see if we can decrease the rates of heart disease in a community,” said Aruni Bhatnagar, a professor of medicine at the University of Louisville, who led the project.

Most previous studies showing the effects of nature on mental and physical health are observational and can’t answer whether people who live in green communities are healthier because they’re wealthier and have access to better health care. 

The HEAL study was set up with a control group and an intervention, meaning something measurable that some of the participants were exposed to during the study but not before. 

Bhatnagar and his team recruited about 750 people living in a 4-mile area of South Louisville cut by a highway. The residents were 25 to 75 years old. 

Nearly 80% were white, and 60% identified as female. Half reported average household incomes of $50,000.

The researchers collected blood, urine, nail and hair samples, as well as health data, from each person before they began their intervention. 

Then, from 2019 to 2022, they planted nearly 8,500 evergreen trees, 630 deciduous trees — the type that lose leaves in the fall — and 45 different types of shrubs in parts of the 4-mile study area, leaving others untouched. 

Last year and this year, they took new samples from residents living in both areas. 

People living in the intervention areas had 13% lower levels of high-sensitivity C-reactive protein , a blood marker associated with heart disease, including stroke, coronary artery disease and heart attack. The drop was similar to starting a regular exercise routine, Bhatnagar said. 

“I wouldn’t have expected such a strong biomarker response, and that speaks to maybe something truly is causal here with how trees impact health,” said Peter James, director of the Center for Occupational and Environmental Health at the University of California, Davis School of Medicine, who wasn’t involved in the new research. 

How trees can improve physical health

Previous research has shown spending time in green spaces boosts mental health .

The new study showed the connection between living among more trees and physical health. 

Trees provide shade and cool the areas where they’re planted, helping quell the urban heat effect that disproportionately affects low-income neighborhoods and neighborhoods of color. Hot weather aggravates heart disease and can cause heatstroke in people without pre-existing conditions. 

Trees also buffer noise, which is linked to higher rates of cardiovascular disease, James said. 

“They provide areas for people to relax, exercise, and probably more importantly, socialize,” Joan Casey, an environmental epidemiologist and associate professor of environmental and occupational health sciences at the University of Washington, said in an email. 

“They also replace other health-harmful land uses, like industrial sites,” she said.

Because one of the city’s major highways cuts through the study area, Bhatnagar and his team believe, trees’ ability to filter air pollution and buffer neighborhoods from constantly breathing in harmful particles could be a primary way the tree-planting intervention appeared to lower inflammation markers in people living in greened areas. 

During the study, the project planted trees only in the parts of South Louisville that had the worst air quality. It took air quality samples before the project, and it is still analyzing how the new tree cover has affected pollution. It’s a complex undertaking, because air quality fluctuates based on the weather — a windy day might increase or decrease air pollution in certain areas, depending on the direction of the wind, and air pollution is worse on hotter days. 

The project plans to plant trees in the control group neighborhoods in another three or four years if the intervention neighborhoods continue to show positive results. It also wants to determine whether tree cover improves sleep or children’s immune systems by encouraging outside play. 

“There is no sort of ultimate proof,” Bhatnagar said. “But this is the strongest evidence of any study that’s ever been done on trees and their relationship to health.” 

Growing evidence shows the importance of ensuring green spaces are equitably distributed around cities, which is currently not the case . 

Casey said it’s important that city planners be careful not to create “green gentrification” when they create more equitable access to green spaces in cities — that is, when spaces such as water fronts are restored and housing prices increase as a result, making it unaffordable for current residents to continue living there once a green space is completed.

“The take-home message here is that nature is not an amenity; green spaces are not a perk for the wealthy. They are essential for us as human beings,” James said. 

Kaitlin Sullivan is a contributor for NBCNews.com who has worked with NBC News Investigations. She reports on health, science and the environment and is a graduate of the Craig Newmark Graduate School of Journalism at City University of New York.

Anne Thompson is NBC News’ chief environmental affairs correspondent.