Neuroscience

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Posts tagged obesity

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Smoking may dull obese women’s ability to taste fat and sugar

Cigarette smoking among obese women appears to interfere with their ability to taste fats and sweets, a new study shows. Despite craving high-fat, sugary foods, these women were less likely than others to perceive these tastes, which may drive them to consume more calories.

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M. Yanina Pepino, PhD, assistant professor of medicine at Washington University School of Medicine in St. Louis, and Julie Mennella, PhD, a biopsychologist at the Monell Center in Philadelphia, where the research was conducted, studied four groups of women ages 21 to 41: obese smokers, obese nonsmokers, smokers of normal weight and nonsmokers of normal weight. The women tasted several vanilla puddings containing varying amounts of fat and were asked to rate them for sweetness and creaminess, a measure of fat content.

“Compared with the other three groups, smokers who were obese perceived less creaminess and sweetness,” Pepino said. “They also derived less pleasure from tasting the puddings.”

The findings are published in the April issue of the journal Obesity.

Pepino cautioned that the study only identified associations between smoking and taste rather than definitive reasons why obese smokers were less likely to detect fat and sweetness. But the findings imply that the ability to perceive fat and sweetness — and to derive pleasure from food — is compromised in female smokers who are obese, which could contribute to the consumption of more calories.

“Obese people often crave high-fat foods,” she said. “Our findings suggest that having this intense craving but not perceiving fat and sweetness in food may lead these women to eat more. Since smoking and obesity are risk factors for cardiovascular and metabolic diseases, the additional burden of craving more fats and sugars, while not fully tasting them, could be detrimental to health.”

Interestingly, it was the combination of smoking and obesity that created something of a “double-whammy” because smokers who were not overweight could perceive fat and sweetness that was similar to women who did not smoke.

Previous studies have linked smoking to increased food cravings and greater consumption of fat, regardless of whether a smoker is obese. Studies also have found that smokers tend to have increased waist-to-hip ratios. That is, they tend to be shaped more like apples than pears, another risk factor for heart disease and metabolic problems.

The findings contribute to a growing body of knowledge that challenges the lingering perception that smoking helps a person maintain a healthy weight.

“Women are much more likely than men to take up smoking as an aid to weight control,” Pepino said. “But there is no good evidence showing that it helps maintain a healthy weight over the long term. And in the case of obese women who smoke, it appears the smoking may make things even worse than previously thought.”

(Source: news.wustl.edu)

Filed under smoking obesity taste perception flavor perception health

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Study finds link between child’s obesity and cognitive function

A new University of Illinois study finds that obese children are slower than healthy-weight children to recognize when they have made an error and correct it. The research is the first to show that weight status not only affects how quickly children react to stimuli but also impacts the level of activity that occurs in the cerebral cortex during action monitoring.

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“I like to explain action monitoring this way: when you’re typing, you don’t have to be looking at your keyboard or your screen to realize that you’ve made a keystroke error. That’s because action monitoring is occurring in your brain’s prefrontal cortex,” said Charles Hillman, a U of I professor of kinesiology and faculty member in the U of I’s Division of Nutritional Sciences.

As an executive control task that requires organizing, planning, and inhibiting, action monitoring requires people to be computational and conscious at all times as they process their behavior. Because these higher-order cognitive processes are needed for success in mathematics and reading, they are linked with success in school and positive life outcomes, he said.

“Imagine a child in a math class constantly checking to make sure she’s carrying the digit over when she’s adding. That’s an example,” he added.

In the study, the scientists measured the behavioral and neuroelectric responses of 74 preadolescent children, half of them obese, half at a healthy weight. Children were fitted with caps that recorded electroencephalographic activity and asked to participate in a task that presented left- or right-facing fish, predictably facing in either the same or the opposite direction. Children were asked to press a button based on the direction of the middle (that is, target) fish. The flanking fish either pointed in the same direction (facilitating) or in the opposite direction (hindering) their ability to respond successfully.

“We found that obese children were considerably slower to respond to stimuli when they were involved in this activity,” Hillman said.

The researchers also found that healthy-weight children were better at evaluating their need to change their behavior in order to avoid future errors.

“The healthy-weight kids were more accurate following an error than the obese children were, and when the task required greater amounts of executive control, the difference was even greater,” he reported.

A second evaluation measured electrical activity in the brain “that occurs at the intersection of thought and action,” Hillman said. “We can measure what we call error-related negativity (ERN) in the electrical pattern that the brain generates following errors. When children made an error, we could see a larger negative response. And we found that healthy-weight children are better able to upregulate the neuroelectric processes that underlie error evaluation.”

Scientists in the Hillman lab and elsewhere have seen a connection between healthy weight and academic achievement, “but a study like this helps us understand what’s happening. There are certainly physiological differences in the brain activity of obese and healthy-weight children. It’s exciting to be able to use functional brain imaging to see the way children’s weight affects the aspects of cognition that influence and underlie achievement,” said postdoctoral researcher and co-author Naiman Khan.

(Source: news.aces.illinois.edu)

Filed under cingulate cortex obesity prefrontal cortex cognitive function psychology neuroscience science

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Understanding Binge Eating and Obesity Researchers at the University of Cambridge have developed a novel method for evaluating the treatment of obesity-related food behavior. In an effort to further scientific understanding of the underlying problem, they have published the first peer-reviewed video of their technique in JoVE, the Journal of Visualized Experiments. In the video, the authors demonstrate their means of objectively studying the drivers and mechanisms of overconsumption in humans. To do this, they assesses their subject’s willingness to work or pay for food, and they simultaneously track the corresponding brain activity using an MRI scanner. “We present alternative ways of exploring attitudes to food by using indirect, objective measures—such as measuring the amount of energy exerted to obtain or view different foods, as well as determining brain responses during the anticipation and consumption of desirable foods,” said the lab’s principal investigator, Dr. Paul Fletcher. He and his colleagues use participant hand-grip intensity (referred to as “grip force” in the video) to calculate the motivation for a given food reward. According to Dr. Fletcher, typical approaches for evaluating anti-obesity type drugs rely on more subjective methods—like having test subjects self-report their ratings of hunger and cravings.   “When a person is asked how much they subjectively desire a food, they may feel pressured to give a ‘correct’ rather than a true answer,” said Dr. Fletcher, “[Our] grip force task may, under certain circumstances, present a more accurate reflection of what they really want.” Dr. Fletcher and his colleagues brought the technique to JoVE after using it in their earlier publication, “Food images engage subliminal motivation to seek food,” published in 2011. They decided to publish a video capturing the protocol “Because it offered the opportunity to demonstrate the methods more fully,” he said. In the video, Dr. Fletcher expands on the purpose of publishing the method with JoVE. “Individuals new to the technique may struggle because there aren’t many examples of grip-force tasks published in the literature, and there are no full and clear descriptions of how to design and set up the tasks,” he said. With rising concerns surrounding obesity, researchers can use the technique presented in the JoVE video to determine the efficacy of a potential emerging market in anti-obesity medicine.

Understanding Binge Eating and Obesity

Researchers at the University of Cambridge have developed a novel method for evaluating the treatment of obesity-related food behavior. In an effort to further scientific understanding of the underlying problem, they have published the first peer-reviewed video of their technique in JoVE, the Journal of Visualized Experiments.

In the video, the authors demonstrate their means of objectively studying the drivers and mechanisms of overconsumption in humans. To do this, they assesses their subject’s willingness to work or pay for food, and they simultaneously track the corresponding brain activity using an MRI scanner.

“We present alternative ways of exploring attitudes to food by using indirect, objective measures—such as measuring the amount of energy exerted to obtain or view different foods, as well as determining brain responses during the anticipation and consumption of desirable foods,” said the lab’s principal investigator, Dr. Paul Fletcher. He and his colleagues use participant hand-grip intensity (referred to as “grip force” in the video) to calculate the motivation for a given food reward.

According to Dr. Fletcher, typical approaches for evaluating anti-obesity type drugs rely on more subjective methods—like having test subjects self-report their ratings of hunger and cravings.  

“When a person is asked how much they subjectively desire a food, they may feel pressured to give a ‘correct’ rather than a true answer,” said Dr. Fletcher, “[Our] grip force task may, under certain circumstances, present a more accurate reflection of what they really want.”

Dr. Fletcher and his colleagues brought the technique to JoVE after using it in their earlier publication, “Food images engage subliminal motivation to seek food,” published in 2011. They decided to publish a video capturing the protocol “Because it offered the opportunity to demonstrate the methods more fully,” he said.

In the video, Dr. Fletcher expands on the purpose of publishing the method with JoVE. “Individuals new to the technique may struggle because there aren’t many examples of grip-force tasks published in the literature, and there are no full and clear descriptions of how to design and set up the tasks,” he said.

With rising concerns surrounding obesity, researchers can use the technique presented in the JoVE video to determine the efficacy of a potential emerging market in anti-obesity medicine.

Filed under binge eating obesity motivation reward processing food reward decision making psychology neuroscience science

163 notes

New contender for ‘fat gene’ found Researchers may have been focusing on the wrong gene. Scientists studying what they thought was a ‘fat gene’ seem to have been looking in the wrong place, according to research published today in Nature. It suggests instead that the real culprit is another gene that the suspected obesity gene interacts with. In 2007, several genome studies identified mutations in a gene called FTO that were strongly associated with an increased risk of obesity and type 2 diabetes in humans. Subsequent studies in mice showed a link between the gene and body mass. So researchers, including Marcelo Nóbrega, a geneticist at the University of Chicago, thought that they had found a promising candidate for a gene that helped cause obesity. The mutations were located in non-coding portions of FTO involved in regulating gene expression. But when Nóbrega looked closer, he found that something was amiss. These regulatory regions contained some elements that are specific for the lungs, one of the few tissues in which FTO is not expressed. “This made us pause,” he says. “Why are there regulatory elements that presumably regulate FTO in the tissue where it isn’t expressed?” This was not the first red flag. Previous attempts to find a link between the presence of the obesity-associated mutations and the expression levels of FTO had been a “miserable failure”, he says. When Nóbrega presented his new results at meetings, he adds that many people came to him to say ‘I just knew there was something wrong here’. So Nóbrega’s team cast the net wider, looking for genes in the broader neighbourhood of FTO whose expression matched that of the mutations, and found IRX3, a gene about half a million base pairs away. IRX3 encodes a transcription factor — a type of protein involved in regulating the expression of other genes — and is highly expressed in the brain, consistent with a role in regulating energy metabolism and eating behaviour. When they examined the looping three-dimensional structure of the chromosome on which both genes sit in mice, zebrafish and human cells, they found that the obesity-associated regions in FTO were physically in contact with the promoter (the initial gene sequence which acts as an on/off switch) of IRX3. So the switches that turn on IRX3 are actually located far away from IRX3 itself, inside another gene. “We think of the genome as a linear thing, but it’s really a complex 3D structure that coils back onto itself,” he says. Distant genes IRX3 also appeared to be strongly linked with obesity. People with one of the obesity-associated mutations showed higher expression of IRX3, but not FTO, in brain tissue samples, the team found. Nóbrega and his colleagues also found that mice lacking the gene weighed 25–30% less than mice with a functional IRX3 gene; did not gain weight on a high-fat diet; were resistant to metabolic disorders such as diabetes and had more of the energy-burning cells known as brown fat. The same results were seen in mice in which the expression of IRX3 was blocked in the hypothalamus, a brain region known to regulate feeding behaviour and energy balance. Inês Barroso, a geneticist at the Wellcome Trust Sanger Institute in Hinxton, UK, says that the work answers some of the questions around the biology of the link found in the genome-wide association studies (GWAS). “That’s always the tricky thing; a GWAS gives you an association, but it’s just a marker on the genome, it doesn’t actually say anything about which gene it’s affecting,” she says. “This strongly suggests that mediation of body mass is going to be through IRX3 rather than FTO.” Nóbrega thinks geneticists should keep in mind this example of unexpected interactions between distant genes when dealing with genetic association studies. “There may be many other cases where people are studying the wrong gene,” he says. “We might be chasing ghosts.”

New contender for ‘fat gene’ found

Researchers may have been focusing on the wrong gene.

Scientists studying what they thought was a ‘fat gene’ seem to have been looking in the wrong place, according to research published today in Nature. It suggests instead that the real culprit is another gene that the suspected obesity gene interacts with.

In 2007, several genome studies identified mutations in a gene called FTO that were strongly associated with an increased risk of obesity and type 2 diabetes in humans. Subsequent studies in mice showed a link between the gene and body mass. So researchers, including Marcelo Nóbrega, a geneticist at the University of Chicago, thought that they had found a promising candidate for a gene that helped cause obesity.

The mutations were located in non-coding portions of FTO involved in regulating gene expression. But when Nóbrega looked closer, he found that something was amiss. These regulatory regions contained some elements that are specific for the lungs, one of the few tissues in which FTO is not expressed. “This made us pause,” he says. “Why are there regulatory elements that presumably regulate FTO in the tissue where it isn’t expressed?”

This was not the first red flag. Previous attempts to find a link between the presence of the obesity-associated mutations and the expression levels of FTO had been a “miserable failure”, he says. When Nóbrega presented his new results at meetings, he adds that many people came to him to say ‘I just knew there was something wrong here’.

So Nóbrega’s team cast the net wider, looking for genes in the broader neighbourhood of FTO whose expression matched that of the mutations, and found IRX3, a gene about half a million base pairs away. IRX3 encodes a transcription factor — a type of protein involved in regulating the expression of other genes — and is highly expressed in the brain, consistent with a role in regulating energy metabolism and eating behaviour.

When they examined the looping three-dimensional structure of the chromosome on which both genes sit in mice, zebrafish and human cells, they found that the obesity-associated regions in FTO were physically in contact with the promoter (the initial gene sequence which acts as an on/off switch) of IRX3. So the switches that turn on IRX3 are actually located far away from IRX3 itself, inside another gene. “We think of the genome as a linear thing, but it’s really a complex 3D structure that coils back onto itself,” he says.

Distant genes

IRX3 also appeared to be strongly linked with obesity. People with one of the obesity-associated mutations showed higher expression of IRX3, but not FTO, in brain tissue samples, the team found. Nóbrega and his colleagues also found that mice lacking the gene weighed 25–30% less than mice with a functional IRX3 gene; did not gain weight on a high-fat diet; were resistant to metabolic disorders such as diabetes and had more of the energy-burning cells known as brown fat. The same results were seen in mice in which the expression of IRX3 was blocked in the hypothalamus, a brain region known to regulate feeding behaviour and energy balance.

Inês Barroso, a geneticist at the Wellcome Trust Sanger Institute in Hinxton, UK, says that the work answers some of the questions around the biology of the link found in the genome-wide association studies (GWAS). “That’s always the tricky thing; a GWAS gives you an association, but it’s just a marker on the genome, it doesn’t actually say anything about which gene it’s affecting,” she says. “This strongly suggests that mediation of body mass is going to be through IRX3 rather than FTO.”

Nóbrega thinks geneticists should keep in mind this example of unexpected interactions between distant genes when dealing with genetic association studies. “There may be many other cases where people are studying the wrong gene,” he says. “We might be chasing ghosts.”

Filed under obesity fat gene FTO gene expression IRX3 GWAS genomics science

149 notes

Neuroscience Study Uncovers New Player in Obesity A new neuroscience study sheds light on the biological underpinnings of obesity. The in vivo study, published in the January 8 issue of The Journal of Neuroscience, reveals how a protein in the brain helps regulate food intake and body weight. The findings reveal a potential new avenue for the treatment of obesity and may help explain why medications that are prescribed for epilepsy and other conditions that interfere with this protein, such as gabapentin and pregabalin, can cause weight gain. The protein – alpha2/delta-1 – has not been linked previously to obesity. A team led by Maribel Rios, Ph.D., associate professor in the department of neuroscience at Tufts University School of Medicine, discovered that alpha2/delta-1 facilitates the function of another protein called brain-derived neurotrophic factor (BDNF). A previous study by Rios determined that BDNF plays a critical role in appetite suppression, while the current study identifies a central mechanism mediating the inhibitory effects of BDNF on overeating. “We know that low levels of the BDNF protein in the brain lead to overeating and dramatic obesity in mice. Deficiencies in BDNF have also been linked to obesity in humans. Now, we have discovered that the alpha2/delta-1 protein is necessary for normal BDNF function, giving us a potential new target for novel obesity treatments,” said Rios, also a member of the cellular and molecular physiology and neuroscience program faculties at the Sackler School of Graduate Biomedical Sciences at Tufts. Rios and colleagues discovered that low levels of BDNF were associated with decreased function of alpha2/delta-1 in the hypothalamus, a brain region that is critical to the regulation of food intake and weight. When the team inhibited the alpha2/delta-1 protein in normal mice, mice ate significantly more food and gained weight. Conversely, when the team corrected the alpha 2/delta-1 deficiency in mice with reduced BDNF levels, overeating and weight gain were mitigated. In addition, blood sugar levels (related to diabetes in humans) were normalized. “We blocked activity of the alpha2/delta-1 protein in mice using gabapentin. These mice ate 39 percent more food, and as a consequence gained substantially more weight than control mice over a seven-day period,” said first author Joshua Cordeira, Ph.D., a graduate of the neuroscience program at the Sackler School and member of Rios’s lab. This study is related to his Ph.D. thesis. “When we re-introduced alpha2/delta-1 in obese mice lacking BDNF in the brain, we saw a 15-20 percent reduction in food intake and a significant reduction in weight gain. Importantly, metabolic disturbances associated with obesity, including hyperglycemia and deficient glucose metabolism, were greatly reduced by restoring the function of alpha2/delta-1,” added Rios. Some individuals who take gabapentin and pregabalin report weight gain. Both gabapentin and pregabalin are anticonvulsants, also used to treat nerve pain from, for example, shingles or diabetes. The findings from the Rios lab suggest that these drugs might contribute to weight gain by interfering with alpha2/delta-1 in the hypothalamus. This new understanding of alpha2/delta-1’s role in appetite may allow researchers to develop complementary treatments that can prevent weight gain for patients taking these medications. “We now know that alpha2/delta-1 plays a critical role in healthy BDNF function. The finding improves our understanding of the intricate neuroscience involved in appetite control. The next phase of our research will be to unravel the mechanisms mediating the satiety effects of alpha2/delta-1 in the hypothalamus,” said Rios. This latest finding builds on Rios’s previous studies of BDNF and its role in regulating body weight. Earlier work by Rios established BDNF as an essential component of the neural circuits governing body weight in adult mice. Rios also determined that BDNF expression in two regions of the brain is required to suppress appetite.

Neuroscience Study Uncovers New Player in Obesity

A new neuroscience study sheds light on the biological underpinnings of obesity. The in vivo study, published in the January 8 issue of The Journal of Neuroscience, reveals how a protein in the brain helps regulate food intake and body weight. The findings reveal a potential new avenue for the treatment of obesity and may help explain why medications that are prescribed for epilepsy and other conditions that interfere with this protein, such as gabapentin and pregabalin, can cause weight gain.

The protein – alpha2/delta-1 – has not been linked previously to obesity. A team led by Maribel Rios, Ph.D., associate professor in the department of neuroscience at Tufts University School of Medicine, discovered that alpha2/delta-1 facilitates the function of another protein called brain-derived neurotrophic factor (BDNF). A previous study by Rios determined that BDNF plays a critical role in appetite suppression, while the current study identifies a central mechanism mediating the inhibitory effects of BDNF on overeating.

“We know that low levels of the BDNF protein in the brain lead to overeating and dramatic obesity in mice. Deficiencies in BDNF have also been linked to obesity in humans. Now, we have discovered that the alpha2/delta-1 protein is necessary for normal BDNF function, giving us a potential new target for novel obesity treatments,” said Rios, also a member of the cellular and molecular physiology and neuroscience program faculties at the Sackler School of Graduate Biomedical Sciences at Tufts.

Rios and colleagues discovered that low levels of BDNF were associated with decreased function of alpha2/delta-1 in the hypothalamus, a brain region that is critical to the regulation of food intake and weight. When the team inhibited the alpha2/delta-1 protein in normal mice, mice ate significantly more food and gained weight. Conversely, when the team corrected the alpha 2/delta-1 deficiency in mice with reduced BDNF levels, overeating and weight gain were mitigated. In addition, blood sugar levels (related to diabetes in humans) were normalized.

“We blocked activity of the alpha2/delta-1 protein in mice using gabapentin. These mice ate 39 percent more food, and as a consequence gained substantially more weight than control mice over a seven-day period,” said first author Joshua Cordeira, Ph.D., a graduate of the neuroscience program at the Sackler School and member of Rios’s lab. This study is related to his Ph.D. thesis.

“When we re-introduced alpha2/delta-1 in obese mice lacking BDNF in the brain, we saw a 15-20 percent reduction in food intake and a significant reduction in weight gain. Importantly, metabolic disturbances associated with obesity, including hyperglycemia and deficient glucose metabolism, were greatly reduced by restoring the function of alpha2/delta-1,” added Rios.

Some individuals who take gabapentin and pregabalin report weight gain. Both gabapentin and pregabalin are anticonvulsants, also used to treat nerve pain from, for example, shingles or diabetes. The findings from the Rios lab suggest that these drugs might contribute to weight gain by interfering with alpha2/delta-1 in the hypothalamus. This new understanding of alpha2/delta-1’s role in appetite may allow researchers to develop complementary treatments that can prevent weight gain for patients taking these medications.

“We now know that alpha2/delta-1 plays a critical role in healthy BDNF function. The finding improves our understanding of the intricate neuroscience involved in appetite control. The next phase of our research will be to unravel the mechanisms mediating the satiety effects of alpha2/delta-1 in the hypothalamus,” said Rios.

This latest finding builds on Rios’s previous studies of BDNF and its role in regulating body weight. Earlier work by Rios established BDNF as an essential component of the neural circuits governing body weight in adult mice. Rios also determined that BDNF expression in two regions of the brain is required to suppress appetite.

Filed under obesity brain-derived neurotrophic factor hypothalamus appetite gabapentin pregabalin neuroscience science

104 notes

Obesity ballooning in developing world: report The number of obese and overweight people in the developing world nearly quadrupled to almost a billion between 1980 and 2008, a think-tank report said on Friday. There are now far more obese or overweight adults in the developing world than in richer countries, the Overseas Development Institute (ODI) said. The London-based institute said more than a third of all adults around the world — 1.46 billion people — were obese or overweight. Between 1980 and 2008, the numbers of people affected in the developing world rose from 250 million to 904 million. In the developed world, the figure rose from 321 million to 557 million. This represented a rise from 23 percent to 34 percent of the world population. "The growing rates of overweight and obesity in developing countries are alarming," said ODI research fellow Steve Wiggins, who co-authored the Future Diets report. "On current trends, globally, we will see a huge increase in the number of people suffering certain types of cancer, diabetes, strokes and heart attacks, putting an enormous burden on public healthcare systems." The report said overweight and obesity rates have almost doubled in China and Mexico since 1980, and risen by a third in South Africa. The study said the rise in obesity was down to diets changing in developing countries where incomes were rising, with people shifting away from cereals and tubers to eating more meat, fats and sugar. The over-consumption of food, coupled with increasingly sedentary lives, was also to blame. The report found that North Africa, the Middle East and South America saw overweight and obesity rates increase to a level similar to Europe, around 58 percent. At 70 percent, North America still has the highest percentage of overweight adults. The report said there seemed to be little will among the public and leaders to take action on influencing diet in the future. "Governments have focused on public awareness campaigns, but evidence shows this is not enough," said Wiggins. "The lack of action stands in stark contrast to the concerted public actions taken to limit smoking in developed countries. "Politicians need to be less shy about trying to influence what food ends up on our plates. The challenge is to make healthy diets viable whilst reducing the appeal of foods which carry a less certain nutritional value." The report gave the example of South Korea as having made efforts to preserve healthy elements of the country’s traditional diet, via public campaigns and education, providing large-scale training for women in preparing healthy, traditional food. The report said it was “only a matter of time” before people would begin to accept and even demand stronger and more effective measures to influence diets.

Obesity ballooning in developing world: report

The number of obese and overweight people in the developing world nearly quadrupled to almost a billion between 1980 and 2008, a think-tank report said on Friday.

There are now far more obese or overweight adults in the developing world than in richer countries, the Overseas Development Institute (ODI) said.

The London-based institute said more than a third of all adults around the world — 1.46 billion people — were obese or overweight.

Between 1980 and 2008, the numbers of people affected in the developing world rose from 250 million to 904 million. In the developed world, the figure rose from 321 million to 557 million.

This represented a rise from 23 percent to 34 percent of the world population.

"The growing rates of overweight and obesity in developing countries are alarming," said ODI research fellow Steve Wiggins, who co-authored the Future Diets report.

"On current trends, globally, we will see a huge increase in the number of people suffering certain types of cancer, diabetes, strokes and heart attacks, putting an enormous burden on public healthcare systems."

The report said overweight and obesity rates have almost doubled in China and Mexico since 1980, and risen by a third in South Africa.

The study said the rise in obesity was down to diets changing in developing countries where incomes were rising, with people shifting away from cereals and tubers to eating more meat, fats and sugar.

The over-consumption of food, coupled with increasingly sedentary lives, was also to blame.

The report found that North Africa, the Middle East and South America saw overweight and obesity rates increase to a level similar to Europe, around 58 percent.

At 70 percent, North America still has the highest percentage of overweight adults.

The report said there seemed to be little will among the public and leaders to take action on influencing diet in the future.

"Governments have focused on public awareness campaigns, but evidence shows this is not enough," said Wiggins.

"The lack of action stands in stark contrast to the concerted public actions taken to limit smoking in developed countries.

"Politicians need to be less shy about trying to influence what food ends up on our plates. The challenge is to make healthy diets viable whilst reducing the appeal of foods which carry a less certain nutritional value."

The report gave the example of South Korea as having made efforts to preserve healthy elements of the country’s traditional diet, via public campaigns and education, providing large-scale training for women in preparing healthy, traditional food.

The report said it was “only a matter of time” before people would begin to accept and even demand stronger and more effective measures to influence diets.

Filed under obesity health nutrition diet medicine science

111 notes

Does obesity reshape our sense of taste? Obesity may alter the way we taste at the most fundamental level: by changing how our tongues react to different foods. In a Nov. 13 study in the journal PLOS ONE, University at Buffalo biologists report that being severely overweight impaired the ability of mice to detect sweets. Compared with slimmer counterparts, the plump mice had fewer taste cells that responded to sweet stimuli. What’s more, the cells that did respond to sweetness reacted relatively weakly. The findings peel back a new layer of the mystery of how obesity alters our relationship to food. “Studies have shown that obesity can lead to alterations in the brain, as well as the nerves that control the peripheral taste system, but no one had ever looked at the cells on the tongue that make contact with food,” said lead scientist Kathryn Medler, PhD, UB associate professor of biological sciences. “What we see is that even at this level — at the first step in the taste pathway — the taste receptor cells themselves are affected by obesity,” Medler said. “The obese mice have fewer taste cells that respond to sweet stimuli, and they don’t respond as well.” The research matters because taste plays an important role in regulating appetite: what we eat, and how much we consume. How an inability to detect sweetness might encourage weight gain is unclear, but past research has shown that obese people yearn for sweet and savory foods though they may not taste these flavors as well as thinner people. Medler said it’s possible that trouble detecting sweetness may lead obese mice to eat more than their leaner counterparts to get the same payoff. Learning more about the connection between taste, appetite and obesity is important, she said, because it could lead to new methods for encouraging healthy eating. “If we understand how these taste cells are affected and how we can get these cells back to normal, it could lead to new treatments,” Medler said. “These cells are out on your tongue and are more accessible than cells in other parts of your body, like your brain.” The new PLOS ONE study compared 25 normal mice to 25 of their littermates who were fed a high-fat diet and became obese. To measure the animals’ response to different tastes, the research team looked at a process called calcium signaling. When cells “recognize” a certain taste, there is a temporary increase in the calcium levels inside the cells, and the scientists measured this change. The results: Taste cells from the obese mice responded more weakly not only to sweetness but, surprisingly, to bitterness as well. Taste cells from both groups of animals reacted similarly to umami, a flavor associated with savory and meaty foods.

Does obesity reshape our sense of taste?

Obesity may alter the way we taste at the most fundamental level: by changing how our tongues react to different foods.

In a Nov. 13 study in the journal PLOS ONE, University at Buffalo biologists report that being severely overweight impaired the ability of mice to detect sweets.

Compared with slimmer counterparts, the plump mice had fewer taste cells that responded to sweet stimuli. What’s more, the cells that did respond to sweetness reacted relatively weakly.

The findings peel back a new layer of the mystery of how obesity alters our relationship to food.

“Studies have shown that obesity can lead to alterations in the brain, as well as the nerves that control the peripheral taste system, but no one had ever looked at the cells on the tongue that make contact with food,” said lead scientist Kathryn Medler, PhD, UB associate professor of biological sciences.

“What we see is that even at this level — at the first step in the taste pathway — the taste receptor cells themselves are affected by obesity,” Medler said. “The obese mice have fewer taste cells that respond to sweet stimuli, and they don’t respond as well.”

The research matters because taste plays an important role in regulating appetite: what we eat, and how much we consume.

How an inability to detect sweetness might encourage weight gain is unclear, but past research has shown that obese people yearn for sweet and savory foods though they may not taste these flavors as well as thinner people.

Medler said it’s possible that trouble detecting sweetness may lead obese mice to eat more than their leaner counterparts to get the same payoff.

Learning more about the connection between taste, appetite and obesity is important, she said, because it could lead to new methods for encouraging healthy eating.

“If we understand how these taste cells are affected and how we can get these cells back to normal, it could lead to new treatments,” Medler said. “These cells are out on your tongue and are more accessible than cells in other parts of your body, like your brain.”

The new PLOS ONE study compared 25 normal mice to 25 of their littermates who were fed a high-fat diet and became obese.

To measure the animals’ response to different tastes, the research team looked at a process called calcium signaling. When cells “recognize” a certain taste, there is a temporary increase in the calcium levels inside the cells, and the scientists measured this change.

The results: Taste cells from the obese mice responded more weakly not only to sweetness but, surprisingly, to bitterness as well. Taste cells from both groups of animals reacted similarly to umami, a flavor associated with savory and meaty foods.

Filed under obesity taste receptor cells taste appetite calcium signaling neuroscience science

111 notes

Drowsy Drosophila shed light on sleep and hunger

Scientists discover key function in molecule that regulates sleep, metabolism and hunger

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Why does hunger keep us awake and a full belly make us tired? Why do people with sleep disorders such as insomnia often binge eat late at night? What can sleep patterns tell us about obesity?

Sleep, hunger and metabolism are closely related, but scientists are still struggling to understand how they interact. Now, Brandeis University researchers have discovered a function in a molecule in fruit flies that may provide insight into the complicated relationship between sleep and food.

In the October issue of the journal Neuron, Brandeis scientists report that sNPF, a neuropeptide long known to regulate food intake and metabolism, is also an important component in regulating and promoting sleep. When researchers activated sNPF in fruit flies, the insects fell asleep almost immediately, awaking only long enough to eat before nodding off again. The flies were so sleepy that once they found a food source, they slept right on top of it for days — like falling asleep on a giant hamburger bun and waking up long enough to take a few nibbles before falling back to sleep.

When researchers returned sNPF functions to normal, the flies resumed their normal level of activity, leaving behind their couch potato ways.

The researchers, led by professor of biology Leslie Griffith, concluded that sNPF has an important regulatory function in sleep in addition to its previously known function coordinating behaviors such as eating and metabolism.

"This paper provides a nice bridge between feeding behavior and sleep behavior with just a single molecule," says Nathan Donelson, a post doctoral fellow in Griffith’s lab and one of the study’s lead authors.

Neurons use neuropeptides to communicate a range of brain functions including learning, metabolism, memory and social behaviors. In humans, Neuropeptide Y functions similarly to sNPF and has been studied as a possible drug target for obesity treatment.

But scientists don’t fully understand how regulating neuropeptide function at specific times and in specific cells affects sleeping and eating. By studying sNPF in fruit flies, scientists can learn which cells, neurotransmitters and genes are involved in eating and sleeping; what processes turn on and inhibit the behaviors, and how sleep cells are relevant to hunger drive.

"Our paper makes a significant step into tying all these things together," says Donelson, "and that is extremely important down the road to our understanding of human health."

(Source: eurekalert.org)

Filed under hunger metabolism learning neuropeptide obesity sleep memory fruit flies neuroscience science

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Scientists identify brain circuitry that triggers overeating The finding shows that certain parts of brain cells could play a critical role in anorexia, bulimia, binge eating disorder, and obesity. Sixty years ago scientists could electrically stimulate a region of a mouse’s brain causing the mouse to eat, whether hungry or not. Now researchers from UNC School of Medicine have pinpointed the precise cellular connections responsible for triggering that behavior. The finding, published September 27 in the journal Science, lends insight into a cause for obesity and could lead to treatments for anorexia, bulimia nervosa, and binge eating disorder, the most prevalent eating disorder in the United States. “The study underscores that obesity and other eating disorders have a neurological basis,” said senior study author Garret Stuber, PhD, assistant professor in the department of psychiatry and department of cell biology and physiology. He’s also a member of the UNC Neuroscience Center. “With further study, we could figure out how to regulate the activity of cells in a specific region of the brain and develop treatments.” Cynthia Bulik, PhD, Distinguished Professor of Eating Disorders at UNC School of Medicine and the Gillings School of Global Public Health, said, “Stuber’s work drills down to the precise biological mechanisms that drive binge eating and will lead us away from stigmatizing explanations that invoke blame and a lack of willpower.” Bulik was not part of the research team. Back in the 1950s, when scientists electrically stimulated a region of the brain called the lateral hypothalamus, they knew that they were stimulating many different types of brain cells. Stuber wanted to focus on one cell type — gaba neurons in the bed nucleus of the stria terminalis, or BNST. The BNST is an outcropping of the amygdala, the part of the brain associated with emotion. The BNST also forms a bridge between the amygdala and the lateral hypothalamus, the brain region that drives primal functions such as eating, sexual behavior, and aggression. The BNST gaba neurons have a cell body and a long strand with branched synapses that transmit electrical signals into the lateral hypothalamus. Stuber and his team wanted to stimulate those synapses by using an optogenetic technique, an involved process that would let him stimulate BNST cells simply by shining light on their synapses. Typically, brain cells don’t respond to light. So Stuber’s team used genetically engineered proteins — from algae — that are sensitive to light and used genetically engineered viruses to deliver them into the brains of mice. Those proteins then get expressed only in the BNST cells, including in the synapses that connect to the hypothalamus. His team then implanted fiber optic cables in the brains of these specially-bred mice, and this allowed the researchers to shine light through the cables and onto BNST synapses. As soon as the light hit BNST synapses the mice began to eat voraciously even though they had already been well fed. Moreover, the mice showed a strong preference for high-fat foods. “They would essentially eat up to half their daily caloric intake in about 20 minutes,” Stuber said. “This suggests that this BNST pathway could play a role in food consumption and pathological conditions such as binge eating.” Stimulating the BNST also led the mice to exhibit behaviors associated with reward, suggesting that shining light on BNST cells enhanced the pleasure of eating. On the flip side, shutting down the BNST pathway caused mice to show little interest in eating, even if they had been deprived of food.  “We were able to really home in on the precise neural circuit connection that was causing this phenomenon that’s been observed for more than 50 years,” Stuber said. The study, which uses technologies highlighted in the new National Institutes of Health Brain Initiative, suggests that faulty wiring in BNST cells could interfere with hunger or satiety cues and contribute to human eating disorders, leading people to eat even when they are full or to avoid food when they are hungry. Further research is needed to determine whether it would be possible to develop drugs that correct a malfunctioning BNST circuit. “We want to actually observe the normal function of these cell types and how they fire electrical signals when the animals are feeding or hungry,” Stuber said. “We want to understand their genetic characteristics – what genes are expressed. For example, if we find cells that become really activated after binge eating, can we look at the gene expression profile to find out what makes those cells unique from other neurons.” And that, Stuber said, could lead to potential targets for drugs to treat certain populations of patients with eating disorders.

Scientists identify brain circuitry that triggers overeating

The finding shows that certain parts of brain cells could play a critical role in anorexia, bulimia, binge eating disorder, and obesity.

Sixty years ago scientists could electrically stimulate a region of a mouse’s brain causing the mouse to eat, whether hungry or not. Now researchers from UNC School of Medicine have pinpointed the precise cellular connections responsible for triggering that behavior. The finding, published September 27 in the journal Science, lends insight into a cause for obesity and could lead to treatments for anorexia, bulimia nervosa, and binge eating disorder, the most prevalent eating disorder in the United States.

“The study underscores that obesity and other eating disorders have a neurological basis,” said senior study author Garret Stuber, PhD, assistant professor in the department of psychiatry and department of cell biology and physiology. He’s also a member of the UNC Neuroscience Center. “With further study, we could figure out how to regulate the activity of cells in a specific region of the brain and develop treatments.”

Cynthia Bulik, PhD, Distinguished Professor of Eating Disorders at UNC School of Medicine and the Gillings School of Global Public Health, said, “Stuber’s work drills down to the precise biological mechanisms that drive binge eating and will lead us away from stigmatizing explanations that invoke blame and a lack of willpower.” Bulik was not part of the research team.

Back in the 1950s, when scientists electrically stimulated a region of the brain called the lateral hypothalamus, they knew that they were stimulating many different types of brain cells. Stuber wanted to focus on one cell type — gaba neurons in the bed nucleus of the stria terminalis, or BNST. The BNST is an outcropping of the amygdala, the part of the brain associated with emotion. The BNST also forms a bridge between the amygdala and the lateral hypothalamus, the brain region that drives primal functions such as eating, sexual behavior, and aggression.

The BNST gaba neurons have a cell body and a long strand with branched synapses that transmit electrical signals into the lateral hypothalamus. Stuber and his team wanted to stimulate those synapses by using an optogenetic technique, an involved process that would let him stimulate BNST cells simply by shining light on their synapses.

Typically, brain cells don’t respond to light. So Stuber’s team used genetically engineered proteins — from algae — that are sensitive to light and used genetically engineered viruses to deliver them into the brains of mice. Those proteins then get expressed only in the BNST cells, including in the synapses that connect to the hypothalamus.

His team then implanted fiber optic cables in the brains of these specially-bred mice, and this allowed the researchers to shine light through the cables and onto BNST synapses. As soon as the light hit BNST synapses the mice began to eat voraciously even though they had already been well fed. Moreover, the mice showed a strong preference for high-fat foods.

“They would essentially eat up to half their daily caloric intake in about 20 minutes,” Stuber said. “This suggests that this BNST pathway could play a role in food consumption and pathological conditions such as binge eating.”

Stimulating the BNST also led the mice to exhibit behaviors associated with reward, suggesting that shining light on BNST cells enhanced the pleasure of eating. On the flip side, shutting down the BNST pathway caused mice to show little interest in eating, even if they had been deprived of food. 

“We were able to really home in on the precise neural circuit connection that was causing this phenomenon that’s been observed for more than 50 years,” Stuber said.

The study, which uses technologies highlighted in the new National Institutes of Health Brain Initiative, suggests that faulty wiring in BNST cells could interfere with hunger or satiety cues and contribute to human eating disorders, leading people to eat even when they are full or to avoid food when they are hungry. Further research is needed to determine whether it would be possible to develop drugs that correct a malfunctioning BNST circuit.

“We want to actually observe the normal function of these cell types and how they fire electrical signals when the animals are feeding or hungry,” Stuber said. “We want to understand their genetic characteristics – what genes are expressed. For example, if we find cells that become really activated after binge eating, can we look at the gene expression profile to find out what makes those cells unique from other neurons.”

And that, Stuber said, could lead to potential targets for drugs to treat certain populations of patients with eating disorders.

Filed under eating disorders obesity anorexia nervosa optogenetics brain cells lateral hypothalamus neuroscience science

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Why One Cream Cake Leads to Another

Continuously eating fatty foods perturbs communication between the gut and brain, which in turn perpetuates a bad diet.

A chronic high-fat diet is thought to desensitize the brain to the feeling of satisfaction that one normally gets from a meal, causing a person to overeat in order to achieve the same high again. New research published today (August 15) in Science, however, suggests that this desensitization actually begins in the gut itself, where production of a satiety factor, which normally tells the brain to stop eating, becomes dialed down by the repeated intake of high-fat food.

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“It’s really fantastic work,” said Paul Kenny, a professor of molecular therapeutics at The Scripps Research Institute in Jupiter, Florida, who was not involved in the study. “It could be a so-called missing link between gut and brain signaling, which has been something of a mystery.”

While pork belly, ice cream, and other high-fat foods produce an endorphin response in the brain when they hit the taste buds, according to Kenny, the gut also sends signals directly to the brain to control our feeding behavior. Indeed, mice nourished via gastric feeding tubes, which bypass the mouth, exhibit a surge in dopamine—a neurotransmitter promoting reinforcement in the brain’s reward circuitry—similar to that experienced by those eating normally.

This dopamine surge occurs in response to feeding in both mice and humans. But evidence suggests that dopamine signaling in the brain is deficient in obese people. Ivan de Araujo, a professor of psychiatry at the Yale School of Medicine, has now discovered that obese mice on a chronic high-fat diet also have a muted dopamine response when receiving fatty food via a direct tube to their stomachs.

To determine the nature of the dopamine-regulating signal emanating from the gut, Araujo and his team searched for possible candidates. “When you look at animals chronically exposed to high-fat foods, you see high levels of almost every circulating factor—leptin, insulin, triglycerides, glucose, et cetera,” he said. But one class of signaling molecule is suppressed. Of these, Araujo’s primary candidate was oleoylethanolamide. Not only is the factor produced by intestinal cells in response to food, he said, but during chronic high-fat exposure, “the suppression levels seemed to somehow match the suppression that we saw in dopamine release.”

Araujo confirmed oleoylethanol’s dopamine-regulating ability in mice by administering the factor via a catheter to the tissues surrounding their guts. “We discovered that by restoring the baseline level of [oleoylethanolamide] in the gut … the high-fat fed animals started having dopamine responses that were indistinguishable from their lean counterparts.”

The team also found that oleoylethanolamide’s effect on dopamine was transmitted via the vagus nerve, which runs between the brain and abdomen, and was dependent on its interaction with a transcription factor called PPAR-a.

Oleoylethanolamide levels are also reduced in fasting animals and increase in response to eating, communicating with the brain to stop further consumption once the belly is full. Indeed, oleoylethanolamide is a known satiety factor. Therefore, when chronic consumption of high-fat food diminishes its production, the satisfaction signal is not achieved, and the brain is essentially “blind to the presence of calories in the gut,” said Araujo, and thus demands more food.

It is not clear why a chronic high-fat diet suppresses the production of oleoylethanolamide. But once the vicious cycle starts, it is hard to break because the brain is receiving its information subconsciously, said Daniele Piomelli, a professor at the University of California, Irvine, and director of drug discovery and development at the Italian Institute of Technology in Genoa.

“We eat what we like, and we think we are conscious of what we like, but I think what this [paper] and others are indicating is that there is a deeper, darker side to liking—a side that we’re not aware of,” Piomelli said. “Because it is an innate drive, you can not control it.” Put another way, even if you could trick your taste buds into enjoying low-fat yogurt, you’re unlikely to trick your gut.

The good news, however, is that “there is no permanent impairment in the [animals’] dopamine levels,” Araujo said. This suggests that if drugs could be designed to regulate the oleoylethanolamide–to-PPAR-a pathway in the gut, Kenny added, it could have “a huge impact on people’s ability to control their appetite.”

(Source: the-scientist.com)

Filed under dopamine dopamine deficiency obesity diet appetite neuroscience science

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