Researchers discover brain circuit linked to food impulsivity

Eating popcorn at a movie (stock image).

Credit: © Zoriana / Adobe Stock

You're on a diet, but the aroma of popcorn in the movie theater lobby triggers a seemingly irresistible craving.

Within seconds, you've ordered a tub of the stuff and have eaten several handfuls.

Impulsivity, or responding without thinking about the consequences of an action, has been linked to excessive food intake, binge eating, weight gain and obesity, along with several psychiatric disorders including drug addiction and excessive gambling.

A team of researchers that includes a faculty member at the University of Georgia has now identified a specific circuit in the brain that alters food impulsivity, creating the possibility scientists can someday develop therapeutics to address overeating.

The team's findings were published recently in the journal Nature Communications.

"There's underlying physiology in your brain that is regulating your capacity to say no to (impulsive eating)," said Emily Noble, an assistant professor in the UGA College of Family and Consumer Sciences who served as lead author on the paper. "In experimental models, you can activate that circuitry and get a specific behavioral response."

Using a rat model, researchers focused on a subset of brain cells that produce a type of transmitter in the hypothalamus called melanin concentrating hormone (MCH).

While previous research has shown that elevating MCH levels in the brain can increase food intake, this study is the first to show that MCH also plays a role in impulsive behavior, Noble said.

"We found that when we activate the cells in the brain that produce MCH, animals become more impulsive in their behavior around food," Noble said.

To test impulsivity, researchers trained rats to press a lever to receive a "delicious, high-fat, high-sugar" pellet, Noble said. However, the rat had to wait 20 seconds between lever presses. If the rat pressed the lever too soon, it had to wait an additional 20 seconds.

Researchers then used advanced techniques to activate a specific MCH neural pathway from the hypothalamus to the hippocampus, a part of the brain involved with learning and memory function.

Results indicated MCH doesn't affect how much the animals liked the food or how hard they were willing to work for the food. Rather, the circuit acted on the animals' inhibitory control, or their ability to stop themselves from trying to get the food."Activating this specific pathway of MCH neurons increased impulsive behavior without affecting normal eating for caloric need or motivation to consume delicious food," Noble said. "Understanding that this circuit, which selectively affects food impulsivity, exists opens the door to the possibility that one day we might be able to develop therapeutics for overeating that help people stick to a diet without reducing normal appetite or making delicious foods less delicious."

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Story Source:

Materials provided by University of Georgia. Original written by Cal Powell. Note: Content may be edited for style and length.

Researchers discover brain circuit linked to food impulsivity

Eating popcorn at a movie 

You're on a diet, but the aroma of popcorn in the movie theater lobby triggers a seemingly irresistible craving.

Within seconds, you've ordered a tub of the stuff and have eaten several handfuls.

Impulsivity, or responding without thinking about the consequences of an action, has been linked to excessive food intake, binge eating, weight gain and obesity, along with several psychiatric disorders including drug addiction and excessive gambling.

A team of researchers that includes a faculty member at the University of Georgia has now identified a specific circuit in the brain that alters food impulsivity, creating the possibility scientists can someday develop therapeutics to address overeating.

The team's findings were published recently in the journal Nature Communications.

"There's underlying physiology in your brain that is regulating your capacity to say no to (impulsive eating)," said Emily Noble, an assistant professor in the UGA College of Family and Consumer Sciences who served as lead author on the paper. "In experimental models, you can activate that circuitry and get a specific behavioral response."

Using a rat model, researchers focused on a subset of brain cells that produce a type of transmitter in the hypothalamus called melanin concentrating hormone (MCH).

While previous research has shown that elevating MCH levels in the brain can increase food intake, this study is the first to show that MCH also plays a role in impulsive behavior, Noble said.

"We found that when we activate the cells in the brain that produce MCH, animals become more impulsive in their behavior around food," Noble said.

To test impulsivity, researchers trained rats to press a lever to receive a "delicious, high-fat, high-sugar" pellet, Noble said. However, the rat had to wait 20 seconds between lever presses. If the rat pressed the lever too soon, it had to wait an additional 20 seconds.

Researchers then used advanced techniques to activate a specific MCH neural pathway from the hypothalamus to the hippocampus, a part of the brain involved with learning and memory function.

Results indicated MCH doesn't affect how much the animals liked the food or how hard they were willing to work for the food. Rather, the circuit acted on the animals' inhibitory control, or their ability to stop themselves from trying to get the food."Activating this specific pathway of MCH neurons increased impulsive behavior without affecting normal eating for caloric need or motivation to consume delicious food," Noble said. "Understanding that this circuit, which selectively affects food impulsivity, exists opens the door to the possibility that one day we might be able to develop therapeutics for overeating that help people stick to a diet without reducing normal appetite or making delicious foods less delicious."

---

Story Source:

Materials provided by University of Georgia. Original written by Cal Powell. Note: Content may be edited for style and length.

Extinct giant ape directly linked to the living orangutan

Modern-day orangutan

By using ancient protein sequencing, researchers have retrieved genetic information from a 1.9 million year old extinct, giant primate that used to live in a subtropical area in southern China. The genetic information allows the researchers to uncover the evolutionary position of Gigantopithecus blacki, a three-meter tall and may be up to 600 kg heavy primate, revealing the orangutan as its closest, living relative.

It is the first time that genetic material this old has been retrieved from a warm, humid environment. The study is published in the scientific journal Nature, and the results are groundbreaking within the field of evolutionary biology, according to Frido Welker, Postdoc at the Globe Institute at the Faculty of Health and Medical Sciences and first author of the study.

'Primates are relatively close to humans, evolutionary speaking. With this study, we show that we can use protein sequencing to retrieve ancient genetic information from primates living in subtropical areas even when the fossil is two million years old. Until now, it has only been possible to retrieve genetic information from up to 10,000-year-old fossils in warm, humid areas. This is interesting, because ancient remains of the supposed ancestors of our species, Homo sapiens, are also mainly found in subtropical areas, particularly for the early part of human evolution. This means that we can potentially retrieve similar information on the evolutionary line leading to humans', says Frido Welker.

Today, scientists know that the human and the chimpanzee lineages split around seven or eight million years ago. With the previous methodologies though, they could only retrieve human genetic information not older than 400,000 years. The new results show the possibility to extend the genetic reconstruction of the evolutionary relationships between our species and extinct ones further back in time, at least up to two million years -- covering a much larger portion of the entire human evolution.

Analyzing ancient dental enamel proteins using mass spectrometry-based proteomics

In a recent study, also published on Nature, Enrico Cappellini, Associate Professor at the Globe Institute and senior author on this study, initially demonstrated, together with an international team of colleagues, the massive potential of ancient protein sequencing.

'By sequencing proteins retrieved from dental enamel about two million years old, we showed it is possible to confidently reconstruct the evolutionary relationships of animal species that went extinct too far away in time for their DNA to survive till now. In this study, we can even conclude that the lineages of orangutan and Gigantopithecus split up about 12 million years ago', says Enrico Cappellini.

Sequencing protein remains two million years old was made possible by stretching to its limits the technology at the base of proteomic discovery: mass spectrometry. State of the art mass spectrometers and the top palaeoproteomics expertise needed to get the best out of such sophisticated instrumentation are key resources deriving from the decade-long strategic collaboration with Jesper Velgaard Olsen, Professor at Novo Nordisk Foundation Center for Protein Research and co-author on this study.

The mystery of Gigantopithecus

The fossil evidence attributed to Gigantopithecus was initially discovered in southern China in 1935, and it is currently limited to just a few lower jaws and lots of teeth. No complete skull and no other bone from the rest of the skeleton has been found so far. As a result, there has been a lot of speculation about the physical appearance of this mysterious animal.

'Previous attempts to understand which could be the living organism most similar to Gigantopithecus could only be based on the comparison of the shape of the fossils with skeletal reference material from living great apes. Ancient DNA analysis was not an option, because Gigantopithecus went extinct approximately 300,000 years ago, and in the geographic area Gigantopithecus occupied no DNA older than approximately 10,000 years has been retrieved so far. Accordingly, we decided to sequence dental enamel proteins to reconstruct its evolutionary relation with living great apes, and we found that orangutan is Gigantopithecus' closest living relative', says Enrico Cappellini.

The study of human evolution by palaeoproteomics will continue in the next years through the recently established "Palaeoproteomics to Unleash Studies on Human History (PUSHH)" Marie Sk?odowska Curie European Training Network (ETN) Programme.

The research is funded mainly by VILLUM FONDEN, the Novo Nordisk Foundation, and the Marie Sklowowska-Curie Actions Individual Fellowship and International Training Network programmes.

---

Story Source:

Materials provided by University of Copenhagen The Faculty of Health and Medical Sciences. Note: Content may be edited for style and length.

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Related Multimedia:

• Images of fossil mandible and artist's rendering of Gigantopithecus blacki

MS linked to variant of common herpes virus

Researchers at Karolinska Institutet have developed a new method to separate between two different types of a common herpes virus (HHV-6) that has been linked to multiple sclerosis. By analyzing antibodies in the blood against the most divergent proteins of herpesvirus 6A and 6B, the researchers were able to show that MS-patients carry the herpesvirus 6A to a greater extent than healthy individuals. The findings, published in Frontiers in Immunology, point to a role for HHV-6A in the development of MS.

Multiple sclerosis, MS, is an autoimmune disease that affects the central nervous system. The cause of the disease is unclear, but one plausible explanation is a virus tricks the immune system to attack the body's own tissue. Human Herpesvirus 6 (HHV-6) has previously been associated with MS, but in those studies it wasn't possible to distinguish between 6A and 6B. Through virus isolation from ill individuals, researchers have been able to show that HHV-6B can cause mild conditions such as roseola in children, but it has been unclear if HHV-6A is the cause of any disease.

According to estimates, as many as 80 percent of all children are infected with the HHV-6 virus before 2 years of age, and many also carry protection in the form of antibodies against this particular virus for the rest of their lives. But since it hasn't been possible to tell the two variants apart post-infection, it has been difficult to say whether HHV-6A or B is a risk factor for MS.

In this study, however, the researchers were able to distinguish between the A and B virus by analyzing antibodies in the blood against the proteins -- immediate early protein 1A and 1B (IE1A and IE1B) -- that diverge the most between the two viruses.

"This is a big breakthrough for both the MS and herpes virus research," says Anna Fogdell-Hahn, associate professor at the Department of Clinical Neuroscience at Karolinska Institutet and one of the study's senior authors. "For one, it supports the theory that HHV-6A could be a contributing factor to the development of MS. On top of that, we are now able, with this new method, to find out how common these two different types of HHV-6 are, something we haven't been able to do previously."

The researchers compared antibody levels in blood samples of some 8,700 MS-patients against more than 7,200 healthy people whose gender, date of birth, date of blood sample and other factors matched those with MS. They concluded that people with MS had a 55 percent higher risk of carrying antibodies against the HHV-6A protein than the control group. In a sub-group of almost 500 people, whose blood samples were drawn before the onset of the disease, the risk of developing MS in the future was more than doubled if they had a 6A viral infection. The younger the people were when the virus was first discovered in the blood, the higher the risk was of developing MS in the future. HHV-6B, on the other hand, was not positively associated with MS. Instead MS-patients had lower levels of antibodies toward IE1B than those without MS.

Antibodies toward Epstein-Barr virus (EBV), another herpes virus that is also associated with MS, were analyzed with the same method and the researchers were able to show that individuals affected with both viruses had an even greater risk of MS. This indicates that several virus infections could be acting jointly to increase the risk of MS.

"Both HHV-6A and 6B can infect our braincells, but they do it in slightly different ways. Therefore, it is now interesting to go forward and attempt to map out exactly how the viruses could affect the onset of MS," says Anna Fogdell-Hahn.

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Story Source:

Materials provided by Karolinska Institutet. Note: Content may be edited for style and length.

Any amount of running linked to significantly lower risk of early death

Woman running

Any amount of running is linked to a significantly lower risk of death from any cause, finds a pooled analysis of the available evidence, published online in the British Journal of Sports Medicine.

If more people took up running -- and they wouldn't have to run far or fast -- there would likely be substantial improvements in population health and longevity, conclude the researchers.

It's not clear how good running is for staving off the risk of death from any cause and particularly from cardiovascular disease and cancer, say the researchers.

Nor is it clear how much running a person needs to do to reap these potential benefits, nor whether upping the frequency, duration, and pace -- in other words, increasing the 'dose' -- might be even more advantageous.

To try and find out, the researchers systematically reviewed relevant published research, conference presentations, and doctoral theses and dissertations in a broad range of academic databases.

They looked for studies on the association between running/jogging and the risk of death from all causes, cardiovascular disease, and cancer.

They found 14 suitable studies, involving 232,149 people, whose health had been tracked for between 5.5 and 35 years. During this time, 25,951 of the study participants died.

When the study data were pooled, any amount of running was associated with a 27% lower risk of death from all causes for both sexes, compared with no running.

And it was associated with a 30% lower risk of death from cardiovascular disease, and a 23% lower risk of death from cancer.

Even small 'doses' -- for example, once weekly or less, lasting less than 50 minutes each time, and at a speed below 6 miles (8 km) an hour, still seemed to be associated with significant health/longevity benefits.

So running for 25 minutes less than the recommended weekly duration of vigorous physical activity could reduce the risk of death. This makes running a potentially good option for those whose main obstacle to doing enough exercise is lack of time, suggest the researchers.

But upping 'the dose' wasn't associated with a further lowering of the risk of death from any cause, the analysis showed.

This is an observational study, and as such, can't establish cause. And the researchers caution that the number of included studies was small and their methods varied considerably, which may have influenced the results.

Nevertheless, they suggest that any amount of running is better than none, concluding: "Increased rates of participation in running, regardless of its dose, would probably lead to substantial improvements in population health and longevity."

Story Source:

Materials provided by BMJ. Note: Content may be edited for style and length.

Any amount of running linked to significantly lower risk of early death

Woman running

Any amount of running is linked to a significantly lower risk of death from any cause, finds a pooled analysis of the available evidence, published online in the British Journal of Sports Medicine.

If more people took up running -- and they wouldn't have to run far or fast -- there would likely be substantial improvements in population health and longevity, conclude the researchers.

It's not clear how good running is for staving off the risk of death from any cause and particularly from cardiovascular disease and cancer, say the researchers.

Nor is it clear how much running a person needs to do to reap these potential benefits, nor whether upping the frequency, duration, and pace -- in other words, increasing the 'dose' -- might be even more advantageous.

To try and find out, the researchers systematically reviewed relevant published research, conference presentations, and doctoral theses and dissertations in a broad range of academic databases.

They looked for studies on the association between running/jogging and the risk of death from all causes, cardiovascular disease, and cancer.

They found 14 suitable studies, involving 232,149 people, whose health had been tracked for between 5.5 and 35 years. During this time, 25,951 of the study participants died.

When the study data were pooled, any amount of running was associated with a 27% lower risk of death from all causes for both sexes, compared with no running.

And it was associated with a 30% lower risk of death from cardiovascular disease, and a 23% lower risk of death from cancer.

Even small 'doses' -- for example, once weekly or less, lasting less than 50 minutes each time, and at a speed below 6 miles (8 km) an hour, still seemed to be associated with significant health/longevity benefits.

So running for 25 minutes less than the recommended weekly duration of vigorous physical activity could reduce the risk of death. This makes running a potentially good option for those whose main obstacle to doing enough exercise is lack of time, suggest the researchers.

But upping 'the dose' wasn't associated with a further lowering of the risk of death from any cause, the analysis showed.

This is an observational study, and as such, can't establish cause. And the researchers caution that the number of included studies was small and their methods varied considerably, which may have influenced the results.

Nevertheless, they suggest that any amount of running is better than none, concluding: "Increased rates of participation in running, regardless of its dose, would probably lead to substantial improvements in population health and longevity."

---

Story Source:

Materials provided by BMJ. Note: Content may be edited for style and length.

Extinct giant ape directly linked to the living orangutan

Modern day orangutan

By using ancient protein sequencing, researchers have retrieved genetic information from a 1.9 million year old extinct, giant primate that used to live in a subtropical area in southern China. The genetic information allows the researchers to uncover the evolutionary position of Gigantopithecus blacki, a three-meter tall and may be up to 600 kg heavy primate, revealing the orangutan as its closest, living relative.

It is the first time that genetic material this old has been retrieved from a warm, humid environment. The study is published in the scientific journal Nature, and the results are groundbreaking within the field of evolutionary biology, according to Frido Welker, Postdoc at the Globe Institute at the Faculty of Health and Medical Sciences and first author of the study.

'Primates are relatively close to humans, evolutionary speaking. With this study, we show that we can use protein sequencing to retrieve ancient genetic information from primates living in subtropical areas even when the fossil is two million years old. Until now, it has only been possible to retrieve genetic information from up to 10,000-year-old fossils in warm, humid areas. This is interesting, because ancient remains of the supposed ancestors of our species, Homo sapiens, are also mainly found in subtropical areas, particularly for the early part of human evolution. This means that we can potentially retrieve similar information on the evolutionary line leading to humans', says Frido Welker.

Today, scientists know that the human and the chimpanzee lineages split around seven or eight million years ago. With the previous methodologies though, they could only retrieve human genetic information not older than 400,000 years. The new results show the possibility to extend the genetic reconstruction of the evolutionary relationships between our species and extinct ones further back in time, at least up to two million years -- covering a much larger portion of the entire human evolution.

Analyzing ancient dental enamel proteins using mass spectrometry-based proteomics

In a recent study, also published on Nature, Enrico Cappellini, Associate Professor at the Globe Institute and senior author on this study, initially demonstrated, together with an international team of colleagues, the massive potential of ancient protein sequencing.

'By sequencing proteins retrieved from dental enamel about two million years old, we showed it is possible to confidently reconstruct the evolutionary relationships of animal species that went extinct too far away in time for their DNA to survive till now. In this study, we can even conclude that the lineages of orangutan and Gigantopithecus split up about 12 million years ago', says Enrico Cappellini.

Sequencing protein remains two million years old was made possible by stretching to its limits the technology at the base of proteomic discovery: mass spectrometry. State of the art mass spectrometers and the top palaeoproteomics expertise needed to get the best out of such sophisticated instrumentation are key resources deriving from the decade-long strategic collaboration with Jesper Velgaard Olsen, Professor at Novo Nordisk Foundation Center for Protein Research and co-author on this study.

The mystery of Gigantopithecus

The fossil evidence attributed to Gigantopithecus was initially discovered in southern China in 1935, and it is currently limited to just a few lower jaws and lots of teeth. No complete skull and no other bone from the rest of the skeleton has been found so far. As a result, there has been a lot of speculation about the physical appearance of this mysterious animal.

'Previous attempts to understand which could be the living organism most similar to Gigantopithecus could only be based on the comparison of the shape of the fossils with skeletal reference material from living great apes. Ancient DNA analysis was not an option, because Gigantopithecus went extinct approximately 300,000 years ago, and in the geographic area Gigantopithecus occupied no DNA older than approximately 10,000 years has been retrieved so far. Accordingly, we decided to sequence dental enamel proteins to reconstruct its evolutionary relation with living great apes, and we found that orangutan is Gigantopithecus' closest living relative', says Enrico Cappellini.

The study of human evolution by palaeoproteomics will continue in the next years through the recently established "Palaeoproteomics to Unleash Studies on Human History (PUSHH)" Marie Sk?odowska Curie European Training Network (ETN) Programme.

The research is funded mainly by VILLUM FONDEN, the Novo Nordisk Foundation, and the Marie Sklowowska-Curie Actions Individual Fellowship and International Training Network programmes.

---

Story Source:

Materials provided by University of Copenhagen The Faculty of Health and Medical Sciences. Note: Content may be edited for style and length.