What you eat can influence how you sleep

Daily intake of fiber, saturated fat and sugar may impact sleep quality

January 14, 2016
Science Daily/American Academy of Sleep Medicine
A new study found that eating less fiber, more saturated fat and more sugar is associated with lighter, less restorative, and more disrupted sleep.

Results show that greater fiber intake predicted more time spent in the stage of deep, slow wave sleep. In contrast, a higher percentage of energy from saturated fat predicted less slow wave sleep. Greater sugar intake also was associated with more arousals from sleep.

"Our main finding was that diet quality influenced sleep quality," said principal investigator Marie-Pierre St-Onge, PhD, assistant professor in the department of medicine and Institute of Human Nutrition at Columbia University Medical Center in New York, N.Y. "It was most surprising that a single day of greater fat intake and lower fiber could influence sleep parameters."

Study results are published in the January issue of the Journal of Clinical Sleep Medicine.

"This study emphasizes the fact that diet and sleep are interwoven in the fabric of a healthy lifestyle," said American Academy of Sleep Medicine President Dr. Nathaniel Watson, who was not involved in the study. "For optimal health it is important to make lifestyle choices that promote healthy sleep, such as eating a nutritious diet and exercising regularly."

The study also found that participants fell asleep faster after eating fixed meals provided by a nutritionist, which were lower in saturated fat and higher in protein than self-selected meals. It took participants an average of 29 minutes to fall asleep after consuming foods and beverages of their choice, but only 17 minutes to fall asleep after eating controlled meals.

"The finding that diet can influence sleep has tremendous health implications, given the increasing recognition of the role of sleep in the development of chronic disorders such as hypertension, diabetes and cardiovascular disease," said St-Onge.

The randomized, crossover study involved 26 adults -- 13 men and 13 women -- who had a normal weight and an average age of 35 years. During 5 nights in a sleep lab, participants spent 9 hours in bed from 10 p.m. to 7 a.m., sleeping for 7 hours and 35 minutes on average per night. Objective sleep data were gathered nightly by polysomnograhy. Sleep data were analyzed from night 3, after 3 days of controlled feeding, and night 5, after one day of ad libitum food intake.

According to the authors, the study suggests that diet-based recommendations might be used to improve sleep in those with poor sleep quality. However, future studies are needed to evaluate this relationship.
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2016/01/160114213443.htm

Brain function differs in obese children

January 25, 2016
Science Daily/Vanderbilt University Medical Center
The brains of children who are obese function differently from those of children of healthy weight, and exhibit an "imbalance" between food-seeking and food-avoiding behaviors, researchers have found. Because of this, mindfulness, a practice used as a therapeutic technique to focus awareness, should be studied as a way to encourage healthy eating and weight loss in children, the new research suggests.

Diet and exercise may not be enough to restore normal weight or prevent overweight children from becoming obese, they conclude. It may be necessary to change their brain function.

In a paper published in the journal Heliyon, the researchers suggest that mindfulness, a practice used as a therapeutic technique to focus awareness, should be studied as a way to encourage healthy eating and weight loss in children.

"Adults, and especially children, are primed towards eating more," said senior author Kevin Niswender, M.D., Ph.D. "This is great from an evolutionary perspective ... but in today's world, full of readily available, highly advertised, energy dense foods, it is putting children at risk of obesity."

"We think mindfulness could recalibrate the imbalance in the brain connections associated with childhood obesity," added co-senior author Ronald Cowan, M.D., Ph.D. "Mindfulness has produced mixed results in adults ... So far there have been few studies showing its effectiveness for weight loss in children."

Childhood obesity in the United States has nearly doubled during the past 30 years, and among adolescents it has tripled. In 2010, a third of U.S. children were considered obese or overweight.

The Vanderbilt study included 38 children, five who were considered obese and six who were overweight. Their eating behaviors were assessed using a questionnaire, and their brain function was assessed using magnetic resonance imaging (MRI).

Three brain regions in adults are potent modulators of eating habits: the nucleus accumbens, associated with reward-motivated behaviors; the frontal pole, associated with impulsivity; and the inferior parietal lobe (IPL), associated with response inhibition, the ability to inhibit or override a response such as overeating.

The researchers used MRI to determine the balance of functional neural connectivity between these eating-related brain regions in children of various weights.

"We wanted to look at the way (their) brains function in more detail so we can better understand what is happening neurologically in children who are overweight and obese," said first author and Vanderbilt graduate student BettyAnn Chodkowski.

They found that as weight increased among children, the connectivity between the inhibition-associated IPL and reward-associated nucleus accumbens decreased, while connectivity between the nucleus accumbens and the impulsivity-associated frontal pole increased.

This suggests that unhealthy eating behaviors and obesity could reflect an imbalance in the functional connectivity of brain areas associated with response inhibition, impulsivity and reward.

The practice of mindfulness can increase response inhibition and decrease impulsivity. Mindfulness has been used to encourage healthy responses to everyday adversities, although few studies have tested its use in the area of healthy eating or weight loss among children.

Among adults, mindfulness has had mixed results when used for weight loss and weight control, which may reflect "the extreme tenaciousness of adult obesity," as well as age-related loss of brain plasticity, the researchers noted.

This supports the importance of early identification of children at risk for obesity, and the need to develop novel methods to treat and prevent it, they concluded.
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2016/01/160125185035.htm

How obesity makes memory go bad

January 26, 2016
Science Daily/University of Alabama at Birmingham
Obesity is associated with epigenetic changes that dysregulate memory-associated genes, and a particular enzyme in brain neurons of the hippocampus appears to be a link between chronic obesity and cognitive decline.

They have found that epigenetic changes dysregulate memory-associated genes, and a particular enzyme in brain neurons of the hippocampus appears to be a link between chronic obesity and cognitive decline. Their work is published in the Jan. 27 issue of Journal of Neuroscience.

Obesity plagues developed nations, and among the numerous negative health outcomes associated with obesity is a memory impairment that is seen in middle-aged and older obese people. The cause of this decline? Experiments with obese rodents have given a clue: altered gene expression in the hippocampus area of the brain. Until now, the reasons gene expression was changed, as well as the mechanism by which obesity leads to pathogenic memory impairment, have not been known.

There was one suspect: epigenetic dysregulation in neurons of the hippocampus. Foundational experiments over the past decade have linked the creation of long-term memories to changes in DNA methylation and hydroxymethylation -- changes caused by epigenetic mechanisms that sit above the level of the genes.

Such lasting molecular changes to DNA appear to play an important role in promoting or suppressing memory formation through their ability to increase or reduce the expression of genes that help brain neurons create new synaptic connections.

UAB researchers have now shown that epigenetic changes are indeed associated with changes in the expression of memory-associated genes within the hippocampus of obese mice, and these epigenetic changes correlate with diminished object location spatial memory in the obese mice. The UAB researchers have also implicated reduced amounts of one particular memory-associated gene product -- SIRT1 -- as the principal pathogenic cause of obesity-induced memory impairment. The hippocampus subregion of the brain is important for consolidation of long-term memory.

Corresponding author J. David Sweatt, Ph.D., first author Frankie D. Heyward, Ph.D., and colleagues in the UAB Department of Neurobiology, Evelyn F. McKnight Brain Institute, write that these data "provide the first evidence that high-fat-diet-induced obesity leads to the time-dependent development of aberrant epigenetic modifications within the hippocampus, as well as corresponding reduction in the expression of various memory-related genes."

Sweatt noted, "We feel this is a very exciting finding that identifies a new linkage between diet, epigenetics and cognitive function, especially in light of the burgeoning obesity epidemic in the U.S. and elsewhere."

This work, they write, "offers a novel working model that may serve as a conceptual basis for the development of therapeutic interventions for obesity-induced memory impairment."

In details about the cause of altered gene expression, the UAB researchers found that:

• Mice with diet-induced obesity at 20 weeks had impaired performance in object location memory tests, and their hippocampus had impaired synaptic plasticity, as measured by long-term potentiation.

• Four memory-associated genes -- Ppargc1a, Ppp1cb, Reln and Sirt1 -- showed significantly decreased gene expression at 23 weeks of diet-induced obesity, as has been seen before, and the latter three had significantly increased DNA methylation in their gene promoter regions. Increased methylation is known to decrease gene expression. Furthermore, the Sirt1 promoter region also had significantly decreased DNA hydroxymethylation. Gene expression increases or decreases as DNA hydroxymethylation increases or decreases.

• Obesity-induced memory impairment develops over time. At just 13 weeks of diet-induced obesity, seven weeks earlier than the experiments above, mice did not have significant object location memory impairment, and at 16 weeks of diet-induced obesity, also seven weeks earlier than above, none of the genes showed significant increases in DNA methylation. Only one gene at 16 weeks -- Ppargc1a -- showed significant decreases in gene expression and DNA hydroxymethylation.

To probe the mechanism by which obesity leads to pathogenic memory impairment, the UAB researchers focused on the gene Sirt1, which makes an enzyme that is active in the neuron during energy expenditure and fat mobilization. This enzyme appears to be depleted and dysfunctional in obesity, and the deletion of the Sirt1 gene in the brain shortly after birth is known to impair memory and the ability to form new neural synapses. These roles for the SIRT1 gene product -- in both high-fat-diet-induced molecular pathology and in memory impairment -- suggest that it might be a link between chronic obesity and cognitive decline.

Heyward, Sweatt and colleagues found that the hippocampus of obese mice had significantly diminished protein expression of SIRT1, and a substrate of the enzyme, acetlylated-p53, was significantly increased, suggesting reduced enzymatic activity. Also, a targeted deletion of Sirt1 in the forebrain region that includes the hippocampus at age 8-12 weeks showed decreased Sirt1 mRNA and protein in the hippocampus, and these mice showed impaired object-location memory when tested two weeks later.

Furthermore, chemical activation of SIRT1 in diet-induced obese mice by feeding them resveratrol showed decreased levels of acetylated-p53, suggesting increased SIRT1 enzymatic activity, and the resveratrol-fed obese mice had a normal object-location memory, as compared with the control obese mice. The resveratrol-fed obese mice did not show an enhanced memory compared with normal mice. This suggests that resveratrol preserved their hippocampus-dependent spatial memory and SIRT1 function in the hippocampus.

Besides Heyward and Sweatt, co-authors of the paper, "Obesity weighs down memory through a mechanism involving the neuroepigenetic dysregulation of Sirt1," are Daniel Gilliam, Mark Coleman, Cristin Gavin, Ph.D., Jing Wang, Ph.D., Garrett Kaas, Ph.D., Richard Trieu, John Lewis and Jerome Moulden, all of the UAB Department of Neurobiology.

Heyward is now a postdoctoral fellow at Harvard Medical School, the Broad Institute and Beth Israel Deaconess Medical Center. While at UAB, Heyward was supported by a UNCF/Merck Graduate Science Research Dissertation Fellowship that helps train and develop African-American biomedical scientists.

About 10 years ago, Sweatt's lab made the seminal discovery that everyday experiences tap into epigenetic mechanisms in subregions of the brain, and the resulting epigenetic changes in DNA are critically important for long-term memory formation and the stable storage of long-term memory. The 2007 Neuron paper "Covalent modification of DNA regulates memory formation," by Courtney Miller, Ph.D., and Sweatt, was the first to show that active regulation of the chemical structure of DNA is involved in learning and experience-driven changes in the brain.

Obesity and cognitive decline

Evidence that suggests a link between the two includes:

• People ages 40-45 who were obese had a 74 percent increased risk of dementia 21 years later, and those who were overweight had a 35 percent greater risk. This study cohort had 10,276 men and women. Whitmer, RA, et al., BMJ 2005.

• A study of 2,223 healthy workers found that a higher body-mass index was associated with lower cognitive scores, after adjustment for age, sex, educational level, blood pressure, diabetes and other co-variables. Also, a higher BMI at baseline was associated with higher cognitive decline at a follow-up five years later. Cournot, M., et al., Neurology 2006.

• Metabolic syndrome in 73 people with an average age of 60 was associated with significant reductions in recall and overall intellectual functioning, compared with age- and education-matched controls. Hassenstab, J.J., et al., Dementia and Geriatric Cognitive Disorders 2010.

• A study of 8,534 twin individuals who were 65 or older showed that being overweight or obese at mid-life, with an average age of 43, was related to later dementia at the older age. Xu, W.L., et al., Neurology 2011.
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2016/01/160126175513.htm

Being overweight linked to poorer memory

February 26, 2016
Science Daily/University of Cambridge
Overweight young adults may have poorer episodic memory -- the ability to recall past events -- than their peers, suggests new research, adding to increasing evidence of a link between memory and overeating. Researchers found an association between high body mass index and poorer performance on a test of episodic memory.

In a preliminary study published in The Quarterly Journal of Experimental Psychology, researchers from the Department of Psychology at Cambridge found an association between high body mass index (BMI) and poorer performance on a test of episodic memory.

Although only a small study, its results support existing findings that excess bodyweight may be associated with changes to the structure and function of the brain and its ability to perform certain cognitive tasks optimally. In particular, obesity has been linked with dysfunction of the hippocampus, an area of the brain involved in memory and learning, and of the frontal lobe, the part of the brain involved in decision making, problem solving and emotions, suggesting that it might also affect memory; however, evidence for memory impairment in obesity is currently limited.

Around 60% of UK adults are overweight or obese: this number is predicted to rise to approximately 70% by 2034. Obesity increases the risk of physical health problems, such as diabetes and heart disease, as well as psychological health problems, such as depression and anxiety.

"Understanding what drives our consumption and how we instinctively regulate our eating behaviour is becoming more and more important given the rise of obesity in society," says Dr Lucy Cheke. "We know that to some extent hunger and satiety are driven by the balance of hormones in our bodies and brains, but psychological factors also play an important role -- we tend to eat more when distracted by television or working, and perhaps to 'comfort eat' when we are sad, for example.

"Increasingly, we're beginning to see that memory -- especially episodic memory, the kind where you mentally relive a past event -- is also important. How vividly we remember a recent meal, for example today's lunch, can make a difference to how hungry we feel and how much we are likely to reach out for that tasty chocolate bar later on."

The researchers tested 50 participants aged 18-35, with body mass indexes (BMIs) ranging from 18 through to 51 -- a BMI of 18-25 is considered healthy, 25-30 overweight, and over 30 obese. The participants took part in a memory test known as the 'Treasure-Hunt Task', where they were asked to hide items around complex scenes (for example, a desert with palm trees) across two 'days'. They were then asked to remember which items they had hidden, where they had hidden them, and when they were hidden. Overall, the team found an association between higher BMI and poorer performance on the tasks.

The researchers say that the results could suggest that the structural and functional changes in the brain previously found in those with higher BMI may be accompanied by a reduced ability to form and/or retrieve episodic memories. As the effect was shown in young adults, it adds to growing evidence that the cognitive impairments that accompany obesity may be present early in adult life.

This was a small, preliminary study and so the researchers caution that further research will be necessary to establish whether the results of this study can be generalised to overweight individuals in general, and to episodic memory in everyday life rather than in experimental conditions.

"We're not saying that overweight people are necessarily more forgetful," cautions Dr Cheke, "but if these results are generalizable to memory in everyday life, then it could be that overweight people are less able to vividly relive details of past events -- such as their past meals. Research on the role of memory in eating suggests that this might impair their ability to use memory to help regulate consumption.

"In other words, it is possible that becoming overweight may make it harder to keep track of what and how much you have eaten, potentially making you more likely to overeat."

Dr Cheke believes that this work is an important step in understanding the role of psychological factors in obesity. "The possibility that there may be episodic memory deficits in overweight individuals is of concern, especially given the growing evidence that episodic memory may have a considerable influence on feeding behaviour and appetite regulation," she says.

Co-author Dr Jon Simons adds: "By recognising and addressing these psychological factors head-on, not only can we come to understand obesity better, but we may enable the creation of interventions that can make a real difference to health and wellbeing."
Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/02/160226133801.htm

Sleep loss boosts hunger, unhealthy food choices

February 29, 2016
Science Daily/University of Chicago Medical Center
Cutting back on sleep boosts levels of a chemical signal that can enhance the pleasure of eating snack foods and increase caloric intake, report investigators. It may be part of a mechanism that encourages overeating, leading to weight gain, they say.

Skimping on sleep has long been associated with overeating, poor food choices and weight gain. Now a new study shows how sleep loss initiates this process, amplifying and extending blood levels of a chemical signal that enhances the joy of eating, particularly the guilty pleasures gained from sweet or salty, high-fat snack foods.

The findings were published Feb. 29, 2016, in the journal SLEEP.

Sleep-deprived participants in this study -- all young, healthy volunteers -- were unable to resist what the researchers called "highly palatable, rewarding snacks," meaning cookies, candy and chips, even though they had consumed a meal that supplied 90 percent of their daily caloric needs two hours before. The effects of sleep loss on appetite were most powerful in the late afternoon and early evening, times when snacking has been linked to weight gain.

"We found that sleep restriction boosts a signal that may increase the hedonic aspect of food intake, the pleasure and satisfaction gained from eating," said Erin Hanlon, PhD, a research associate in endocrinology, diabetes and metabolism at the University of Chicago. "Sleep restriction seems to augment the endocannabinoid system, the same system targeted by the active ingredient of marijuana, to enhance the desire for food intake."

This chemical signal is the endocannabinoid 2-arachidonoylglycerol (2-AG). Blood levels of 2-AG are typically low overnight. They slowly rise during the day, peaking in the early afternoon.

When the study subjects were sleep-deprived, however, endocannabinoid levels rose higher and remained elevated through the evening, beyond the typical 12:30 p.m. peak. During that period, sleep-restricted study subjects reported higher scores for hunger and stronger desire to eat. When given access to snacks, they ate nearly twice as much fat as when they had slept for eight hours.

This increase in circulating endocannabinoid levels, the authors note, "could be a mechanism by which recurrent sleep restriction results in excessive food intake, particularly in the form of snacks, despite minimal increases in energy need."

"The energy costs of staying awake a few extra hours seem to be modest," explained Hanlon. "One study has reported that each added hour of wakefulness uses about 17 extra calories. That adds up to about 70 calories for the four hours of lost sleep. But, given the opportunity, the subjects in this study more than made up for it by bingeing on snacks, taking in more than 300 extra calories. Over time, that can cause significant weight gain."

Obesity and sleep restriction have become extremely common. According to the Centers for Disease Control and Prevention, about a third of Americans get less than seven hours of sleep a night and more than a third of adults in the United States are obese. A 2013 Gallup poll found that U.S. adults sleep an average of 6.8 hours per night. Forty percent of adults report sleeping six hours or less.

Hanlon and colleagues designed the study to help understand how the endocannabinoid system connected short sleep with weight gain. Her team recruited 14 healthy men and women in their 20s as volunteers. The researchers monitored the subjects' hunger and eating habits in two situations: one four-day stay in the University's Clinical Research Center during which they spent 8.5 hours in bed each night (averaging 7.5 hours of sleep), and another four-day stay when they spent only 4.5 hours in bed (4.2 hours asleep).

The participants ate identical meals three times a day, at 9 a.m., 2 p.m., and 7 p.m. Researchers measured levels of the hormone ghrelin, which boosts appetite, and leptin, which signals fullness, in their blood. Previous studies have linked high ghrelin and low leptin levels to reduced sleep time and increased appetite.

For the first time, however, they also measured blood levels of endocannabinoids. After a normal night's sleep, 2-AG levels were low in the morning. They peaked in the early afternoon, soon after lunchtime, then decreased.

After restricted sleep, however, 2-AG levels rose to levels about 33 percent higher than those seen after normal sleep. They also peaked about 90 minutes later, at 2 p.m., and remained elevated until about 9 p.m.

After the period of restricted sleep, study subjects reported a significant increase in hunger levels. This was prominent soon after their second meal of the day, the time when 2-AG levels were highest. Sleep deprived study subjects expressed greater desire to eat. When asked, they estimated that they could eat much more than they predicted the day after a full night's sleep.

After the fourth night of restricted sleep, subjects were offered an array of snack foods. Despite having eaten a large meal less than two hours before being offered snacks, subjects in the restricted sleep phase of the study had trouble limiting their snack consumption. They chose foods that provided 50 percent more calories, including twice the amount of fat, as when they were completing the normal sleep phase.

These results support "the novel insight that sleep restriction leads not only to increased caloric intake," but also to "changes in the hedonic aspects of food consumption," wrote Frank Scheer, PhD, of the Medical Chronobiology Program at Harvard University's Brigham and Women's Hospital, in a commentary. The increase in 2-AG following sleep restriction, he added, "may be part of the mechanism by which people overeat."

Despite the study's limitations -- small size, short duration, limited sampling frequency -- the findings are clearly significant and consistent with the epidemiologic evidence, the authors note. They are also "relevant to normal life conditions."

This tells us that "if you have a Snickers bar, and you've had enough sleep, you can control your natural response," Hanlon explained. "But if you're sleep deprived, your hedonic drive for certain foods gets stronger, and your ability to resist them may be impaired. So you are more likely to eat it. Do that again and again, and you pack on the pounds."
Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/02/160229221045.htm

Can mindful eating help lower risk of type 2 diabetes, cardiovascular disease?

New research suggests mindfulness could improve glucose levels, heart health

March 9, 2016
Science Daily/Wiley
Given the high stress levels, extended periods of screen time and regular social outings many Americans experience day-to-day in environments where high-calorie foods are readily available, it can be easy to fall into the habit of mindless eating -- where we're too distracted to pay attention to how much, what and why we're eating.

Given the high stress levels, extended periods of screen time and regular social outings many Americans experience day-to-day in environments where high-calorie foods are readily available, it can be easy to fall into the habit of mindless eating -- where we're too distracted to pay attention to how much, what and why we're eating. Research suggests that practicing mindfulness -- or taking the time to bring awareness to present-moment experiences with an open attitude of curiosity and non-judgment -- can be effective in allowing us to make more thoughtful food choices and recognize when we are hungry, satisfied or full. The latest research in this area led by Jennifer Daubenmier, PhD, Assistant Professor at the Osher Center for Integrative Medicine at the University of California, San Francisco, suggests that the impact of mindful eating could be even greater.

"Whether eating snacks while watching the game or grazing by the dessert tray at the office event, we often find ourselves overeating not because we're hungry, but because the food looks delicious, we're distracted, or we wish to soothe away unpleasant feelings," explains Dr. Daubenmier. "Our study suggests that mindful eating can go further than making healthy food choices and recognizing when we're full; it could improve glucose levels and heart health to a greater extent than behavioral weight-loss programs that do not teach mindful eating."

Dr. Daubenmier and her colleagues evaluated the effects of a mindfulness-based weight-loss intervention on adults with obesity, and although no statistically significant differences in weight loss were found compared to the control group, the mindfulness intervention showed greater improvements in certain cardiometabolic outcomes tied to Type 2 Diabetes and cardiovascular disease up to one year after the intervention ended. The research is published in the March issue of Obesity, the scientific journal of The Obesity Society.

To conduct the study, the researchers randomized nearly 200 adults with obesity to a mindfulness intervention or an active attention control group over a five-and-a-half month period, with a subsequent one-year follow up. Both groups were given identical diet and exercise guidelines. Participants in the mindfulness intervention received added training on mindfulness meditation and how to practice awareness of their thoughts, feelings, and bodily sensations during eating and exercise. At 18 months after the start of the intervention, participants in the mindfulness program lost an estimated 4.3% of body weight on average, which was 3.7 pounds more than those in the control group but not enough to reach statistical significance. Nevertheless, the authors found that the mindfulness program had more positive effects on fasting blood glucose at 18 months and a ratio of triglycerides to HDL-cholesterol levels at 12 months (a difference of -4.1 mg/dL and -0.57, respectively), both of which are linked to Type 2 Diabetes and cardiovascular disease.

"Most behavioral weight-loss interventions do not place as much emphasis on managing mindless eating, and previous studies on the topic have not included attention controls or long term follow-up to better study the contribution of mindfulness components over time," said Deborah Tate, PhD, spokesperson for The Obesity Society. "This research points to some of the potential benefits of enhancing the mindfulness components of behavioral weight loss."
Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/03/160309082810.htm

Losing weight with a high-protein diet can help adults sleep better

March 24, 2016
Science Daily/Purdue University
Overweight and obese adults who are losing weight with a high-protein diet are more likely to sleep better, according to new research. The study also has studied how dietary protein quantity, sources and patterns affect appetite, body weight and body composition.

"Most research looks at the effects of sleep on diet and weight control, and our research flipped that question to ask what are the effects of weight loss and diet -- specifically the amount of protein -- on sleep," said Wayne Campbell, a professor of nutrition science. "We found that while consuming a lower calorie diet with a higher amount of protein, sleep quality improves for middle-age adults. This sleep quality is better compared to those who lost the same amount of weight while consuming a normal amount of protein."

These findings are published in the American Journal of Clinical Nutrition, which is affiliated with the American Society for Nutrition. The research was funded by Beef Checkoff, National Pork Board, National Dairy Council, Purdue Ingestive Behavior Research Center and National Institutes of Health.

A pilot study found that in 14 participants, consuming more dietary protein resulted in better sleep after four weeks of weight loss. Then, in the main study, 44 overweight or obese participants were included to consume either a normal-protein or a higher-protein weight loss diet. After three weeks of adapting to the diet, the groups consumed either 0.8 or 1.5 grams of protein for each kg of body weight daily for 16 weeks. The participants completed a survey to rate the quality of their sleep every month throughout the study. Those who consumed more protein while losing weight reported an improvement in sleep quality after three and four months of dietary intervention.

A dietitian designed a diet that met each study participant's daily energy need and 750 calories in fats and carbohydrates were trimmed per day while maintaining the protein amount based on whether they were in the higher- or normal-protein group. The sources of protein used in the two studies varied from beef, pork, soy, legumes and milk protein.

"Short sleep duration and compromised sleep quality frequently lead to metabolic and cardiovascular diseases and premature death," said Jing Zhou, a doctoral student in nutrition science and the study's first author. "Given the high prevalence of sleep problems it's important to know how changes to diet and lifestyle can help improve sleep."

Campbell's lab also has studied how dietary protein quantity, sources and patterns affect appetite, body weight and body composition.

"This research adds sleep quality to the growing list of positive outcomes of higher-protein intake while losing weight, and those other outcomes include promoting body fat loss, retention of lean body mass and improvements in blood pressure," Campbell said. "Sleep is recognized as a very important modifier of a person's health, and our research is the first to address the question of how a sustained dietary pattern influences sleep. We've showed an improvement in subjective sleep quality after higher dietary protein intake during weight loss, which is intriguing and also emphasizes the need for more research with objective measurements of sleep to confirm our results."

The other co-authors are Jung Eun Kim, a postdoctoral research associate in nutrition science; Cheryl Armstrong, a research associate in nutrition science; and Ningning Chen, a graduate student in statistics.

Campbell, whose expertise and research focuses on understanding how protein nutrition and exercise influence adults' health as they age, served as a member of the 2015 Dietary Guidelines Advisory Committee, which helped provide the scientific foundation for the nation's 2015-2020 Dietary Guidelines for Americans.
Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/03/160324133028.htm