Eating Disoders News & Resources

Cocoa May Help Fight Obesity-Related Inflammation

Eating Disorders News | 14 June 2013

A few cups of hot cocoa may not only fight off the chill of a winter's day, but they could also help obese people better control inflammation-related diseases, such as diabetes, according to Penn State researchers.

Mice that were fed cocoa with a high-fat diet experienced less obesity-related inflammation than mice fed the same high-fat diet without the supplement, said Joshua Lambert, associate professor of food science. The mice ate the human equivalent of 10 tablespoons of cocoa powder -- about four or five cups of hot cocoa -- during a 10-week period.

"What surprised me was the magnitude of the effect," Lambert said. "There wasn't as big of an effect on the body weight as we expected, but I was surprised at the dramatic reduction of inflammation and fatty liver disease."

The researchers reported that several indicators of inflammation and diabetes in the mice that were fed the cocoa supplement were much lower than the mice that were fed the high-fat diet without the cocoa powder and almost identical to the ones found that were fed a low-fat diet in the control group. For example, they had about 27 percent lower plasma insulin levels than the mice that were not fed cocoa. High levels of insulin can signal that a patient has diabetes.

The cocoa powder supplement also reduced the levels of liver triglycerides in mice by a little more than 32 percent, according to Lambert, who worked with Yeyi Gu, graduate student in food science, and Shan Yu, a graduate student in physiology. Elevated triglyceride levels are a sign of fatty liver disease and are related to inflammation and diabetes.

The mice also saw a slight but significant drop in the rate of body weight gain, according to the researchers, who reported their findings in the online version of the European Journal of Nutrition.

While researchers have linked obesity-related chronic inflammation to several diseases, including type 2 diabetes and fatty liver disease, the reason for the inflammation response is not completely known. Lambert said two theories on inflammation and obesity that have emerged may help explain cocoa's role in mitigating inflammation. In one theory, Lambert said excess fat may activate a distress signal that causes immune cells to become activated and cause inflammation. The cocoa may reduce the precursors that act as a distress signal to initiate this inflammatory response.

Lambert said that another theory is that excess fat in the diet interferes with the body's ability to keep a bacterial component called endotoxin from entering the bloodstream through gaps between cells in the digestive system -- gut barrier function -- and alerting an immune response. The cocoa in this case may help improve gut barrier function.

Cocoa, although commonly consumed in chocolate, actually has low-calorie content, low-fat content and high-fiber content.

"Most obesity researchers tend to steer clear of chocolate because it is high in fat, high in sugar and is usually considered an indulgence," Lambert said. "However, cocoa powder is low in fat and low in sugar. We looked at cocoa because it contains a lot of polyphenolic compounds, so it is analogous to things like green tea and wine, which researchers have been studying for some of their health benefits."

Lambert said he expects future research will be conducted to better identify why the cocoa powder is effective in treating inflammation, as well as determine if the treatment is suitable for humans.

The National Institutes of Health supported this work.

Reducing Caloric Intake Delays Nerve Cell Loss

Eating Disorders News | 10 June 2013

Study points to role of protein in anti-aging benefits of calorie restriction. Activating an enzyme known to play a role in the anti-aging benefits of calorie restriction delays the loss of brain cells and preserves cognitive function in mice, according to a study published in the May 22 issue of The Journal of Neuroscience. The findings could one day guide researchers to discover drug alternatives that slow the progress of age-associated impairments in the brain. 

Previous studies have shown that reducing calorie consumption extends the lifespan of a variety of species and decreases the brain changes that often accompany aging and neurodegenerative diseases such as Alzheimer’s. There is also evidence that caloric restriction activates an enzyme called Sirtuin 1 (SIRT1), which studies suggest offers some protection against age-associated impairments in the brain. 

In the current study, Li-Huei Tsai — director of the Picower Institute for Learning and Memory and Picower Professor of Neuroscience at MIT — along with postdoc Johannes Gräff and others at MIT tested whether reducing caloric intake would delay the onset of nerve cell loss that is common in neurodegenerative disease, and if so, whether SIRT1 activation was driving this effect. The group not only confirmed that caloric restriction delays nerve cell loss, but also found that a drug that activates SIRT1 produces the same effects.

“There has been great interest in finding compounds that mimic the benefits of caloric restriction that could be used to delay the onset of age-associated problems and/or diseases,” says Dr. Luigi Puglielli, who studies aging at the University of Wisconsin, Madison, and was not involved in this study. “If proven safe for humans, this study suggests such a drug could be used as a preventive tool to delay the onset of neurodegeneration associated with several diseases that affect the aging brain."

In the study, Tsai’s team first decreased the normal diets of mice genetically engineered to rapidly undergo changes in the brain associated with neurodegeneration by 30 percent. Following three months on the diet, the mice completed several learning and memory tests. “We not only observed a delay in the onset of neurodegeneration in the calorie-restricted mice, but the animals were spared the learning and memory deficits of mice that did not consume reduced-calorie diets,” Tsai says.

Curious if they could recreate the benefits of caloric restriction without changing the animals’ diets, the scientists gave a separate group of mice a drug that activates SIRT1. Similar to what the researchers found in the mice exposed to reduced-calorie diets, the mice that received the drug had less cell loss and better cellular connectivity than the mice that did not receive the drug. Additionally, the mice that received the drug treatment performed as well as normal mice in learning and memory tests.

“The question now is whether this type of treatment will work in other animal models, whether it’s safe for use over time, and whether it only temporarily slows down the progression of neurodegeneration or stops it altogether,” Tsai says.

The research was supported by the National Institute on Aging and the Swiss National Science Foundation.

Sweeteners Can Alter Metabolism

Eating Disorders News | 31 May 2013

In a small study, researchers analyzed the sweetener sucralose (Splenda) in 17 severely obese people who do not have diabetes and don’t use artificial sweeteners regularly.

“Our results indicate that this artificial sweetener is not inert—it does have an effect,” says first author M. Yanina Pepino, research assistant professor of medicine at Washington University School of Medicine in St. Louis. “And we need to do more studies to determine whether this observation means long-term use could be harmful.”

Pepino’s team studied people with an average body mass index (BMI) of just over 42; a person is considered obese when BMI reaches 30. They gave subjects either water or sucralose to drink before they consumed a glucose challenge test. The glucose dosage is very similar to what a person might receive as part of a glucose-tolerance test.

The researchers wanted to learn whether the combination of sucralose and glucose would affect insulin and blood sugar levels.

“We wanted to study this population because these sweeteners frequently are recommended to them as a way to make their diets healthier by limiting calorie intake,” Pepino says. The research is available online in the journal Diabetes Care.

Every participant was tested twice. Those who drank water followed by glucose in one visit drank sucralose followed by glucose in the next. In this way, each subject served as his or her own control group.

Metobolic reaction

“When study participants drank sucralose, their blood sugar peaked at a higher level than when they drank only water before consuming glucose,” Pepino explained. “Insulin levels also rose about 20 percent higher. So the artificial sweetener was related to an enhanced blood insulin and glucose response.”

The elevated insulin response could be a good thing, she pointed out, because it shows the person is able to make enough insulin to deal with spiking glucose levels. But it also might be bad because when people routinely secrete more insulin, they can become resistant to its effects, a path that leads to type 2 diabetes.

It has been thought that artificial sweeteners, such as sucralose, don’t have an effect on metabolism. They are used in such small quantities that they don’t increase calorie intake. Rather, the sweeteners react with receptors on the tongue to give people the sensation of tasting something sweet without the calories associated with natural sweeteners, such as table sugar.

But recent findings in animal studies suggest that some sweeteners may be doing more than just making foods and drinks taste sweeter.

One finding indicates that the gastrointestinal tract and the pancreas can detect sweet foods and drinks with receptors that are virtually identical to those in the mouth. That causes an increased release of hormones, such as insulin. Some animal studies also have found that when artificial sweeteners activate receptors in the gut, the absorption of glucose also increases.

Pepino, who is part of the university’s Center for Human Nutrition, says those studies could help explain how sweeteners may affect metabolism, even at very low doses. But most human studies involving artificial sweeteners haven’t found comparable changes.

Sucralose and obesity mystery

“Most of the studies of artificial sweeteners have been conducted in healthy, lean individuals,” Pepino says. “In many of these studies, the artificial sweetener is given by itself. But in real life, people rarely consume a sweetener by itself. They use it in their coffee or on breakfast cereal or when they want to sweeten some other food they are eating or drinking.”

Just how sucralose influences glucose and insulin levels in people who are obese is still somewhat of a mystery.

“Although we found that sucralose affects the glucose and insulin response to glucose ingestion, we don’t know the mechanism responsible,” says Pepino. “We have shown that sucralose is having an effect. In obese people without diabetes, we have shown sucralose is more than just something sweet that you put into your mouth with no other consequences.”

She says further studies are needed to learn more about the mechanism through which sucralose may influence glucose and insulin levels, as well as whether those changes are harmful. A 20 percent increase in insulin may or may not be clinically significant, she added.

“What these all mean for daily life scenarios is still unknown, but our findings are stressing the need for more studies,” she says. “Whether these acute effects of sucralose will influence how our bodies handle sugar in the long term is something we need to know.”

Brain Chemistry Changes Sustain Obesity

Eating Disorders News | 21 May 2013

With obesity reaching epidemic levels in some parts of the world, scientists have only begun to understand why it is such a persistent condition. A study in the Journal of Biological Chemistry adds substantially to the story by reporting the discovery of a molecular chain of events in the brains of obese rats that undermined their ability to suppress appetite and to increase calorie burning.

A complex set of neurochemical processes, newly unraveled, shows that obesity can sustain itself, impeding hormones that would curb appetite or increase the burn rate for calories. “This is so novel. Nobody has ever looked at that”. It’s a vicious cycle, involving a breakdown in how brain cells process key proteins that allows obesity to beget further obesity. But in a finding that might prove encouraging in the long term, the researchers at Brown University and Lifespan also found that they could intervene to break that cycle by fixing the core protein-processing problem.

Before the study, scientists knew that one mechanism in which obesity perpetuates itself was by causing resistance to leptin, a hormone that signals the brain about the status of fat in the body. But years ago senior author Eduardo A. Nillni, professor of medicine at Brown University and a researcher at Rhode Island Hospital, observed that after meals obese rats had a dearth of another key hormone — alpha-MSH — compared to rats of normal weight.

Alpha-MSH has two jobs in parts of the hypothalamus region of the brain. One is to suppress the activity of food-seeking brain cells. The second is to signal other brain cells to produce the hormone TRH, which prompts the thyroid gland to spur calorie burning activity in the body.

In the obese rats alpha-MSH was low, despite an abundance of leptin and despite normal levels of gene expression both for its biochemical precursor protein called pro-opiomelanocortin (POMC) and for a key enzyme called PC2 that processes POMC in brain cells. There had to be more to the story than just leptin, and it wasn’t a problem with expressing the needed genes.

Nillni and his co-authors, including lead authors Isin Cakir and Nicole Cyr, conducted the new study to find out where the alpha-MSH deficit was coming from. Nillni said he suspected that the problem might lie in the brain cells’ mechanism for processing the POMC protein to make alpha-MSH.

Protein processing problems

To do their work, the team fed some rats a high-calorie diet and fed others a normal diet for 12 weeks. The overfed rats developed the condition of “diet-induced obesity.” The team then studied the hormone levels and brain cell physiology of the rats. They also tested their findings by experimenting with the biochemistry of key individual cells on the lab bench.

They found that in the obese rats, a key “machine” in the brain cells’ assembly line of protein-making, called the endoplasmic reticulum (ER), becomes stressed and overwhelmed. The overloaded ER apparently fumbles the proper handling of PC2, perhaps discarding it because it can’t be folded up properly. The PC2 levels they measured in obese rats, for example, were 53 percent lower than in normal rats. Alpha-MSH peptides were also barely more than half as abundant in obese rats as they were in healthy rats.

“In our study we showed that what actually prevents the production of more alpha-MSH peptide is that ER stress was decreasing the biosynthesis of POMC by affecting one key enzyme that is essential for the formation of alpha-MSH,” Nillni said. “This is so novel. Nobody ever looked at that.”

Novel as it was, the story — a stressed ER mishandles PC2, which leaves POMC unfolded, which impedes alpha-MSH production — needed experimental confirmation.

The team provided that confirmation in several ways: In obese rats they measured elevated levels of known markers of ER stress. They also purposely induced ER stress in cells using pharmacological agents and saw that both PC2 and Alpha-MSH levels dropped.

Next they conducted an experiment to see if fixing ER stress would improve alpha-MSH production. They treated lean and obese rats for two days with a chemical called TUDCA, which is known to alleviate ER stress. If ER stress is responsible for alpha-MSH production problems, the researchers would see alpha-MSH recover in obese rats treated with TUDCA. Sure enough, while TUDCA didn’t increase alpha-MSH production in normal rats, it increased it markedly in the obese rats.

Similarly on the benchtop they took mouse neurons that produce PC2 and POMC and pretreated some with a similar chemical called PBA that prevents ER stress. They left others untreated. Then they induced ER stress in all the cells. Under that ER stress, those that had been pretreated with PBA produced about twice as much PC2 as those that had not.

Nillni cautioned that although his team found ways to restore PC2 and alpha-MSH by treating ER stress in living rats and individual cells, the agents used in the study are not readily applicable as medicines for treating obesity in humans. There could well be unknown and unwanted side effects, for example, and TUDCA is not approved for human use by the U.S. Food and Drug Administration.

But by laying out the exact mechanism responsible for why the brains of the obese rats failed to curb appetite or spur greater calorie burning, Nillni said, the study points drug makers to several opportunities where they can intervene to break this new, vicious cycle that helps obesity to perpetuate itself.

“Understanding the central control of energy-regulating neuropeptides during diet-induced obesity is important for the identification of therapeutic targets to prevent and or mitigate obesity pathology,” the authors wrote.

In addition to Nillni, Cakir and Cyr, other authors of the paper are Mario Perello, Bogdan Litvinov, Amparo Romero, and Ronald Stuart.

The Biology Behind Binge Eating

Eating Disorders News | 17 May 2013

Female rats are much more likely to binge eat than male rats, according to new research that provides some of the strongest evidence yet that biology plays a role in eating disorders.

The study, by Michigan State University scientists, is the first to establish sex differences in rates of binge eating in animals and has implications for humans. Binge eating is one of the core symptoms of most eating disorders, including bulimia nervosa and the binge/purge subtype of anorexia nervosa, and females are four to 10 times more likely than males to have an eating disorder.

“Most theories of why eating disorders are so much more prevalent in females than males focus on the increased cultural and psychological pressure that girls and women face,” said Kelly Klump, lead author and professor of psychology. “But this study suggests that biological factors likely contribute as well, since female rats do not experience the psychosocial pressures that humans do, such as pressures to be thin.”

Klump and colleagues ran a feeding experiment with 30 female and 30 male rats over a two-week period, replacing the rodents’ food pellets periodically with vanilla frosting. They found that the rate of binge eating “proneness” (i.e., the tendency to consume the highest amount of frosting across all feeding tests) was up to six times higher in female as compared to male rats.

The tendency to binge eat may be related to the brain’s natural reward system, or the extent to which someone likes and seeks reward, Klump said. The MSU researchers currently are testing the rats to see if female brains are more sensitive and/or responsive to rewarding stimuli (e.g., high-fat, high-sugar food) and the chemicals that trigger reward behavior.

The answers could ultimately help improve therapy – both counseling and medications – for those with eating disorders.

“This research suggests there is probably a biological difference between males and females that we need to explore to understand risk factors and mechanisms,” Klump said.

The study is published online in the International Journal of Eating Disorders. Klump’s co-authors are Cheryl Sisk, psychology professor, and graduate students Sarah Racine and Britny Hildebrandt.

Calories Are Main Attraction in Foods

Eating Disorders News | 10 May 2013

People like food because it contains calories they need to survive. However, researchers from The John B Pierce Laboratory and Yale have discovered an interesting twist to the basic biology story: Calories trigger responses in areas of the brain that control eating behavior independently of how much the subject likes the flavor.

“The implication is that calories don’t need to increase liking to influence our eating,” said Dana Small, associate professor of psychiatry, associate fellow of the Pierce Laboratory, and senior author of the study to be published in the May 20 edition of the journal Current Biology.

The findings shed light on how food cues trigger eating, insights that can help explain overeating and obesity, say the researchers.

The Yale team was interested in teasing out the signals that allow the brain to assess the nutritional value of the food.

Fourteen subjects were tested for preferences for flavors of novel drinks without calories.  Later, calories were added to one of the drinks by adding an undetectable carbohydrate.

The subjects consumed this flavored beverage and one without calories repeatedly over three weeks. The effect of consuming these drinks on blood glucose was also measured. Following this conditioning, subjects’ brains were then scanned as they sampled non-caloric versions of both flavored drinks.  As predicted, participants liked the calorie-paired flavor. The team found that a change in blood glucose produced by drinking the flavor that had once contained calories strongly predicted responses in regions of the brain known to guide feeding.

“What was striking was that this happened completely independently from changes in liking,” Small said.

This helps explain why eating — and over-eating — are often unrelated to how much a person likes the food, say the researchers. It also suggests that individuals with altered glucose metabolism, like people with diabetes, will be more susceptible to food cues because they have increased glucose responses to food.

Ivan E de Araujo was lead author of the paper. Other Yale authors are Tammy Lin and Maria G. Veldhuizen. The National Institute of Diabetes and Digestive and Kidney Diseases funded the study.

Binge Eating Curbed by Deep Brain Stimulation

Eating Disorders News | 26 April 2013

Deep brain stimulation (DBS) in a precise region of the brain appears to reduce caloric intake and prompt weight loss in obese animal models, according to a new study led by researchers at the University of Pennsylvania. The study, reported in the Journal of Neuroscience, reinforces the involvement of dopamine deficits in increasing obesity-related behaviors such as binge eating, and demonstrates that DBS can reverse this response via activation of the dopamine type-2 receptor.

"Based on this research, DBS may provide therapeutic relief to binge eating, a behavior commonly seen in obese humans, and frequently unresponsive to other approaches," said senior author Tracy L. Bale, PhD, associate professor of neuroscience in Penn’s School of Veterinary Medicine’s Department of Animal Biology and in the Perelman School of Medicine’s Department of Psychiatry. DBS is currently used to reduce tremors in Parkinson's disease and is under investigation as a therapy for major depression and obsessive-compulsive disorder.

Nearly 50 percent of obese people binge eat, uncontrollably consuming palatable highly caloric food within a short period of time. In this study, researchers targeted the nucleus accumbens, a small structure in the brain reward center known to be involved in addictive behaviors. Mice receiving the stimulation ate significantly less of the high fat food compared to mice not receiving DBS. Following stimulation, mice did not compensate for the loss of calories by eating more. However, on days when the device was turned off, binge eating resumed.

Researchers also tested the long-term effects of DBS on obese mice that had been given unlimited access to high-fat food. During four days of continuous stimulation, the obese mice consumed fewer calories and, importantly, their body weight dropped. These mice also showed improvement in their glucose sensitivity, suggestive of a reversal of type 2 diabetes.

“These results are our best evidence yet that targeting the nucleus accumbens with DBS may be able to modify specific feeding behaviors linked to body weight changes and obesity,” Bale added.

“Once replicated in human clinical trials, DBS could rapidly become a treatment for people with obesity due to the extensive groundwork already established in other disease areas,” said lead author Casey Halpern, MD, resident in the Department of Neurosurgery of the Perelman School of Medicine at the University of Pennsylvania.

The study was funded by the National Institutes of Health (DA022605 and HL091911). In addition to Drs. Bale and Halpern, Penn experts include Anand Tekriwal from the College of Arts and Sciences, John Wolf from Neurosurgery and Jeffrey Keating from Neurology. They were joined by colleagues in Psychology at the University of Buffalo.

Over-Exercise May Signal Heightened Suicide Risk in Bulimic Individuals

Eating Disorders News | 17 April 2013

Over-exercise in females with bulimia nervosa is linked to suicidality, April Smith, Ph.D., of Miami University in Ohio and colleagues report in the April 30Psychiatry Research. In a first study, which included 204 women who met full or partial criteria for a DSM-IV diagnosis of bulimia nervosa, the researchers found that the frequency of over-exercise—defined as "hard exercise as a means of controlling weight or shape"—significantly predicted suicidal gestures and suicide attempts, even when other bulimic behaviors such as vomiting, purging, and fasting were considered.

They then attempted to replicate this finding in a nonclinical sample of 171 college students. The students were evaluated for symptoms of bulimia nervosa, including over-exercise, as well as for "acquired capability of suicide" (that is, fearlessness about lethal self-injury). The researchers found that over-exercise predicted "acquired capability of suicide" even when other bulimia nervosa symptoms were considered.

And in a third study, this one of 467 college students, Smith and colleagues found that over-exercise predicted pain insensitivity over and above other bulimic behaviors. They thus suspect that over-exercise might lead to suicidality by increasing pain and in turn pain tolerance, and the pain tolerance in turn might make a person less fearful of death. "These results may help explain the increased rate of suicidal behavior displayed by people with bulimia nervosa," the researchers said. "And given these findings, an important treatment target for individuals with bulimia nervosa who are engaging in over-exercise may be to teach healthy exercise..."

For picky eaters, genes matter more than food

Eating Disorders News | 12 April 2013

Genes play a major role in some people’s tendency to avoid new foods, but that doesn’t mean they can’t be swayed, researchers say.

Parents may plead, cajole, or entice their children to try new foods, but some kids just won’t budge. New research reveals that the reason these kids fear new foods has less to do with what’s on their plate and more to do with their genes.

The work, led by Myles Faith, an associate professor of nutrition at the University of North Carolina at Chapel Hill’s Gillings School of Global Public Health, adds to the growing body of knowledge that genes play a significant role in children’s eating behavior, including the tendency to avoid new foods.

“In some respects, food neophobia, or the aversion to trying new foods, is similar to child temperament or personality,” says Faith, whose work appears in the journal Obesity.

“Some children are more genetically susceptible than others to avoid new foods. However, that doesn’t mean that they can’t change their behaviors and become a little less picky.”

The study looked at 66 pairs of twins between ages 4 and 7 years old, and found that genes explain 72 percent of the variation among children in the tendency to avoid new foods, while the rest was influenced by environment. Previous research has shown a similar genetic influence for food neophobia in 8-to-11-year-olds (78 percent) and adults (69 percent), suggesting that the impact of genes on food neophobia is constant across the developmental spectrum.

Faith and his team also examined the relationship between food neophobia and body fat measures in both parent and child. Unexpectedly, the researchers found that if the parent was heavier, the child was heavier only if he or she avoided trying new foods.

“It’s unexpected, but the finding certainly invites interesting questions about how food neophobia and temperament potentially shape longer-term eating and influence body weight,” says Faith.

On the environmental side, the findings suggest that parents should consider each child’s idiosyncrasies, even for siblings in the same household, when thinking about how to increase a child’s acceptance of new foods.

For example, parents can serve as role models and provide repeated exposure to new foods at home, or show their child how much they enjoy the food being avoided. They might also provide a choice of several new items from which a child could select.

“Each child may respond differently to each approach, and research needs to examine new interventions that take into account children’s individuality,” says Faith. “But what we do know through this and other emerging science is that this individuality includes genetic uniqueness.”

Protein-Rich Breakfasts Prevent Unhealthy Snacking in the Evening, MU Researcher Finds

Eating Disorders News | 29 March 2013

For a new study, 20 overweight or obese adolescent females ages 18-20 either skipped breakfast, consumed a high-protein breakfast consisting of eggs and lean beef, or ate a normal-protein breakfast of ready-to-eat cereal. Every breakfast consisted of 350 calories and was matched for dietary fat, fiber, sugar, and energy density.

The high-protein breakfast contained 35 grams of protein. Participants completed questionnaires and provided blood samples throughout the day. Prior to dinner, a brain scan using functional magnetic resonance imaging (fMRI) was performed to track brain signals that control food motivation and reward-driven eating behavior.

As reported in the American Journal of Clinical Nutrition, eating the high-protein breakfast led to increased fullness or “satiety” along with reductions in brain activity that is responsible for controlling food cravings. It also reduced evening snacking on high-fat and high-sugar foods compared to when breakfast was skipped or when a normal protein, ready-to-eat cereal breakfast was consumed, says Heather Leidy, assistant professor in the department of nutrition and exercise physiology at the University of Missouri.

“Eating a protein-rich breakfast impacts the drive to eat later in the day, when people are more likely to consume high-fat or high-sugar snacks,” Leidy says. “These data suggest that eating a protein-rich breakfast is one potential strategy to prevent overeating and improve diet quality by replacing unhealthy snacks with high quality breakfast foods.”

People who normally skip breakfast might be skeptical about consuming food in the morning, but Leidy says it only takes about three days for the body to adjust to eating early in the day.

Study participants ate egg and beef-based foods such as burritos or egg-based waffles with applesauce and a beef sausage patty as part of a high-protein breakfast; Leidy also suggests eating plain Greek yogurt, cottage cheese, or ground pork loin as alternatives to reach the 35 grams of protein.

Future research will examine whether regularly consuming high-protein breakfasts improves body weight management in young people.