SSIB Press Releases


Blue light at night increases the consumption of sweets in rats

A new study demonstrates that just one hour of exposure to blue light at night – the kind of light produced by the screens of our many devices - raises blood sugar levels and increases sugar consumption in male rats. This study, led by Anayanci Masís-Vargas and colleagues from the University of Strasbourg and University of Amsterdam, was presented this week at the annual conference of the Society for the Study of Ingestive Behavior (SSIB) in Utrecht, Netherlands.

Previous research has shown a strong correlation between obesity and the levels of artificial light at night. Much of the artificial light we are now exposed to comes from LED lights and LED screens, which emit high levels of blue light. Retinal cells of the eye are sensitive to this blue light and directly convey information to areas of the brain that regulate appetite.

In their study, Masís-Vargas and colleagues, exposed rats to nighttime blue light and measured their food consumption and glucose tolerance the following day. It should be noted that, in order to better model human light exposure, the rats used in this study were diurnal, meaning awake during the day and asleep at night, rather than the typical nocturnal laboratory rats which are awake during nighttime hours. The authors found that after only one hour of nocturnal blue light exposure, glucose tolerance was altered in male rats, a warning sign of pre-diabetes.

To investigate what happens with appetite control and food choice after exposure to blue light at night, the rats were given the option to choose among a nutritionally balanced food (standard rodent food), water, lard, and sugar water. After the exposure to blue light, they observed that the male animals drank more sugar that night than during the nights with no blue light exposure.

These studies show clearly that being exposed to light, especially blue light, at night is disruptive and that screen use at night may increase our tendency to snack on sugary foods and disrupt our ability to process that sugar, especially in males. Though the rats were tested after only one night of light exposure, over time, this could lead to weight gain and the development of diabetes.

“Limiting the amount of time that we spend in front of screens at night is, for now, the best measure to protect ourselves from the harmful effects of blue light. In case it is necessary to be exposed to devices at night, I would recommend the use of apps and night mode features on the devices, which turn the screens more orange and less blue or the use of blue light filtering googles that are already available in the market.” Masís-Vargas says.

Research citation:
Acute exposure to blue light at night impairs glucose tolerance, alters insulin secretion and increase sugar intake in a diurnal rodent. Anayanci Masís-Vargas2,3, David Hicks1, Andries Kalsbeek2,3, Jorge Mendoza1
1Light, Vision and the Brain Team, Institute de Neurosciences Cellulaires et Intégratives Strasbourg, France, 2 Hypothalamic Integration Mechanisms, Netherlands Institute of Neuroscience Amsterdam, Netherlands, 3 Department of Endocrinology and Metabolism, Amsterdam UMC Amsterdam, Netherlands
Presented July 2019, Society for the Study of Ingestive Behavior, Utrecht, Netherlands

Contact:
Jorge Mendoza, PhD
jmendoza@inci-cnrs.unistra.fr
+33 03 88 45 66 96


Perception of lower socioeconomic standing stimulates appetite

Recent research suggests that the psychological consequences of being in a disadvantaged position in society may stimulate appetite and increase eating regardless of one’s ability to access healthier foods. These findings, out from Nanyang Technological University in Singapore and the Singapore Institute for Clinical Sciences, add a new dimension to previous findings suggesting that the increased risk for obesity among people who are poorer and socioeconomically disadvantaged is due primarily to economic barriers that prevent access to healthier foods and other unhealthy behaviors associated with poverty.

These intriguing findings, presented by Dr. Bobby Cheon at the annual meeting of the Society for the Study of Ingestive Behavior this week, involved making research participants feel like they have inadequate socioeconomic resources compared to other people and measuring the effects on eating behaviors. Participants in the study were led to make comparisons of financial, economic, and social status resources (e.g., having a respected position in society) with others who were either much better off or much worse off than them. This approach of experimentally manipulating whether people perceive themselves as having sufficient or inadequate socioeconomic standing compared to others allowed the researchers to directly test whether the mere perception of socioeconomic disadvantage influences food preferences and eating behaviors.

Across multiple studies, the researchers found that participants who were led to feel they had fewer resources and opportunities compared to others ate more calories from snacks and meals offered during the experiment, served themselves larger portion sizes of foods, and showed increased ability to detect differences in calories between beverages. Participants who experienced feelings of socioeconomic disadvantage also had elevated levels of ghrelin – often referred to as the “hunger hormone” – providing a biological explanation for the desire to eat more under these conditions.

“If feelings of deprivation and inadequacy produced by perceived socioeconomic inequality can stimulate appetite and food intake, then it’s possible that feeling that important needs in one’s life have been satisfied may produce the opposite effect of reducing excessive food intake,” said Cheon. To test this, research participants were assigned to complete a daily gratitude journal for 2 weeks, in which they listed things that they were grateful for each day. Compared to a control group that wrote about events that occurred each day, male participants in the gratitude journal group showed a reduction in desired portions of a variety of foods.

Although inadequate access to healthy foods is often blamed for obesity in populations with lower socioeconomic status, this research shows that the psychological consequences of social and economic inequality are also detrimental to health. The research team plans to continue to test methods, like heightening gratitude, to psychologically protect people from engaging in potentially unhealthy eating behaviors in response to perceived socioeconomic inequality and insecurities.

Research citation:
Social inequality as an obesogenic environment: Implications for socioeconomic disparities in obesity.
BK Cheon, Nanyang Technological University & Singapore Institute for Clinical Sciences, Singapore.
Presented July 2019, Society for the Study of Ingestive Behavior, Utrecht, Netherlands.

Contact:
Bobby Cheon, Ph.D.
bkcheon@ntu.edu.sg


“Hunger hormone” enhances memory

A team of neuroscience researchers at the University of Southern California have identified a surprising new role for the “hunger hormone” ghrelin. Ghrelin has previously been recognized for its unique role in sending hunger signals from the gut to the brain, but, as presented this week at the annual meeting of the Society for the Study of Ingestive Behavior, these new findings suggest that it may also be important for memory control.

Ghrelin is produced in the stomach and secreted in anticipation of eating, and is known for its role to increase hunger. “For example, ghrelin levels would be high if you were at a restaurant, looking forward to a delicious dinner that was going to be served shortly,” said Dr. Elizabeth Davis, lead author on the study. Once it is secreted, ghrelin binds to specialized receptors on the vagus nerve – a nerve that communicates a variety of signals from the gut to the brain. “We recently discovered that in addition to influencing the amount of food consumed during a meal, the vagus nerve also influences memory function,” said Dr. Scott Kanoski, senior author of the study. The team hypothesized that ghrelin is a key molecule that helps the vagus nerve promote memory.

Using an approach called RNA interference to reduce the amount of ghrelin receptor, the researchers blocked ghrelin signaling in the vagus nerve of laboratory rats. When given a series of memory tasks, animals with reduced vagal ghrelin signaling were impaired in a test of episodic memory, a type of memory that involves remembering what, when, and where something occurred, such as recalling your first day of school. For the rats, this required remembering a specific object in a specific location.

The team also investigated whether vagal ghrelin signaling influences feeding behavior. They found that when the vagus nerve could not receive the ghrelin signal, the animals ate more frequently, yet consumed smaller amounts at each meal. Dr. Davis thinks these results may be related to the episodic memory problems. “Deciding to eat or not to eat is influenced by the memory of the previous meal,” says Davis. “Ghrelin signaling to the vagus nerve may be a shared molecular link between remembering a past meal and the hunger signals that are generated in anticipation of the next meal.”

These novel findings add to our understanding of how episodic memories are generated, as well as the relationship between memory and eating behavior. In the future, researchers may be able to develop strategies for improving memory capacity in humans by manipulating ghrelin signaling from the gut to the brain.

Research citation:
Vagal afferent ghrelin signaling promotes episodic memory and influences meal patterns in rats
Elizabeth A Davis1, Andrea N Suarez1, Clarissa M Liu1, Guillaume de Lartigue2, Scott E Kanoski 1
1 University of Southern California Los Angeles, CA, USA; 2 University of Florida Gainesville, FL, USA
Presented July 2019, Society for the Study of Ingestive Behavior, Utrecht, Netherlands

Contact:
Dr. Scott Kanoski
kanoski@usc.edu
213-821-5762
www.kanoski-lab.com


Brain stimulation enhances motivation to work for food

Electrical stimulation of the brain through the vagus nerve increases the motivations to work for food, according to recent findings of a research group at the University of Tübingen. These findings, which were presented at the annual meeting of the Society for the Study of Ingestive Behavior this week in Utrecht, Netherlands, demonstrate a novel method to alter motivation to obtain food.

“Vigorous work is costly and has to be recuperated by energy intake. That makes it vital for us to know when it is worth the effort. The vagus nerve helps set the tone for actions by signaling, for example, if energy is readily available for that action or not,” says Dr. Nils B. Kroemer, the Principal Investigator of the study and junior group leader of the University’s Neuroscience of Motivation, Action, and Desire Laboratory (neuroMADLAB) . “We knew that vagus nerve stimulation changes dopamine levels in animals and that chronic stimulation improves depressive symptoms in humans, but it was not known if it could acutely improve motivation. We found that it may provide a much-needed technique to rapidly change reward-related behavior such as eating”.

The researchers invited 81 hungry participants to their laboratory on two occasions. Everyone was offered a tasty breakfast, but there was a catch. Participants had to exert physical effort to win reward points that could be “cashed in” for their favorite cereals. At one of the two sessions, participants completed the task while receiving electrical stimulation of the vagus nerve; during the other session, they received placebo stimulation. Results showed that stimulation boosted how vigorously participants exerted effort for the rewards at stake compared to the control condition.

“This ambitious experiment is one of the first to study motivational changes during acute vagus nerve stimulation,'' said Monja P. Neuser, a Ph.D. student in the neuroMADLAB and lead study author. “The motivational effects elicited by the stimulation are very promising and encourage us to further unravel the exact neural mechanisms. We think that the stimulation increases dopamine levels in the brain, which is known to enhance vigor. “

By using concurrent functional neuroimaging, researchers of the neuroMADLAB will continue investigating how non-invasive vagus nerve stimulation can be administered to maximize its benefits. Most notably, researchers plan to apply this technique in people suffering from anhedonia—an absence of desire to engage in normally pleasurable activities such as eating—to determine whether it increases their motivation to seek out and consume food.

Research citation:
Going with your gut: tVNS increases invigoration for food rewards
MP Neuser1, V Teckentrup1, M Walter1,2,3, NB Kroemer1
1 Eberhard Karls University Tübingen, Germany
2 Otto-von-Guericke University Magdeburg, Germany
3 Leibniz Institute for Neurobiology, Magdeburg, Germany
Presented July 2019 at the Society for the Study of Ingestive Behavior, Utrecht, NL

Contact:
Dr. rer. nat. Nils Kroemer, Dipl.-Psych.
#: 0049 7071/ 29-82021
nils.kroemer@uni-tuebingen.de
https://www.medizin.uni-tuebingen.de/en-de
www.neuromadlab.de


Food and alcohol reduce activity in “hunger neurons” via different brain pathways

How does the brain process rewards? Researchers at the University of Pennsylvania are investigating how the brain responds differently to two commonly ingested rewards – food and alcohol – to understand how they alter neural activity and behavior. Their findings were presented this week in Utrecht, Netherlands at the 2019 Annual Meeting of the Society for the Study of Ingestive Behavior (SSIB), one of the leading venues for research on eating and drinking.

In a study led by Dr. Amber Alhadeff, neural activity was measured in hungry mice consuming either food or alcohol. “Our modern neuroscience toolkit now allows us to monitor neural activity in behaving mice when we give them access to different kinds of rewards. This gives us unprecedented access into the mechanisms that control motivation and behavior,” said Alhadeff. The study demonstrates that food and alcohol have similar effects on neurons that are known to be involved in food intake and reward. However, different pathways carry signals to the brain following ingestion of either food or alcohol. They found that the vagus nerve, a highway of information from the gastrointestinal tract to the brain, is responsible for transmitting food signals to “hunger neurons.” Alcohol, on the other hand, does not utilize vagal signaling to communicate with these same hunger neurons, but likely accesses them, and suppresses their activity, directly through the bloodstream.

These divergent pathways of information flow could help explain why food and alcohol have different effects on our behavior, according to senior author Dr. J. Nicholas Betley. When the researchers measured how alcohol affects food intake, they unexpectedly found that it has little effect on feeding behavior, despite its significant calorie content. “When we observed this, we started to think that mice don’t actually compute the caloric content of alcohol” said Betley. Indeed, the University of Pennsylvania team went on to show that stimulation of “hunger neurons” in the brain robustly drives food intake, but has no effect on alcohol intake. In the future, these findings will be useful for determining the different mechanisms through which food and drugs impact neural activity and motivation for different rewards, providing insight into the underpinnings of obesity and substance abuse.

Research citation:

Nutrients and drugs of abuse modulate hypothalamic neuron activity via distinct pathways
Amber L. Alhadeff, Nitsan Goldstein, J. Nicholas Betley
University of Pennsylvania Philadelphia, PA, USA
Presented July 2019, Society for the Study of Ingestive Behavior, Utrecht, Netherlands

Contact:
Dr. Amber L. Alhadeff
amberla@sas.upenn.edu
610-533-8326


Insulin nasal spray may boost cognitive function in obese adolescents by improving brain connectivity
Researchers at the Modern Diet and Physiology Research Center and Department of Pediatrics at Yale School of Medicine are investigating whether insulin delivered directly to the brain by nasal inhalation can enhance communication between brain regions and improve cognition in adolescents with obesity and prediabetes. Led by Dr. Dana Small, preliminary findings from a two-year study suggest that intranasal insulin improves brain and cognitive function in adolescents with obesity.

Insulin is primarily recognized for its role in regulation of blood sugar and metabolism. But insulin also travels to the brain where it influences a wide range of functions including memory, mood, and appetite. In type 2 diabetes, cells throughout the body become insensitive to insulin and when this happens in the brain, it may lead to cognitive impairment and an increased risk of developing dementia later in life.

Capitalizing on the fact that intranasal inhalation of insulin delivers insulin directly to the brain, Dr. Small and her team are investigating the link between brain insulin sensitivity and cognitive function in adolescents with obesity. Preliminary cross-sectional findings presented this week at the annual meeting for the Society for the Study of Ingestive Behavior in Utrecht, Netherlands, found that intranasal insulin delivery improved performance on a memory task in adolescents with high BMI. Compared to inhalation of a placebo, the intranasal insulin also significantly increased connectivity between left and right dorsolateral prefrontal cortex – key brain areas for cognitive performance and cognitive control.

While data collection is ongoing, the preliminary cross-sectional findings suggest that not only is obesity associated with poorer memory, but that this impairment can be reversed by intranasal insulin. The researchers plan to continue this work to better understand the role of factors such as body fat levels and diabetic status on neurocognition, as well as evaluation of the effects of changes in these measures over time.

Research citation:
Effects of intranasal insulin on brain connectivity and cognition in overweight/obese adolescents
Tuki N. Attuquayefio, Iris Hovens, Alex Difeliceantonio, Michael Farrugia, Kathryn Wall, Nicola Santoro, Sonia Caprio, Dana Small
Yale University New Haven, CT, USA
Presented July 2019, Society for the Study of Ingestive Behavior, Utrecht, Netherlands

Contact:
Tuki Attuquayefio
tuki.attuquayefio@yale.edu
(203) 390 7707


Exercise improves brain function in overweight and obese individuals
New findings out of the University of Tübingen show that, on top of its benefits for metabolism, mood, and general health, exercise also improves brain function. In recent studies, researchers learned that obese and overweight individuals are prone to insulin resistance in the brain, where it provides information about current nutritional status, as well as the rest of the body. So researchers wanted to know whether exercise can improve insulin sensitivity in the brain and improve cognition in overweight individuals.

In the current study, led by Dr. Stephanie Kullmann, 22 sedentary adults with overweight or obesity (an average BMI of 31) underwent two brain scans before and after an 8-week exercise intervention, including cycling and walking. Brain function was measured before and after using an insulin nasal spray to investigate insulin sensitivity of the brain. Participants were also assessed for cognition, mood, and peripheral metabolism.

Even though the exercise intervention only resulted in a marginal weight loss, brain functions important for metabolism “normalized” only after 8-weeks. Exercise increased regional blood flow in areas of the brain important for motor control and reward processes, both of which depend on the neurotransmitter dopamine. Dopamine is an important neurotransmitter for learning new motor skills and in reward-related learning and this research shows that exercise significantly improves dopamine-related brain function. One area in particular, the striatum, had enhanced sensitivity to insulin after the 8-weeks of exercise such that the brain response of a person with obesity after exercise training resembled the response of a person with normal-weight. Interestingly, the greater the improvement in brain function, the more belly fat a person lost during the course of the exercise intervention. Behaviorally, participants reported an improvement in mood and task switching, which is an indicator for improved executive function.

“The bottom line is that exercise improves brain function”, said Kullmann. “And increasing insulin sensitivity in dopamine-related brain regions through exercise may help decrease the risk of a person to develop type 2 diabetes, along with the benefits for mood and cognition”.

Research citation:
Exercise improves brain insulin action and executive function in adults with overweight and obesity
Stephanie Kullmann, Lore Wagner, Ralf Veit, Christoph Hoffmann, Patrick Schneeweiss, Andreas Niess, Hubert Preissl, Hans-Ulrich Häring, Günter Schnauder, Andreas Fritsche, Cora Weigert, Anja Böhm, Martin Heni
University of Tübingen, Tübingen, Germany
Presented July 2019, Society for the Study of Ingestive Behavior, Utrecht, Netherlands

Contact:
Stephanie Kullmann
stephanie.kullmann@med.uni-tuebingen.de


Intermittent fasting protects mice from type 2 diabetes
Every-other-day fasting substantially reduces the likelihood of developing type 2 diabetes in mice eating a fat-rich diet, according to new research out of the German Institute of Human Nutrition Potsdam-Rehbruecke. These findings, presented this week at the annual meeting of the Society for the Study of Ingestive Behavior in Utrecht, Netherlands, suggest that periodic fasting can reduce fat accumulation in the pancreas and, in turn, prevent the onset of type 2 diabetes. “We observed that pancreatic fat cells directly affect islet insulin secretion and that this can be altered by eating patterns” said Dr. Mandy Stadion, a post-doctoral research fellow who led this study.

“It is well known that a fatty liver promotes the development of type 2 diabetes and that intermittent fasting improves insulin sensitivity by reducing liver fat in mice and men,” explained Professor Annette Schürmann, head of the Department Experimental Diabetology at the German Institute of Human Nutrition and senior author of the study. “However, little is known about the formation of fat cells in the pancreas during obesity, their detailed impact on islet-cell function and whether intermittent fasting can prevent a fatty pancreas.”

For these studies the researchers provided one group of diabetes-prone mice with unlimited access to a high-fat diet. These mice were subjected to food restriction every other day (intermittent fasting). Compared to the control condition, intermittent fasting resulted in remarkably reduced pancreatic fat - similar to levels of diabetes-resistant mice - as well as in lower blood sugar levels and improved islet-cell function.

“We believe that the elevated insulin secretion of pancreatic islet cells, particularly from diabetes-prone mice, initiates a more rapid loss of function and finally islet cell-death,”explaned Schürmann. And while this loss of function ultimately contributes to the development of type 2 diabetes, the researchers are optimistic the finding that intermittent fasting can prevent the fat accumulation that leads to increased insulin may reveal a new path forward in the therapeutic prevention and treatment of diabetes.

Research citation:
Intermittent fasting reduces pancreatic fat and prevents type 2 diabetes in mice
Mandy Stadion, Charline Quiclet, Anneke Gässler, Christian Baumeier, Tim J. Schulz, Annette Schürmann
German Institute for Human Nutrition Potsdam-Rehbruecke, Potsdam, Germany; German Center for Diabetes Research (DZD) München-Neuherberg, Germany
Presented July 2019, Society for the Study of Ingestive Behavior, Utrecht, Netherlands

Contact:
Mandy Stadion, PhD
stadion@dife.de
+49 (0) 33200 88 2140
@Leibniz_DIfE