Do Gut Bacteria Rule Our Minds?

It sounds like science fiction, but it seems that bacteria within us — which outnumber our own cells about 100-fold — may very well be affecting both our cravings and moods to get us to eat what they want, and often are driving us toward obesity.

In an article published this week in the journal BioEssays, researchers from UC San Francisco, Arizona State University and University of New Mexico concluded from a review of the recent scientific literature that microbes influence human eating behavior and dietary choices to favor consumption of the particular nutrients they grow best on, rather than simply passively living off whatever nutrients we choose to send their way.

Bacterial species vary in the nutrients they need. Some prefer fat, and others sugar, for instance. But they not only vie with each other for food and to retain a niche within their ecosystem — our digestive tracts — they also often have different aims than we do when it comes to our own actions, according to senior author Athena Aktipis, PhD, co-founder of the Center for Evolution and Cancer with the Helen Diller Family Comprehensive Cancer Center at UCSF.

While it is unclear exactly how this occurs, the authors believe this diverse community of microbes, collectively known as the gut microbiome, may influence our decisions by releasing signaling molecules into our gut. Because the gut is linked to the immune system, the endocrine system and the nervous system, those signals could influence our physiologic and behavioral responses.

“Bacteria within the gut are manipulative,” said Carlo Maley, PhD, director of the UCSF Center for Evolution and Cancer and corresponding author on the paper. “There is a diversity of interests represented in the microbiome, some aligned with our own dietary goals, and others not.”

Fortunately, it’s a two-way street. We can influence the compatibility of these microscopic, single-celled houseguests by deliberating altering what we ingest, Maley said, with measurable changes in the microbiome within 24 hours of diet change.

“Our diets have a huge impact on microbial populations in the gut,” Maley said. “It’s a whole ecosystem, and it’s evolving on the time scale of minutes.”

There are even specialized bacteria that digest seaweed, found in humans in Japan, where seaweed is popular in the diet.

Research suggests that gut bacteria may be affecting our eating decisions in part by acting through the vagus nerve, which connects 100 million nerve cells from the digestive tract to the base of the brain.

“Microbes have the capacity to manipulate behavior and mood through altering the neural signals in the vagus nerve, changing taste receptors, producing toxins to make us feel bad, and releasing chemical rewards to make us feel good,” said Aktipis, who is currently in the Arizona State University Department of Psychology.

In mice, certain strains of bacteria increase anxious behavior. In humans, one clinical trial found that drinking a probiotic containing Lactobacillus casei improved mood in those who were feeling the lowest.

Maley, Aktipis and first author Joe Alcock, MD, from the Department of Emergency Medicine at the University of New Mexico, proposed further research to test the sway microbes hold over us. For example, would transplantation into the gut of the bacteria requiring a nutrient from seaweed lead the human host to eat more seaweed?

The speed with which the microbiome can change may be encouraging to those who seek to improve health by altering microbial populations. This may be accomplished through food and supplement choices, by ingesting specific bacterial species in the form of probiotics, or by killing targeted species with antibiotics. Optimizing the balance of power among bacterial species in our gut might allow us to lead less obese and healthier lives, according to the authors.

“Because microbiota are easily manipulatable by prebiotics, probiotics, antibiotics, fecal transplants, and dietary changes, altering our microbiota offers a tractable approach to otherwise intractable problems of obesity and unhealthy eating,” the authors wrote.

The authors met and first discussed the ideas in the BioEssays paper at a summer school conference on evolutionary medicine two years ago. Aktipis, who is an evolutionary biologist and a psychologist, was drawn to the opportunity to investigate the complex interaction of the different fitness interests of microbes and their hosts and how those play out in our daily lives. Maley, a computer scientist and evolutionary biologist, had established a career studying how tumor cells arise from normal cells and evolve over time through natural selection within the body as cancer progresses.

In fact, the evolution of tumors and of bacterial communities are linked, points out Aktipis, who said some of the bacteria that normally live within us cause stomach cancer and perhaps other cancers.

“Targeting the microbiome could open up possibilities for preventing a variety of disease from obesity and diabetes to cancers of the gastro-intestinal tract. We are only beginning to scratch the surface of the importance of the microbiome for human health,” she said.

Highly processed foods linked to addictive eating

A new University of Michigan study confirms what has long been suspected: highly processed foods like chocolate, pizza and French fries are among the most addictive.

This is one of the first studies to examine specifically which foods may be implicated in “food addiction,” which has become of growing interest to scientists and consumers in light of the obesity epidemic.

Previous studies in animals conclude that highly processed foods, or foods with added fat or refined carbohydrates (like white flour and sugar), may be capable of triggering addictive-like eating behavior. Clinical studies in humans have observed that some individuals meet the criteria for substance dependence when the substance is food.

Despite highly processed foods generally known to be highly tasty and preferred, it is unknown whether these types of foods can elicit addiction-like responses in humans, nor is it known which specific foods produce these responses, said Ashley Gearhardt, U-M assistant professor of psychology.

Unprocessed foods, with no added fat or refined carbohydrates like brown rice and salmon, were not associated with addictive-like eating behavior.

Individuals with symptoms of food addiction or with higher body mass indexes reported greater problems with highly processed foods, suggesting some may be particularly sensitive to the possible “rewarding” properties of these foods, said Erica Schulte, a U-M psychology doctoral student and the study’s lead author.

“If properties of some foods are associated with addictive eating for some people, this may impact nutrition guidelines, as well as public policy initiatives such as marketing these foods to children,” Schulte said.

Nicole Avena, assistant professor of pharmacology and systems therapeutics at Icahn School of Medicine at Mount Sinai in New York City, and a co-author on the study, explained the significance of the findings.

“This is a first step towards identifying specific foods, and properties of foods, which can trigger this addictive response,” she said. “This could help change the way we approach obesity treatment. It may not be a simple matter of ‘cutting back’ on certain foods, but rather, adopting methods used to curtail smoking, drinking and drug use.”

Future research should examine whether addictive foods are capable of triggering changes in brain circuitry and behavior like drugs of abuse, the researchers said.

Eating is addictive

People can become addicted to eating for its own sake but not to consuming specific foods such as those high in sugar or fat, research suggests.

An international team of scientists has found no strong evidence for people being addicted to the chemical substances in certain foods.

The brain does not respond to nutrients in the same way as it does to addictive drugs such as heroin or cocaine, the researchers say.

Instead, people can develop a psychological compulsion to eat, driven by the positive feelings that the brain associates with eating.

“This is a behavioural disorder and could be categorised alongside conditions such as gambling addiction”, say scientists at Edinburgh.

They add that the focus on tackling the problem of obesity should be moved from food itself towards the individual’s relationship with eating.

The study, which examined the scientific evidence for food addiction as a substance-based addiction, is published in Neuroscience & Biobehavioral Reviews.

The researchers also say that the current classification of mental disorders, which does not permit a formal diagnosis of eating addiction, could be redrawn.

However, more research would be needed to define a diagnosis, the scientists add.

They add that the focus on tackling the problem of obesity should be moved from food itself towards the individual’s relationship with eating.

Headcanon: Never leave your food unattended when you’re having dinner/lunch with Skye. Or if you’re eating something in general. Because once you get distracted she will just take it from you and eat it herself. It doesn’t matter if it’s something to drink or to eat she’ll just take it without asking you if you don’t pay attention.

Brain reward circuits respond differently to 2 kinds of sugar

The brain responds differently to two kinds of sugar, according to a report today at the American College of Neuropsychopharmacology annual meeting in Phoenix Arizona. The study suggests that fructose heightens the response of brain reward circuits to food cues, promoting feeding behavior.

Currently, roughly two out of three U.S. adults are overweight and one out of three is obese. Changes in lifestyle and dietary intake during the past quarter century are thought to be the main culprits, with the increase in fructose consumption of particular concern. Fructose is the simple sugar found in fruit, but it is added to many foods as a “refined sugar” in the form of high-fructose corn syrup. By comparison, glucose, the primary energy source for the body, is usually produced through the breakdown of complex carbohydrates. Fructose ingestion produces smaller increases in circulating satiety hormones than glucose ingestion. Further, administration of fructose directly into the brain provokes feeding in rodents, whereas glucose administered this way promotes satiety, or the feeling of being full. Preliminary studies in people have also shown that glucose reduces activity in the hypothalamus, an event that is associated with metabolic satiety, whereas fructose does not.

Using functional magnetic resonance imaging (fMRI), Kathleen Page at the Keck School of Medicine of the University of Southern California (USC) and her colleagues in the Department of Psychology at the University of Southern California extended this work. They examined brain responses and motivation to eat when research volunteers viewed images of food (like chocolate cake) after they drank a beverage containing either glucose or fructose. The participants were 24 young men and women, 16 to 25 years of age. They viewed images of food during fMRI scans of their brains and reported how much they wanted to eat. The food cues produced activation in the nucleus accumbens, a part of the brain’s “reward circuit”, and increased the desire for food. Activation in the nucleus accumbens was greater after consuming the fructose drink compared to the glucose drink. The fructose drink also resulted in greater ratings of hunger and motivation to eat compared to the glucose drink. These neural and behavioral responses to high-calorie food stimuli could promote eating, and more so after consuming fructose compared to glucose.

These studies have important public health implications in a society that is inundated with high-sugar foods and tantalizing food stimuli. They suggest that consumption of fructose may promote overeating.

autisticbutchgabrielle  asked:

I just saw a Ghastly produce the illusion of a mongoose to scare Ekans ("A snake's natural predator is a mongoose"--this was a talking Ghastly) and Koffing... idk if there are mongoose Pokemon, but that's something to consider maybe...

ym instan t though t was of zangoose bu t its referr ed 2 as the cat ferre t pokemon  instead (& doestn look lik 1 at all rly), other wise  yungoos  Coudl b a possibil ity once we learn mo re abt it in s un & moon . it do es look Soor ta simil ar 2 th e illusio n it makes

eith er way this is v inter estign & somethign 2 consider 

Consuming Sweets Forms Memories That May Control Eating Habits

Eating sweet foods causes the brain to form a memory of a meal, according to researchers at Georgia State University, Georgia Regents University and Charlie Norwood VA Medical Center.

The findings, published online in the journal Hippocampus, show that neurons in the dorsal hippocampus, the part of the brain that is critical for episodic memory, are activated by consuming sweets. Episodic memory is the memory of autobiographical events experienced at a particular time and place.

In the study, a meal consisting of a sweetened solution, either sucrose or saccharin, significantly increased the expression of the synaptic plasticity marker called activity-regulated cytoskeleton-associated protein (Arc) in dorsal hippocampal neurons in rats. Synaptic plasticity is a process that is necessary for making memories.

“We think that episodic memory can be used to control eating behavior,” said Marise Parent, professor in the Neuroscience Institute at Georgia State. “We make decisions like ‘I probably won’t eat now. I had a big breakfast.’ We make decisions based on our memory of what and when we ate.”

That possibility is supported by the researchers’ previous work, which showed that temporarily inactivating dorsal hippocampal neurons following a sucrose meal—the period during which the memory of a meal forms—accelerates the onset of the next meal and causes rats to eat more.

Forming memories of meals is important to a healthy diet. A London-based study shows that disrupting the encoding of the memory of a meal in humans, such as by watching television, increases the amount of food they consume during the next meal. Researchers have found that people with amnesia will eat again if presented with food, even if they’ve already eaten, because they have no memory of the meal.

To understand energy regulation and the causes of obesity, scientists must consider how the brain controls meal onset and frequency, Parent said.

Studies have found that increased snacking is correlated positively with obesity, and obese individuals snack more frequently than people who aren’t obese. Research also shows that over the past three decades, children and adults are eating more snacks per day and deriving more of their daily calories from snacks, mostly in the form of desserts and sweetened beverages.

In the future, the research team would like to determine if nutritionally balanced liquid or solid diets that typically contain protein, fat and carbohydrates have a similar effect on Arc expression in dorsal hippocampal neurons and whether increases in Arc expression are necessary for the memory of sweet foods.

Eating habits, body fat related to differences in brain chemistry

People who are obese may be more susceptible to environmental food cues than their lean counterparts due to differences in brain chemistry that make eating more habitual and less rewarding, according to a National Institutes of Health study published in Molecular Psychiatry.

Researchers at the NIH Clinical Center found that, when examining 43 men and women with varying amounts of body fat, obese participants tended to have greater dopamine activity in the habit-forming region of the brain than lean counterparts, and less activity in the region controlling reward. Those differences could potentially make the obese people more drawn to overeat in response to food triggers and simultaneously making food less rewarding to them. A chemical messenger in the brain, dopamine influences reward, motivation and habit formation.

“While we cannot say whether obesity is a cause or an effect of these patterns of dopamine activity, eating based on unconscious habits rather than conscious choices could make it harder to achieve and maintain a healthy weight, especially when appetizing food cues are practically everywhere,” said Kevin D. Hall, Ph.D., lead author and a senior investigator at National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of NIH. “This means that triggers such as the smell of popcorn at a movie theater or a commercial for a favorite food may have a stronger pull for an obese person – and a stronger reaction from their brain chemistry – than for a lean person exposed to the same trigger.”

Study participants followed the same eating, sleeping and activity schedule. Tendency to overeat in response to triggers in the environment was determined from a detailed questionnaire. Positron emission tomography (PET) scans evaluated the sites in the brain where dopamine was able to act.

According to the Centers for Disease Control and Prevention, more than one-third of U.S. adults are obese. Obesity-related conditions include heart disease, type 2 diabetes and certain types of cancer, some of the leading causes of preventable death.

“These findings point to the complexity of obesity and contribute to our understanding of how people with varying amounts of body fat process information about food,” said NIDDK Director Griffin P. Rodgers, M.D. “Accounting for differences in brain activity and related behaviors has the potential to inform the design of effective weight-loss programs.”

The study did not demonstrate cause and effect among habit formation, reward, dopamine activity, eating behavior and obesity. Future research will examine dopamine activity and eating behavior in people over time as they change their diets, physical activity, and their weight.

(Image caption: Alternative mechanisms for driving food consumption. Eating not only is a necessity, it is a learned response to hunger, too. a) In the positive-valance mechanism, hungry animals learn that eating feels good. b) In the negative-valence mechanism, hunger feels bad to animals, and they learn that eating makes these bad feelings dissipate)

Another reason why your diet is doomed – “Hunger” neurons promote negative feelings

Dieting challenges evolution

In its simplest terms, weight loss occurs when the amount of energy consumed in the form of food is less than the amount of energy burned. This can be accomplished by eating less or exercising more. With either approach, the goal is to create a caloric debt that will be resolved by burning stored carbohydrate, protein, or fat. Challenges to losing the holiday weight (alternatively a beer gut, Freshman Fifteen, etc.) are simple: eating feels good and being hungry is uncomfortable. Behaviors that evolved as survival mechanisms to ensure that an animal feeds itself become inconvenient and potentially detrimental side effects in industrialized human populations where cardiovascular disease, diabetes, and obesity, rather than starvation, pose greater risks to long-term survival.

To explain the less commonly researched “discomfort when hungry” phenomenon, researchers at the Howard Hughes Medical Institute (HHMI) Janelia Research Campus hypothesized that specific hypothalamic neurons stimulate food-seeking behaviors to eliminate the negative feelings associated with energy deficit (Betley et al. 2015).

The Hunger Games  – Neural manipulation suggests AGRP signals are negative

Previously demonstrated by other groups, hypothalamic AGRP neurons (agouti-related protein-expressing neurons) fire during energy deficit, such as food restriction, and quickly lead to food-seeking behavior and food-consumption. To determine whether these neurons were associated with positive signals (such as those associated with food reward) versus negative signals (such as those associated with the uncomfortable feelings of hunger), mice either with photoactivatable AGRP neurons (STOCK Agrptm1(cre)Lowl/J 012899 X B6;129S-Gt(ROSA)26Sortm32(CAG-COP4*H134R/EYFP)Hze/J 012569 F1 hybrids) or with virally-transduced AGRP neurons that could be inhibited pharmacologically were subjected to flavor and place preference tests.

In flavor preference tests, AGRP neuron activation reduced an animal’s preference for previously preferred flavored gel compared to unstimulated controls, suggesting that a once tasty flavor was now a less pleasant experience. In contrast, mouse preferences for a preferred gel increased when AGRP neurons in food-restricted mice were pharmacologically inhibited compared to the preferences of untreated controls, suggesting that AGRP inhibition relieved negative feelings. In complementary place preference experiments in which mice were offered two experimental chambers to explore, well-fed mice avoided chambers in which they had previously received AGRP stimulation, indicating AGRP stimulation was undesirable. Similarly, food-restricted mice spent more time in chambers where they had previously received AGRP inhibition, indicating that relief from AGRP simulation was preferred. Together, these results suggest that AGRP neurons stimulate negative signals and generate Pavlovian responses learned through these negative experiences.

AGRP neurons anticipate feeding and turn off

To support their behavioral studies, the HHMI Janelia group performed deep brain imaging in freely-moving AGRP-specific calcium reporter mice using miniature head-mounted fluorescent microscopes. As expected, food-restricted mice showed higher fluorescent signals than mice fed ad libitum, demonstrating that food restriction activates AGRP neurons. Calcium signals quickly diminished when food-restricted mice were allowed to eat. Interestingly, the calcium signals dropped before eating began, including cases where food was visible but not accessible for consumption. In contrast, calcium signals dropped slightly when mice were presented a wooden pellet resembling food, but quickly returned when the mice discovered that the wooden pellet was not food. Together, these experiments indicate that AGRP neuron activity is reduced when feeding cues are present. Further, the rapidity with which the AGRP signals terminate upon feeding or recommence upon presentation with non-food items strengthen the hypothesis that AGRP neurons promote negative, rather than positive, signals.

Collectively, these results indicate that energy homeostasis depends, in part, on alleviating negative signals produced during hunger. Findings from this study corroborate the negative emotions people experience when dieting and point to alternative avenues to regulate food intake. The negative-valence mechanism that AGRP neurons utilize contrasts with the majority of hunger-associated neurons previously studied, which stimulate reward pathways and result in positive feelings when hunger is satisfied. Certainly, then, fine control of energy homeostasis is accomplished by possessing both kinds of neurons.

Hunger-spiking neurons could help control autoimmune diseases

Neurons that control hunger in the central nervous system also regulate immune cell functions, implicating eating behavior as a defense against infections and autoimmune disease development, Yale School of Medicine researchers have found in a new study published in the Proceedings of the National Academies of Sciences (PNAS).

Autoimmune diseases have been on a steady rise in the United States. These illnesses develop when the body’s immune system turns on itself and begins attacking its own tissues. The interactions between different kinds of T cells are at the heart of fighting infections, but they have also been linked to autoimmune disorders.

“We’ve found that if appetite-promoting AgRP neurons are chronically suppressed, leading to decreased appetite and a leaner body weight, T cells are more likely to promote inflammation-like processes enabling autoimmune responses that could lead to diseases like multiple sclerosis,” said lead author Tamas Horvath, the Jean and David W. Wallace Professor of Biomedical Research and chair of comparative medicine at Yale School of Medicine.

“If we can control this mechanism by adjusting eating behavior and the kinds of food consumed, it could lead to new avenues for treating autoimmune diseases,” he added.

Horvath and his research team conducted their study in two sets of transgenic mice. In one set, they knocked out Sirt1, a signaling molecule that controls the hunger-promoting neuron AgRP in the hypothalamus. These Sirt1-deficient mice had decreased regulatory T cell function and enhanced effector T cell activity, leading to their increased vulnerability in an animal model of multiple sclerosis.

“This study highlights the important regulatory role of the neurons that control appetite in peripheral immune functions,” said Horvath. “AgRP neurons represent an important site of action for the body’s immune responses.”

The team’s data support the idea that achieving weight loss through the use of drugs that promote a feeling of fullness “could have unwanted effects on the spread of autoimmune disorders,” he notes.

Do Certain Words Entice Us to Eat High-Calorie Foods?

New research shows that brain responses to written food words differ between lean individuals and those with obesity, and suggests that both stress and genetics could influence excess eating.

The pair of studies led by Susan Carnell, PhD, member of The Obesity Society (TOS) and Assistant Professor of Psychiatry and Behavioral Sciences at Johns Hopkins University School of Medicine, reinforces the need to better understand how the external food environment interacts with our biology, and may aid the development of behavioral interventions to help individuals with obesity or those at high risk for the disease. The findings were presented during an oral presentation, and a poster presentation on Wednesday, Nov. 4, at The Obesity Society Annual Meeting at ObesityWeekSM 2015 in Los Angeles, CA.

In recent years, obesity researchers have greatly enhanced our understanding of “food cues,” which are internal or external environmental factors that influence the desire to eat. They come in many forms including emotions, images, smells, tastes and even food words. Food words could be considered a relatively minimal food cue compared with images or smells; however, because they are ubiquitous in advertising and other contexts they have significant potential to impact eating behavior.

In one study, the research team found that individuals with obesity were more likely to consume energy-dense foods (foods high in calories per unit of weight) compared to those of normal weight after experiencing stress. As seen in brain imaging scans, neural responses to high-calorie compared with low-calorie food words was also increased for individuals with obesity under both stressed and non-stressed conditions. To conduct the study, seventeen participants with obesity and 12 at normal weight underwent a functional magnetic resonance imaging (fMRI) scan during which they viewed words describing high-calorie foods, low-calorie foods and non-foods, and rated how much they wanted to eat each food item.

“Our study found that individuals with obesity had a stronger response to words associated with high-calorie foods - such as chocolate spread and chicken wings - in a widespread neural circuit spanning multiple areas of the brain,” said Dr. Carnell. “When we subjected individuals to a combined social and physiological stressor, both individuals with obesity and those of normal weight showed slightly altered responses to high-calorie food words, but only those with obesity ate more at a subsequent meal. This suggests that people with obesity show a consistently different response to mere words describing foods than lean individuals. This could contribute to excess intake of energy-dense foods in both stressful and non-stressful environments.”

In the second study, the research team identified an association between higher genetic obesity risk in teenagers based on several known obesity-associated genetic variants and subjective responses to food words. In addition, one specific genetic variant, MC4R, was associated with greater intake of high-calorie foods during a laboratory test meal, while another, FTO, was associated with lower scores on a questionnaire measuring self-regulation of food intake.

A genetic variant is a genetic difference that makes one individual or population different from another.

“We all have tiny differences in our genome that affect how we interact with the surrounding environment,” says Carnell. “While some of the genetic variants we see may have helped people maintain a healthy body weight in the past, they could now be working against us, making certain populations more susceptible to obesity and diabetes.”

To conduct the study, the research team genotyped 35 adolescents between 14 and 19 years old with varying familial risk for obesity. Subjective appetite responses to food and non-food words were measured using a computer paradigm, and food consumption was measured in a laboratory meal that followed. Participants also filled out a questionnaire measuring habitual self-regulation of intake.

“While we know that certain genetic variants are tied to obesity, our study provides additional insight into how these particular obesity-associated genetic variants may be working – by increasing appetite and food intake,” said Leora Benson, MS, research coordinator for the study. “The fact that many of these genetic variants act through eating behavior is exciting because behavior can be changed,” adds Carnell. “This research tells us that there may be ways we can help prevent individuals with these variants from developing obesity.”

The new understandings gleaned from these two studies could help the clinical research community identify behavioral treatment strategies based on reducing the impact of food cues, particularly for those at high risk for obesity.

“It may be  possible to train our brains to react differently to certain food cues,” said Martin Binks, PhD, FTOS, Secretary Treasurer of and spokesperson for The Obesity Society. “This research is a step toward better understanding how food words – relatively minimal food cues – may influence food consumption and how other common experiences like stress may interact with associated food cues to influence eating behavior. These types of studies may eventually lead to more effective behavioral strategies.”