1. Nutrition has benefits for brain network organization

    September 20, 2017 by Ashley

    From the University of Illinois at Urbana-Champaign press release:

    Nutrition has been linked to cognitive performance, but researchers have not pinpointed what underlies the connection. A new study by University of Illinois researchers found that monounsaturated fatty acids — a class of nutrients found in olive oils, nuts and avocados — are linked to general intelligence, and that this relationship is driven by the correlation between MUFAs and the organization of the brain’s attention network.

    The study of 99 healthy older adults, recruited through Carle Foundation Hospital in Urbana, compared patterns of fatty acid nutrients found in blood samples, functional MRI data that measured the efficiency of brain networks, and results of a general intelligence test. The study was published in the journal NeuroImage.

    “Our goal is to understand how nutrition might be used to support cognitive performance and to study the ways in which nutrition may influence the functional organization of the human brain,” said study leader Aron Barbey, a professor of psychology. “This is important because if we want to develop nutritional interventions that are effective at enhancing cognitive performance, we need to understand the ways that these nutrients influence brain function.”

    “In this study, we examined the relationship between groups of fatty acids and brain networks that underlie general intelligence. In doing so, we sought to understand if brain network organization mediated the relationship between fatty acids and general intelligence,” said Marta Zamroziewicz, a recent Ph.D. graduate of the neuroscience program at Illinois and lead author of the study.

    Studies suggesting cognitive benefits of the Mediterranean diet, which is rich in MUFAs, inspired the researchers to focus on this group of fatty acids. They examined nutrients in participants’ blood and found that the fatty acids clustered into two patterns: saturated fatty acids and MUFAs.

    “Historically, the approach has been to focus on individual nutrients. But we know that dietary intake doesn’t depend on any one specific nutrient; rather, it reflects broader dietary patterns,” said Barbey, who also is affiliated with the Beckman Institute for Advanced Science and Technology at Illinois.

    The researchers found that general intelligence was associated with the brain’s dorsal attention network, which plays a central role in attention-demanding tasks and everyday problem solving. In particular, the researchers found that general intelligence was associated with how efficiently the dorsal attention network is functionally organized used a measure called small-world propensity, which describes how well the neural network is connected within locally clustered regions as well as across globally integrated systems.

    In turn, they found that those with higher levels of MUFAs in their blood had greater small-world propensity in their dorsal attention network. Taken together with an observed correlation between higher levels of MUFAs and greater general intelligence, these findings suggest a pathway by which MUFAs affect cognition.

    “Our findings provide novel evidence that MUFAs are related to a very specific brain network, the dorsal attentional network, and how optimal this network is functionally organized,” Barbey said. “Our results suggest that if we want to understand the relationship between MUFAs and general intelligence, we need to take the dorsal attention network into account. It’s part of the underlying mechanism that contributes to their relationship.”

    Barbey hopes these findings will guide further research into how nutrition affects cognition and intelligence. In particular, the next step is to run an interventional study over time to see whether long-term MUFA intake influences brain network organization and intelligence.

    “Our ability to relate those beneficial cognitive effects to specific properties of brain networks is exciting,” Barbey said. “This gives us evidence of the mechanisms by which nutrition affects intelligence and motivates promising new directions for future research in nutritional cognitive neuroscience.”


  2. Study suggests you are what you think you eat

    by Ashley

    From the British Psychological Society (BPS) press release:

    Despite eating the same breakfast, made from the same ingredients, people consumed more calories throughout the day when they believed that one of the breakfasts was less substantial than the other.

    The research, funded by the Rural and Environment Science and Analytical Services at the Rowett Institute, is the key finding of research led by Steven Brown from Sheffield Hallam University which is being presented today at the annual conference of the British Psychological Society’s Division of Health Psychology.

    Previous studies have investigated the link between how filling we expect liquids (e.g. drinks) or semi-solids (e.g. smoothies/soups) to be and people’s subsequent feelings of hunger up to three hours later.

    These initial expectations have also been shown to be an important determinant of how much people eat at a meal provided a short time later. The current research shows that a similar effect can be seen when using solid foods (i.e. an omelette) and that the influence of those expectations is still present after a longer period of time (four hours later and the total day’s calorific intake).

    A total of 26 participants took part. Over two visits, participants believed they were eating either a two or four egg omelette for breakfast. However, both of the omelettes actually contained three eggs.

    When the participants believed that the omelette was smaller they reported themselves to be significantly hungrier after two hours, they consumed significantly more of a pasta lunch and, in total, consumed significantly more calories throughout the day than when the same participants believed that they were eating a larger omelette.

    Steven Brown said, “Previous studies have shown that a person’s expectations can have an impact on their subsequent feelings of hunger and fullness and, to a degree, their later calorie consumption. Our work builds on this with the introduction of solid food and measured people’s subsequent consumption four hours later, a period of time more indicative of the gap between breakfast and lunch.

    “We were also able to measure participants’ consumption throughout the rest of the day and found that total intake was lower when participants believed that they had eaten a larger breakfast.

    “As part of the study, we were able to take blood samples from participants throughout their visits. Having analysed levels of ghrelin, a known hunger hormone, our data also suggest that changes in reported hunger and the differences in later consumption are not due to a differences in participants’ physical response to the food.

    Therefore, memory for prior consumption, as opposed to physiological factors, may be a better target for investigating why expectations for a meal have an effect on subsequent feelings of hunger and calorie intake.”


  3. Study finds active ingredient in sugarcane may help with stress-related insomnia

    September 18, 2017 by Ashley

    From the University of Tsukuba press release:

    Everyone empirically knows that stressful events certainly affect sound sleep. Scientists in the Japanese sleep institute found that the active component rich in sugarcane and other natural products may ameliorate stress and help having sound sleep.

    In today’s world ever-changing environment, demanding job works and socio-economic factors enforces sleep deprivation in human population. Sleep deprivation induces tremendous amount of stress, and stress itself is one of the major factors responsible for sleep loss or difficulty in falling into sleep. Currently available sleeping pills does not address stress component and often have severe side effects. Sleep loss is also associated with certain other diseases including obesity, cardiovascular diseases, depression, anxiety, mania deficits etc.

    The research group led by Mahesh K. Kaushik and Yoshihiro Urade of the International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, found that octacosanol reduces stress and restores stress-affected sleep back to normal.

    Octacosanol is abundantly present in various everyday foods such as sugarcane (thin whitish layer on surface), rice bran, wheat germ oil, bee wax etc. The crude extract is policosanol, where octacosanol is the major constituent. Policosanol and octacosanol have already been used in humans for various other medical conditions.

    In the current study, authors made an advancement and investigated the effect of octacosanol on sleep regulation in mildly stressed mice by oral administration. Octacosanol reduced corticosterone level in blood plasma, which is a stress marker. The octacosanol-administered mice also showed normal sleep, which was previously disturbed due to stress. They therefore claim that the octacosanol mitigates stress in mice and restores stress-affected sleep to normal in mice. The sleep induced by octacosanol was similar to natural sleep and physiological in nature. However, authors also claimed that octacosanol does not affect sleep in normal animals. These results clearly demonstrated that octacosanol is an active compound that has potential to reduce stress and to increase sleep, and it could potentially be useful for the therapy of insomnia caused by stress. Octacosanol can be considered safe for human use as a therapy, because it is a food-based compound and believed to show no side effects.

    Octacosanol/policosanol supplements are used by humans for functions such as lipid metabolism, cholesterol lowering or to provide strength. However, well-planned clinical studies need to be carried out to confirm its effect on humans for its stress-mitigation and sleep-inducing potentials. “Future studies include the identification of target brain area of octacosanol, its BBB permeability, and the mechanism via which octacosanol lowers stress,” Kaushik says.


  4. Nutrition has benefits for brain network organization

    September 15, 2017 by Ashley

    From the University of Illinois at Urbana-Champaign press release:

    Nutrition has been linked to cognitive performance, but researchers have not pinpointed what underlies the connection. A new study by University of Illinois researchers found that monounsaturated fatty acids — a class of nutrients found in olive oils, nuts and avocados — are linked to general intelligence, and that this relationship is driven by the correlation between MUFAs and the organization of the brain’s attention network.

    The study of 99 healthy older adults, recruited through Carle Foundation Hospital in Urbana, compared patterns of fatty acid nutrients found in blood samples, functional MRI data that measured the efficiency of brain networks, and results of a general intelligence test. The study was published in the journal NeuroImage.

    “Our goal is to understand how nutrition might be used to support cognitive performance and to study the ways in which nutrition may influence the functional organization of the human brain,” said study leader Aron Barbey, a professor of psychology. “This is important because if we want to develop nutritional interventions that are effective at enhancing cognitive performance, we need to understand the ways that these nutrients influence brain function.”

    “In this study, we examined the relationship between groups of fatty acids and brain networks that underlie general intelligence. In doing so, we sought to understand if brain network organization mediated the relationship between fatty acids and general intelligence,” said Marta Zamroziewicz, a recent Ph.D. graduate of the neuroscience program at Illinois and lead author of the study.

    Studies suggesting cognitive benefits of the Mediterranean diet, which is rich in MUFAs, inspired the researchers to focus on this group of fatty acids. They examined nutrients in participants’ blood and found that the fatty acids clustered into two patterns: saturated fatty acids and MUFAs.

    “Historically, the approach has been to focus on individual nutrients. But we know that dietary intake doesn’t depend on any one specific nutrient; rather, it reflects broader dietary patterns,” said Barbey, who also is affiliated with the Beckman Institute for Advanced Science and Technology at Illinois.

    The researchers found that general intelligence was associated with the brain’s dorsal attention network, which plays a central role in attention-demanding tasks and everyday problem solving. In particular, the researchers found that general intelligence was associated with how efficiently the dorsal attention network is functionally organized used a measure called small-world propensity, which describes how well the neural network is connected within locally clustered regions as well as across globally integrated systems.

    In turn, they found that those with higher levels of MUFAs in their blood had greater small-world propensity in their dorsal attention network. Taken together with an observed correlation between higher levels of MUFAs and greater general intelligence, these findings suggest a pathway by which MUFAs affect cognition.

    “Our findings provide novel evidence that MUFAs are related to a very specific brain network, the dorsal attentional network, and how optimal this network is functionally organized,” Barbey said. “Our results suggest that if we want to understand the relationship between MUFAs and general intelligence, we need to take the dorsal attention network into account. It’s part of the underlying mechanism that contributes to their relationship.”

    Barbey hopes these findings will guide further research into how nutrition affects cognition and intelligence. In particular, the next step is to run an interventional study over time to see whether long-term MUFA intake influences brain network organization and intelligence.

    “Our ability to relate those beneficial cognitive effects to specific properties of brain networks is exciting,” Barbey said. “This gives us evidence of the mechanisms by which nutrition affects intelligence and motivates promising new directions for future research in nutritional cognitive neuroscience.”


  5. Lutein, found in leafy greens, may counter cognitive aging

    August 19, 2017 by Ashley

    From the University of Illinois at Urbana-Champaign press release:

    Spinach and kale are favorites of those looking to stay physically fit, but they also could keep consumers cognitively fit, according to a new study from University of Illinois researchers.

    The study, which included 60 adults aged 25 to 45, found that middle-aged participants with higher levels of lutein — a nutrient found in green leafy vegetables such as spinach and kale, as well as avocados and eggs — had neural responses that were more on par with younger individuals than with their peers. The findings were published in the journal Frontiers in Aging Neuroscience.

    “Now there’s an additional reason to eat nutrient-rich foods such as green leafy vegetables, eggs and avocados,” said Naiman Khan, a professor of kinesiology and community health at Illinois. “We know these foods are related to other health benefits, but these data indicate that there may be cognitive benefits as well.”

    Most other studies have focused on older adults, after there has already been a period of decline. The Illinois researchers chose to focus on young to middle-aged adults to see whether there was a notable difference between those with higher and lower lutein levels.

    “As people get older, they experience typical decline. However, research has shown that this process can start earlier than expected. You can even start to see some differences in the 30s,” said Anne Walk, a postdoctoral scholar and first author of the paper. “We want to understand how diet impacts cognition throughout the lifespan. If lutein can protect against decline, we should encourage people to consume lutein-rich foods at a point in their lives when it has maximum benefit.”

    Lutein is a nutrient that the body can’t make on its own, so it must be acquired through diet. Lutein accumulates in brain tissues, but also accumulates in the eye, which allows researchers to measure levels without relying on invasive techniques.

    The Illinois researchers measured lutein in the study participants’ eyes by having participants look into a scope and respond to a flickering light. Then, using electrodes on the scalp, the researchers measured neural activity in the brain while the participants performed a task that tested attention.

    “The neuro-electrical signature of older participants with higher levels of lutein looked much more like their younger counterparts than their peers with less lutein,” Walk said. “Lutein appears to have some protective role, since the data suggest that those with more lutein were able to engage more cognitive resources to complete the task.”

    Next, Khan’s group is running intervention trials, aiming to understand how increased dietary consumption of lutein may increase lutein in the eye, and how closely the levels relate to changes in cognitive performance.

    “In this study we focused on attention, but we also would like to understand the effects of lutein on learning and memory. There’s a lot we are very curious about,” Khan said.


  6. Green tea ingredient may ameliorate memory impairment, brain insulin resistance, and obesity

    August 16, 2017 by Ashley

    From the Federation of American Societies for Experimental Biology press release:

    A study published online in The FASEB Journal, involving mice, suggests that EGCG (epigallocatechin-3-gallate), the most abundant catechin and biologically active component in green tea, could alleviate high-fat and high-fructose (HFFD)-induced insulin resistance and cognitive impairment. Previous research pointed to the potential of EGCG to treat a variety of human diseases, yet until now, EGCG’s impact on insulin resistance and cognitive deficits triggered in the brain by a Western diet remained unclear.

    “Green tea is the second most consumed beverage in the world after water, and is grown in at least 30 countries,” said Xuebo Liu, Ph.D., a researcher at the College of Food Science and Engineering, Northwest A&F University, in Yangling, China. “The ancient habit of drinking green tea may be a more acceptable alternative to medicine when it comes to combatting obesity, insulin resistance, and memory impairment.”

    Liu and colleagues divided 3-month-old male C57BL/6J mice into three groups based on diet:

    1) a control group fed with a standard diet,

    2) a group fed with an HFFD diet, and 3) a group fed with an HFFD diet and 2 grams of EGCG per liter of drinking water.

    For 16 weeks, researchers monitored the mice and found that those fed with HFFD had a higher final body weight than the control mice, and a significantly higher final body weight than the HFFD+EGCG mice. In performing a Morris water maze test, researchers found that mice in the HFFD group took longer to find the platform compared to mice in the control group. The HFFD+EGCG group had a significantly lower escape latency and escape distance than the HFFD group on each test day. When the hidden platform was removed to perform a probe trial, HFFD-treated mice spent less time in the target quadrant when compared with control mice, with fewer platform crossings. The HFFD+EGCG group exhibited a significant increase in the average time spent in the target quadrant and had greater numbers of platform crossings, showing that EGCG could improve HFFD-induced memory impairment.

    “Many reports, anecdotal and to some extent research-based, are now greatly strengthened by this more penetrating study,” said Thoru Pederson, Ph.D., Editor-in-Chief of The FASEB Journal.


  7. Using omega 3 fatty acids to treat Alzheimer’s and other diseases?

    August 3, 2017 by Ashley

    From the Louisiana State University Health Sciences Center press release:

    Understanding how dietary essential fatty acids work may lead to effective treatments for diseases and conditions such as stroke, Alzheimer’s disease, age-related macular degeneration, Parkinson’s disease and other retinal and neurodegenerative diseases. The key is to be able to intervene during the early stages of the disease. That is the conclusion of a Minireview by Nicolas Bazan, MD, PhD, Boyd Professor and Director, and Aram Asatryan, PhD, postdoctoral researcher, at the Neuroscience Center of Excellence at LSU Health New Orleans School of Medicine published in the Journal of Biological Chemistry‘s Thematic Minireview Series: Inflammatory transcription confronts homeostatic disruptions.

    Docosahexaenoic acid (DHA), a key essential Omega-3 fatty acid, produces signaling molecules called docosanoids in response to disruptions in the state of equilibrium within cells caused by injury or disease. Neuroprotectin D1 (NDP1) is a docosanoid that the Bazan lab discovered and found protects neurons by controlling which and how certain genes in the retina and brain respond.

    Research shows that the preclinical events in Alzheimer’s disease including neuroinflammation, damage to dendritic spines — small doorknob-shaped protrusions that help transmit electrical signals to the cell — and problems with cell-to-cell communication coincide with decreased DHA content in the brain. The neuroprotective bioactivity of NPD1 includes inflammatory modulating properties as well as features that promote cell survival, both of which contribute to restoring a stable state of equilibrium, or homeostasis, within the cell.

    In experimental models of stroke, researchers at LSU Health New Orleans Neuroscience Center led by Bazan have shown that the administration of NPD1 reduces the size of stroke damage and also saves tissue in the rim surrounding the stroke core, which remains viable for a short time.

    Research has demonstrated that DHA from the liver is also retained and concentrated in photoreceptor cells and that retinal degeneration occurs when photoreceptor cells fail to capture DHA. When a gene that regulates the uptake of DHA is turned off, photoreceptor cells die and a single amino acid mutation in this receptor can cause retinitis pigmentosa.

    Cells die through a variety of mechanisms. Contributors include a family of reactive oxygen species — compounds formed continuously as by-products of aerobic metabolism such as from reactions to drugs and environmental toxins, or when the levels of antioxidants are diminished creating oxidative stress, as well as inflammation and the disease process. Cell death is considered to be reversible until a first “point of no return” checkpoint is passed. The authors describe how NPD1 acts to stop cells from passing that checkpoint in cell death activation pathways including apoptosis, necrosis, necroptosis, pyroptosis, and pyronecrosis, among others.

    The Minireview summarizes the effects of the essential fatty acid family member DHA and its bioactive derivative NPD1 in the context of a specific target of gene regulation. The authors also describe the mechanism of a pathway of regulation by a bioactive lipid that has a significant impact on cellular homeostasis — how NPD1 activates pro-survival genes and suppresses pro-death genes.

    “The organizational and functional complexity of the brain raises new questions regarding how the cellular events described here operate in response to disrupted homeostasis to attain neuroprotection in pathological conditions,” notes Bazan. “It is our hope that this knowledge will contribute to managing early stages of such devastating diseases as Alzheimer’s, stroke, traumatic brain injury, age-related macular degeneration, Parkinson’s and others.”


  8. Study suggests natural plant compound may reduce mental effects of aging

    July 28, 2017 by Ashley

    From the Salk Institute press release:

    Salk scientists have found further evidence that a natural compound in strawberries reduces cognitive deficits and inflammation associated with aging in mice. The work, which appeared in the Journals of Gerontology Series A in June 2017, builds on the team’s previous research into the antioxidant fisetin, finding it could help treat age-related mental decline and conditions like Alzheimer’s or stroke.

    “Companies have put fisetin into various health products but there hasn’t been enough serious testing of the compound,” says Pamela Maher, a senior staff scientist in Salk’s Cellular Neurobiology Laboratory and senior author of the paper. “Based on our ongoing work, we think fisetin might be helpful as a preventative for many age-associated neurodegenerative diseases, not just Alzheimer’s, and we’d like to encourage more rigorous study of it.”

    Maher, who works in the lab of David Schubert, the head of Salk’s Cellular Neurobiology Lab, has been studying fisetin for over a decade. Previous research by the lab found that fisetin reduced memory loss related to Alzheimer’s in mice genetically modified to develop the disease. But that study focused on genetic (familial) AD, which accounts for only 1 to 3 percent of cases. By far the bigger risk factor for developing what is termed sporadic AD, as well as other neurodegenerative disorders, is simply age. For the current inquiry, Maher turned to a strain of laboratory mice that age prematurely to better study sporadic AD. By 10 months of age, these mice typically show signs of physical and cognitive decline not seen in normal mice until two years of age.

    The Salk team fed the 3-month-old prematurely aging mice a daily dose of fisetin with their food for 7 months. Another group of the prematurely aging mice was fed the same food without fisetin. During the study period, mice took various activity and memory tests. The team also examined levels of specific proteins in the mice related to brain function, responses to stress and inflammation.

    “At 10 months, the differences between these two groups were striking,” says Maher. Mice not treated with fisetin had difficulties with all the cognitive tests as well as elevated markers of stress and inflammation. Brain cells called astrocytes and microglia, which are normally anti-inflammatory, were now driving rampant inflammation. Mice treated with fisetin, on the other hand, were not noticeably different in behavior, cognitive ability or inflammatory markers at 10 months than a group of untreated 3-month-old mice with the same condition. Additionally, the team found no evidence of acute toxicity in the fisetin-treated mice, even at high doses of the compound.

    “Mice are not people, of course,” says Maher, “But there are enough similarities that we think fisetin warrants a closer look, not only for potentially treating sporadic AD but also for reducing some of the cognitive effects associated with aging, generally.”

    Next, Maher hopes to partner with another group or company in order to conduct clinical trials of fisetin with human subjects.


  9. Mouse study suggests sense of smell affects metabolism

    July 26, 2017 by Ashley

    From the University of California – Berkeley press release:

    Our sense of smell is key to the enjoyment of food, so it may be no surprise that in experiments at the University of California, Berkeley, obese mice who lost their sense of smell also lost weight.

    What’s weird, however, is that these slimmed-down but smell-deficient mice ate the same amount of fatty food as mice that retained their sense of smell and ballooned to twice their normal weight.

    In addition, mice with a boosted sense of smell — super-smellers — got even fatter on a high-fat diet than did mice with normal smell.

    The findings suggest that the odor of what we eat may play an important role in how the body deals with calories. If you can’t smell your food, you may burn it rather than store it.

    These results point to a key connection between the olfactory or smell system and regions of the brain that regulate metabolism, in particular the hypothalamus, though the neural circuits are still unknown.

    “This paper is one of the first studies that really shows if we manipulate olfactory inputs we can actually alter how the brain perceives energy balance, and how the brain regulates energy balance,” said Céline Riera, a former UC Berkeley postdoctoral fellow now at Cedars-Sinai Medical Center in Los Angeles.

    Humans who lose their sense of smell because of age, injury or diseases such as Parkinson’s often become anorexic, but the cause has been unclear because loss of pleasure in eating also leads to depression, which itself can cause loss of appetite.

    The new study, published this week in the journal Cell Metabolism, implies that the loss of smell itself plays a role, and suggests possible interventions for those who have lost their smell as well as those having trouble losing weight.

    “Sensory systems play a role in metabolism. Weight gain isn’t purely a measure of the calories taken in; it’s also related to how those calories are perceived,” said senior author Andrew Dillin, the Thomas and Stacey Siebel Distinguished Chair in Stem Cell Research, professor of molecular and cell biology and Howard Hughes Medical Institute Investigator. “If we can validate this in humans, perhaps we can actually make a drug that doesn’t interfere with smell but still blocks that metabolic circuitry. That would be amazing.”

    Riera noted that mice as well as humans are more sensitive to smells when they are hungry than after they’ve eaten, so perhaps the lack of smell tricks the body into thinking it has already eaten. While searching for food, the body stores calories in case it’s unsuccessful. Once food is secured, the body feels free to burn it.

    Zapping olfactory neurons

    The researchers used gene therapy to destroy olfactory neurons in the noses of adult mice but spare stem cells, so that the animals lost their sense of smell only temporarily — for about three weeks — before the olfactory neurons regrew.

    The smell-deficient mice rapidly burned calories by up-regulating their sympathetic nervous system, which is known to increase fat burning. The mice turned their beige fat cells — the subcutaneous fat storage cells that accumulate around our thighs and midriffs — into brown fat cells, which burn fatty acids to produce heat. Some turned almost all of their beige fat into brown fat, becoming lean, mean burning machines.

    In these mice, white fat cells — the storage cells that cluster around our internal organs and are associated with poor health outcomes — also shrank in size.

    The obese mice, which had also developed glucose intolerance — a condition that leads to diabetes — not only lost weight on a high-fat diet, but regained normal glucose tolerance.

    On the negative side, the loss of smell was accompanied by a large increase in levels of the hormone noradrenaline, which is a stress response tied to the sympathetic nervous system. In humans, such a sustained rise in this hormone could lead to a heart attack.

    Though it would be a drastic step to eliminate smell in humans wanting to lose weight, Dillin noted, it might be a viable alternative for the morbidly obese contemplating stomach stapling or bariatric surgery, even with the increased noradrenaline.

    “For that small group of people, you could wipe out their smell for maybe six months and then let the olfactory neurons grow back, after they’ve got their metabolic program rewired,” Dillin said.

    Dillin and Riera developed two different techniques to temporarily block the sense of smell in adult mice. In one, they genetically engineered mice to express a diphtheria receptor in their olfactory neurons, which reach from the nose’s odor receptors to the olfactory center in the brain. When diphtheria toxin was sprayed into their nose, the neurons died, rendering the mice smell-deficient until the stem cells regenerated them.

    Separately, they also engineered a benign virus to carry the receptor into olfactory cells only via inhalation. Diphtheria toxin again knocked out their sense of smell for about three weeks.

    In both cases, the smell-deficient mice ate as much of the high-fat food as did the mice that could still smell. But while the smell-deficient mice gained at most 10 percent more weight, going from 25-30 grams to 33 grams, the normal mice gained about 100 percent of their normal weight, ballooning up to 60 grams. For the former, insulin sensitivity and response to glucose — both of which are disrupted in metabolic disorders like obesity — remained normal.

    Mice that were already obese lost weight after their smell was knocked out, slimming down to the size of normal mice while still eating a high-fat diet. These mice lost only fat weight, with no effect on muscle, organ or bone mass.

    The UC Berkeley researchers then teamed up with colleagues in Germany who have a strain of mice that are supersmellers, with more acute olfactory nerves, and discovered that they gained more weight on a standard diet than did normal mice.

    “People with eating disorders sometimes have a hard time controlling how much food they are eating and they have a lot of cravings,” Riera said. “We think olfactory neurons are very important for controlling pleasure of food and if we have a way to modulate this pathway, we might be able to block cravings in these people and help them with managing their food intake.”


  10. Your hands may reveal the struggle to maintain self-control

    July 25, 2017 by Ashley

    From the Ohio State University press release:

    It takes just a few seconds to choose a cookie over an apple and wreck your diet for the day.

    But what is happening during those few seconds while you make the decision?

    In a new study, researchers watched in real time as people’s hands revealed the struggle they were under to choose the long-term goal over short-term temptation. The work represents a new approach to studying self-control.

    In one key experiment, participants viewed pictures of a healthy and an unhealthy food choice on opposite sides of the top of a computer screen and moved a cursor from the center bottom to select one of the foods.

    People who moved the cursor closer to the unhealthy treat (even when they ultimately made the healthy choice) later showed less self-control than did those who made a more direct path to the healthy snack.

    Our hand movements reveal the process of exercising self-control,” said Paul Stillman, co-author of the study and postdoctoral researcher in psychology at The Ohio State University.

    “You can see the struggle as it happens. For those with low self-control, the temptation is actually drawing their hand closer to the less-healthy choice.”

    The results may shed light on a scholarly debate about what’s happening in the brain when humans harness willpower.

    Stillman conducted the study with Melissa Ferguson, professor of psychology, and Danila Medvedev, a former undergraduate student, both from Cornell University. Their research will appear in the journal Psychological Science.

    The study involved several experiments. In one, 81 college students made 100 decisions involving healthy versus unhealthy food choices.

    In each trial, they clicked a “Start” button at the bottom of the screen. As soon as they did, two images appeared in the upper-left and upper-right corners of the screen, one a healthy food (such as Brussels sprouts) and the other an unhealthy one (such as a brownie).

    They were told to choose as quickly as possible which of the two foods would most help them meet their health and fitness goals. So there was a “correct” answer, even if they were tempted by a less healthy treat.

    Before the experiment began, the participants were told that after they finished they would be given one of the foods they chose in the experiment. At the end, however, they could freely choose whether they wanted an apple or a candy bar.

    The results showed that those who chose the candy bar at the end of the experiment — those with lower self-control — had tended to veer closer to the unhealthy foods on the screen.

    “The more they were pulled toward the temptation on the computer screen, the more they actually chose the temptations and failed at self-control,” Stillman said.

    But for those with higher levels of self-control, the path to the healthy food was more direct, indicating that they experienced less conflict.

    In two other studies, similar results occurred in a completely different scenario, in which college students could decide whether they would rather accept $25 today or $45 in 180 days. Those with lower levels of self-control had mouse trajectories that were clearly different from those with higher self-control, suggesting differences in how they were dealing with the decisions.

    “This mouse-tracking metric could be a powerful new tool to investigate real-time conflict when people have to make decisions related to self-control,” he said.

    The findings also offer new evidence in a debate about how decision-making in self-control situations unfolds, Stillman said.

    When the researchers mapped the trajectories people took with the cursor in the first experiment, they observed that most participants did not automatically start directly toward the unhealthy treat before abruptly switching course back to the healthy food. Rather, the trajectories appear curved, as if both the temptation and goal were competing from the beginning.

    Why is that important?

    Some researchers have argued that there are two systems in our brain that are involved in a self-control decision: one that’s impulsive and a second that overcomes the impulses to exert willpower. But if that were the case, the trajectories seen in this study should look different than they do, Stillman said.

    If dual systems underlie these choices, there should be a relatively straight line toward the unhealthy food while people are under the influence of the impulsive first system and then an abrupt change in direction toward the healthy food as the system in charge of self-control kicks in.

    “That’s not what we found,” Stillman said. “Our results suggest a more dynamical process in which the healthy and unhealthy choices are competing from the very beginning in our brains and there isn’t an abrupt change in thinking. That’s why we get these curved trajectories.”

    Stillman said these results should help lead to a more accurate view of how our cognitive processes unfold to allow us to resist temptation.