TAG: "Obesity"

Sense of smell may reveal weight bias


Prejudice against overweight people is likely more pervasive than previously thought.

By Rebecca Kendall, UCLA

Could our reaction to an image of an overweight or obese person affect how we perceive odor? A trio of researchers, including two from UCLA, says yes.

The researchers discovered that visual cues associated with overweight or obese people can influence one’s sense of smell, and that the perceiver’s body mass index matters, too. Participants with higher BMI tended to be more critical of heavier people, with higher-BMI participants giving scents a lower rating when scent samples were matched with an obese or overweight individual.

The findings, published online in the International Journal of Obesity and scheduled to be presented today (March 18) at the annual conference of the American Psychosomatic Society, suggest that the extent of negative bias toward overweight and obese people may be greater than previously believed.

“You wouldn’t think that not liking someone’s weight could then be seen in a totally different sensory modality, which makes us think, ‘How else is weight stigma affecting our lives that we don’t even know about?’” said A. Janet Tomiyama, a UCLA assistant professor of psychology. Tomiyama conducted the research with Angela Incollingo Rodriguez, a UCLA doctoral student in psychology, and Andrew Ward, a professor of psychology at Swarthmore College.

“This is the first step in proving that the consequences of weight stigma could be very widespread in ways that we don’t even know,” Tomiyama said.

Incollingo Rodriguez, the report’s lead author, said while some people are overtly biased, others are more subtle about it and may not even be aware that they harbor negative feelings toward heavy people.

“There are no checks and balances on weight stigma in the way you would see with racism, sexism or homophobia,” Tomiyama said.

In two related studies, the researchers showed subjects one of two sets of images. Both sets contained photographs of different people — half who were visibly overweight or obese, and half who were normal weight or thin — along with a series of “distractor” objects.

With each image they viewed, participants were asked to smell a container of lotion tinted with a different food coloring. Although all of the “scent samples” were actually fragrance free, the researchers wanted to test whether participants would perceive them to have different smells — and whether their reactions could be associated with the images they were viewing at the same time.

As each image appeared, the experimenter placed the scent sample under the participant’s nose. Participants were instructed to rate each scent of 1 to 11.  The more positive the rating, the more positive the reported smell.

The researchers found that when overweight or obese people were on the screen, participants gave worse ratings to the scent samples. Images of average-sized or thin people tended to trigger higher ratings.

The correlation between visual stimuli and sense of smell is well-established: Previous research has connected the perception of foul odors to feelings of disgust.

“Right now, we only have a couple of ways to measure implicit attitudes, such as an implicit-association test measure,” Incollingo Rodriguez said. “We wanted to see if looking at something you find unappealing or unpleasant could influence how you evaluate a smell that has nothing to do with weight. This shows that something is happening implicitly, and we may have tapped into a new methodology for assessing people.”

She said weight bias can affect people’s everyday lives in many different ways, including how they are treated in social situations, the quality of medical care they receive, and hiring and promotion decisions.

“It also undermines people’s motivation to diet and exercise,” Incollingo Rodriguez said. “If anything, stigma is a barrier to these lifestyle changes that people commonly use to lose weight.”

Weight bias can also affect people’s health, including by increasing their cortisol levels and by causing them to eat more. In 2014, a study by Tomiyama in the journal JAMA Pediatrics showed that simply being called “fat” at age 10 increased a girl’s chances of becoming overweight by the time she turned 19.

“By being aware of our deep-seated attitudes regarding weight, we can begin to change our behavior,” Incollingo Rodriguez said.

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Necklace and smartphone app can help people track food intake


UCLA-developed app could help battle obesity, heart disease and diabetes.

WearSens rests loosely above the sternum and uses highly sensitive sensors to capture vibrations from the action of swallowing.

By Bill Kisliuk, UCLA

A sophisticated necklace developed by researchers at the UCLA Henry Samueli School of Engineering and Applied Science can monitor food and drink intake, which could help wearers track and improve their dietary habits.

The inventors of the WearSens device say it could help battle obesity, heart disease, diabetes and other problems related to nutrition.

Majid Sarrafzadeh, a distinguished professor of computer science and co-director of UCLA’s Wireless Health Institute, led a team that created the device and an algorithm that translates data from the necklace, and tested it on 30 people who ate a variety of foods.

The researchers found that WearSens can differentiate between solids and liquids with 87 percent accuracy, between hot drinks and room-temperature drinks with 90 percent accuracy, and between food items with different textures with 80 percent accuracy. Researchers say those figures will improve as users calibrate the device based on their eating habits.

The research was published online by the IEEE Sensors Journal.

“Today, many people try to track their food intake with journals, but this is often not effective or convenient,” Sarrafzadeh said. “This technology allows individuals and health care professionals to monitor intake with greater accuracy and more immediacy.”

WearSens rests loosely above the sternum and uses highly sensitive piezoelectric sensors to capture vibrations from the action of swallowing. Piezoelectric sensors produce voltage based on the mechanical stress — or movement or pressure — that is applied to them.

When the wearer eats or drinks, skin and muscle motion from the lower trachea trigger the sensors, and the necklace transmits the signals to a smartphone, where the UCLA-developed algorithm converts the data into information about the food or beverage. The phone displays data about the volume of food or liquid consumed and can offer advice or analysis; for example, that the wearer is eating more than in previous days or that the person should drink more water.

With the WearSens device, the sensor information is translated using a spectrogram, which offers a visual representation of vibrations picked up by the sensors. Spectrograms are often used in speech therapy and seismology, among other applications.

“The breakthroughs are in the design of the necklace, which is simple and does not interfere with daily activity, and in identifying statistical measures that distinguish food intake based on spectrogram images generated from piezoelectric sensor signals,” said Nabil Alshurafa, a graduate student researcher at UCLA who is a co-inventor of the device and the first author of the research.

The study’s other authors are co-inventor Haik Kalantarian, a graduate student researcher; Shruti Sarin and Behnam Shahbazi, also graduate student researchers; Jason Liu, who was a UCLA graduate student at the time he worked on the research; and postdoctoral researcher Mohammad Pourhomayoun.

The team is continuing to refine the algorithms and the necklace’s design. The researchers hope WearSens will be available to the public later this year.

The technology is available for licensing via the UCLA Office of Intellectual Property and Industry-Sponsored Research, which facilitates the conversion of UCLA research to benefit the public.

The research was supported by the National Science Foundation.

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Partnership to broaden fitness opportunities for Los Angeles adolescents


UCLA Health System partners with Sound Body Sound Mind Foundation.

Students at East Valley High School workout on new equipment that was provided as part of a new program called UCLA Health Sound Body Sound Mind. (Photo by WorldWise Productions)

By Roxanne Moster, UCLA

UCLA Health System and the Sound Body Sound Mind Foundation have formed a partnership to provide practical ways to combat childhood obesity and promote healthy lifestyles in Los Angeles. The new entity, UCLA Health Sound Body Sound Mind, funded by a $3 million pledge from Sound Body Sound Mind, will replicate the foundation’s existing program model.

The announcement was made today at North Hollywood’s East Valley High School during the unveiling of a new, state-of-the art fitness center provided by UCLA Health Sound Body Sound Mind.

“We are proud to establish UCLA Health Sound Body Sound Mind as a means of strengthening preventive health solutions for middle school and high school students,” said Dr. David Feinberg, president of the UCLA Health System. “By encouraging students to embrace fitness in their adolescent years, we intend to address bad habits and inactivity before they become an integral part of their lives.”

“Our ultimate goal is to ensure that every student has the opportunity, knowledge and tools to pursue a healthy lifestyle through physical fitness,” said Bill Simon, co-founder of Sound Body Sound Mind. “Our collaboration with UCLA Health System will allow us access to their world-renowned resources and personnel. Ultimately, we believe this partnership will allow us to reach our goals faster and more effectively as we bring to bear the experience of both our organizations on this challenge.”

UCLA Health Sound Body Sound Mind will provide under-resourced schools with commercial-grade fitness equipment and an innovative curriculum designed to build students’ competence and confidence in a range of physical activities. The $3 million gift will enable UCLA Health System to expand its preventive care solutions among the city’s most vulnerable adolescent populations. The project exemplifies UCLA Health System’s commitment to community engagement.

Anastasia Loukaitou-Sideris, a UCLA professor of urban planning and associate dean of the Luskin School of Public Affairs, also has collaborated with the Robert F. Kennedy Community Schools to evaluate the effectiveness of the Sound Body Sound Mind curriculum and find ways to improve community health through additional research and publications.

According to the Los Angeles County Department of Public Health, 42 percent of children in L.A. County are overweight or obese and therefore have a higher risk for serious chronic health problems. More than one-third of children and adolescents were overweight or obese, according to a 2012 study by the Children’s Defense Fund.

UCLA Health Sound Body Sound Mind will give students the tools they need to take charge of their health by ensuring that they have access to fitness resources.

“Our population-based approach identifies and focuses on low-socioeconomic schools and formulates the best physical fitness resources for each school,” said Nathan Nambiar, executive director of the Sound Body Sound Mind Foundation. “This program will help to improve the health of thousands of young Angelenos, and over the long term it may drive down health care costs and help boost economic productivity.”

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Obesity poses serious health risks for moms and their babies


‘Eating for two’ no longer holds weight.

By Shari Roan, U Magazine

Veronica Romero was 21 years old and worried. Pregnant with her first child, she was putting on a lot of weight. Her obstetrician leveled with her: “You’re gaining too much.” But as she approached 50 pounds of weight gain near the end of her pregnancy, Romero felt helpless.

“I tried to watch what I was eating, but it was so hard. Pregnant women get cravings, and my cravings were sugary,” she recalled.

“I tried to eat carrots and small appetizers, but it didn’t work. I was disappointed. I didn’t want to get bigger.” The pregnancy set into motion a health crisis on two fronts: for Romero, now 38, and her son, Anthony, now 17. Romero eventually grew to nearly 300 pounds, and Anthony became a big baby, then a chubby toddler and now an obese adolescent.

This mother-child pair is not unique. The obesity tsunami that has washed across the United States over the past four decades has swept up pregnant women and their offspring too. In fact, pregnant women today are considered by some medical authorities to be at the nexus of the obesity crisis. Abundant research has revealed that pregnancy is a key period of increased risk for developing obesity in women and that obesity in pregnancy may genetically “program” offspring to become overweight or obese later in life.

The concept, commonly known as fetal programming, is rapidly altering the fields of obstetrics and pediatrics, said Dr. Sherin Devaskar, Mattel Executive Endowed Chair of the Department of Pediatrics, physician-in-chief of Mattel Children’s Hospital UCLA and assistant vice chancellor of children’s health. “There have been many studies to prove beyond a doubt that fetal programming is real. If a mother is obese, her babies are at very high risk for obesity and chronic disease.”

In the United States, more than half of all pregnant women are overweight or obese, according to the American College of Obstetricians and Gynecologists. An estimated 9 percent of babies are born macrosomic — weighing too much for their gestational age. Fetal macrosomia is typically defined as a birth weight of more than 9 pounds, 15 ounces, regardless of gestational age.

However, obesity in pregnancy can also result in babies who are born prematurely or underweight. These infants also seem to be predisposed to obesity and related diseases, such as diabetes and heart disease, later in life, Devaskar explained.

More than three decades ago, Dr. David Barker, a British physician and epidemiologist, linked birth weight, either excessively high or low, to a heightened risk of heart disease, type 2 diabetes and obesity in offspring. He posited that these diseases had their roots, at least in part, in under- or over-nutrition during pregnancy. If a pregnant woman is under-nourished, her infant is prone to low birth weight with a rapid “catch-up” gain in body fat later when exposed to plentiful food. If a pregnant woman is over-nourished, her infant is prone to high birth weight and a booming growth trajectory that increases the risk of obesity later in life.

The amount of nutrients provided to a developing fetus, as well as the type of nutrients, appears to chemically modify genes that predispose a child to obesity and obesity-related diseases, said  Devaskar, whose own research on the subject resulted in her election to the prestigious Institute of Medicine in 2012. Her current research focuses on whether or not it’s possible to further modify those genes to reverse the propensity to gain weight. “In the fetus, the organs are still developing,” she explained. “It’s a critical window of development, and it’s very plastic at that time. Any insult — whether it’s from diet, drugs or toxins — creates a permanent mark that lasts for one’s lifetime. The hypothalamus — the part of the brain governing metabolism and hunger — is already programmed. The infant is used to seeing so much nutrition coming from the mother. These children are ever-hungry; they are born hypersensitive to high-calorie foods. Their insulin sensitivity is low, so they are at high risk for developing diabetes, obesity and heart disease.”

In 2009, the Institute of Medicine issued revolutionary new guidelines to begin to address obesity in pregnancy. The group put tighter limits on weight gain in pregnancy, warning doctors to help their patients stay within a healthy range and even strictly limit weight gain in obese pregnant women to 11 to 20 pounds.

“It’s a major change,” said Dr. Aisling Murphy, assistant professor in the Division of Maternal-Fetal Medicine. “More recent data have suggested that obese women really don’t need to be gaining as much weight as women who enter pregnancy at a normal weight.”

Moreover, doctors are encouraging pregnant women to exercise — something many women had been fearful of doing. “Sometimes, women are under the impression that they shouldn’t be walking or going to the gym when they are pregnant. That is not the case,” Murphy said. “They really should be active.”

In addition to the risk of fetal programming, obesity during pregnancy is linked to several other potential complications. The chances of developing both hypertension and gestational diabetes are higher in pregnant women who are obese. About 7 percent of pregnant women in the United States develop gestational diabetes. Studies show that these women have an increased likelihood of developing type 2 diabetes later in life. In essence, gestational diabetes often isn’t a “temporary” condition that goes away after childbirth.

Obesity during pregnancy also raises the risk of some types of birth defects and other complications, such as an increased risk of Cesarean section or complications during childbirth, Murphy noted.

While two decades ago, few pregnant women were given extra resources and support they needed to manage weight gain, overweight or obese women who are planning to have children are now encouraged to seek pre-conception counseling, where they are given advice and resources to help them lose weight before becoming pregnant. And pregnant women who are obese are typically referred to a registered dietician for assistance with a healthy diet. Breastfeeding for at least six months is highly recommended to help the mother lose weight.

“If we can take care of young women before pregnancy and during pregnancy, we will end up with a healthier society, and it will bring down health care costs dramatically,” Dr. Devaskar said.

Read the complete story in the latest issue of U Magazine.

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UCSF researchers redefine role of brain’s ‘hunger circuit’


Unexpected findings have implications for anti-obesity therapies.

By Pete Farley, UC San Francisco

Using techniques developed only over the past few years, UC San Francisco researchers have completed experiments that overturn the scientific consensus on how the brain’s “hunger circuit” governs eating.

Because of this circuit’s potential role in obesity, it has been extensively studied by neuroscientists and has attracted intense interest among pharmaceutical companies. According to the UCSF scientists, their unexpected new findings could reshape basic research on feeding behavior as well as strategies for the development of new anti-obesity drugs.

Scientists have generally believed that the hunger circuit, made up of two groups of cells known as AgRP and POMC neurons, senses long-term changes in the body’s hormone and nutrient levels, and that the activation of AgRP neurons directly drives eating. But the new work shows that the AgRP-POMC circuit responds within seconds to the mere presence of food, and that AgRP neurons motivate animals to seek and obtain food, rather than directly prompting them to consume it.

“No one would have predicted this. It’s one of the most surprising results in the field in a long time,” said Zachary Knight, Ph.D., assistant professor of physiology at UCSF. “These findings really change our view of what this region of the brain is doing.”

It has been known for 75 years that a region at the base of the brain called the hypothalamus exerts profound control over eating behavior. As neuroscientists refined this observation over the ensuing decades, they zeroed in first on a small area of the hypothalamus known as the arcuate nucleus, and more recently on AgRP and POMC neurons, two small populations of cells within that nucleus.

These two groups of cells, which collectively occupy an area smaller than a millimeter in the mouse brain, are functionally organized in a seesaw-like fashion: when AgRP neurons are active, POMC neurons are not, and vice versa.

Hundreds of experiments in which scientists added hormones or nutrients to brain slices while recording the activity of AgRP and POMC neurons have laid the foundation of the dominant model of how the hunger circuit works. As we grow hungry, this view holds, gradual changes in hormone levels send signals that begin to trigger AgRP neurons, the activity of which eventually drives us to eat. As we become sated, circulating nutrients such as glucose activate POMC neurons, which suppresses the desire to eat more food.

Yiming Chen, a graduate student in Knight’s lab, was expecting to build on the prevailing model of the hunger circuit when he began experiments using newly developed fiber optic devices that allowed him to record AgRP-POMC activity in real time as mice were given food after a period of fasting. “No one had actually recorded the activity of these neurons in a behaving mouse, because the cells in this region are incredibly heterogeneous and located deep within the brain,” said Chen. “The technology to do this experiment has only existed for a few years.”

But as reported in the Feb. 19 online issue of Cell, just seconds after food was given to the mice, and before they had begun to eat, Chen saw AgRP activity begin to plummet, and POMC activity correspondingly begin to rise.

“Our prediction was that if we gave a hungry mouse some food, then slowly, over many minutes, it would become satiated and we would see these neurons slowly change their activity,” Knight said. “What we found instead was very surprising. If you simply give food to the mouse, almost immediately the neurons reversed their activation state. This happens when the mouse first sees and smells the food, before they even take a bite.”

The researchers found that the AgRP-POMC circuit could be quickly “reset,” with POMC cell activity dampened and AgRP neurons again beginning to fire, if the food were taken away. The magnitude of the transition from AgRP to POMC activity was also directly correlated with the palatability of the food offered: peanut butter and chocolate, both of which are much preferred by mice over standard lab chow, caused a stronger and more rapid reversal of AgRP-POMC activity. The AgRP-POMC responses also depended on the accessibility of the food. A slower and weaker transition was seen if the mice were able to detect the presence of peanut butter through smell, but couldn’t see the food.

These results show that, while slow, hunger-induced changes in hormones and nutrients activate AgRP neurons over the long term, these neurons are rapidly inactivated by the sight and smell of food alone. A major implication of this discovery, Knight and Chen said, is that the function of AgRP neurons is to motivate hungry animals to seek and find food, not to directly control eating behavior itself.

The fact that more accessible and more palatable, energy-rich foods engage POMC neurons and shut down AgRP activity more strongly suggests that the circuit also has “anticipatory” aspects, by which these neurons predict the nutritional value of a forthcoming meal and adjust their activity accordingly.

Both of these roles of the AgRP-POMC circuit make sense, said the researchers: if an animal has successfully obtained food, the most adaptive brain mechanism would suppress the motivation to continue searching; likewise, since energy-dense foods alleviate hunger for longer periods, discovery of these foods should more strongly tamp down the hunger circuit and the desire to seek additional nutrition.

“Evolution has made these neurons a key control point in the hunger circuit, but it’s primarily to control the discovery of food,” said Knight. “It’s controlling the motivation to go out and find food, not the intake of food itself.”

So far, clinical trials of drugs that target AgRP-related pathways have been disappointing, Knight said, and he believes the new research may provide a new perspective on these efforts. “What probably drives obesity is the rewarding aspect of food. When you want dessert after you’ve finished dinner, it’s because it tastes good, and that doesn’t require hunger at all,” Knight said. “Finding that this circuitry primarily controls food discovery rather than eating changes our view of what we might be manipulating with drugs targeting AgRP pathways. We might be manipulating the decision to go to the grocery store, not necessarily the decision to take the next bite of food.”

Other members of the Knight laboratory participating in the research were Yen-Chu Lin, research specialist, and graduate student Tzu-Wei Kuo. The research was supported by the New York Stem Cell Foundation, the Rita Allen Foundation, the McKnight Foundation, the Alfred P. Sloan Foundation, a NARSAD Young Investigator Grant from the Brain and Behavior Research Foundation, the Esther A. and Joseph Klingenstein Foundation, the Program for Breakthrough Biomedical Research, the UCSF Diabetes Center Obesity Pilot Program, and the National Institutes of Health.

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Molecular link between obesity, type 2 diabetes reveals potential therapy


UC San Diego researchers find that inflammatory molecule LTB4 promotes insulin resistance.

By Heather Buschman, UC San Diego

Obesity causes inflammation, which can in turn lead to type 2 diabetes. What isn’t well established is how inflammation causes diabetes — or what we can do to stop it. Researchers at the UC San Diego School of Medicine have discovered that the inflammatory molecule LTB4 promotes insulin resistance, a first step in developing type 2 diabetes. What’s more, the team found that genetically removing the cell receptor that responds to LTB4, or blocking it with a drug, improves insulin sensitivity in obese mice. The study is published today (Feb. 23) by Nature Medicine.

“This study is important because it reveals a root cause of type 2 diabetes,” said Jerrold M. Olefsky, M.D., professor of medicine, associate dean for scientific affairs and senior author of the study. “And now that we understand that LTB4 is the inflammatory factor causing insulin resistance, we can inhibit it to break the link between obesity and diabetes.”

Here’s what’s happening in obesity, according to Olefsky’s study. Extra fat, particularly in the liver, activates resident macrophages, the immune cells living there. These macrophages then do what they’re supposed to do when activated — release LTB4 and other immune signaling molecules to call up an influx of new macrophages. Then, in a positive feedback loop, the newly arriving macrophages also get activated and release even more LTB4 in the liver.

This inflammatory response would be a good thing if the body was fighting off an infection. But when inflammation is chronic, as is the case in obesity, all of this extra LTB4 starts activating other cells, too. Like macrophages, nearby liver, fat and muscle cells also have LTB4 receptors on their cell surfaces and are activated when LTB4 binds them. Now, in obesity, those cells become inflamed as well, rendering them resistant to insulin.

Once Olefsky and his team had established this mechanism in their obese mouse models, they looked for ways to inhibit it. First, they genetically engineered mice that lack the LBT4 receptor. When that approach dramatically improved the metabolic health of obese mice, they also tried blocking the receptor with a small molecule inhibitor. This particular compound was at one time being tested in clinical trials, but was dropped when it didn’t prove all that effective in treating its intended ailment. Olefsky’s team fed the prototype drug to their mice and found that it worked just as well as genetic deletion at preventing — and reversing — insulin resistance.

“When we disrupted the LTB4-induced inflammation cycle either through genetics or a drug, it had a beautiful effect — we saw improved metabolism and insulin sensitivity in our mice,” Olefsky said. “Even though they were still obese, they were in much better shape.”

Co-authors of this study include Pingping Li, Da Young Oh, Gautam Bandyopadhyay, William S. Lagakos, Saswata Talukdar, Olivia Osborn, Andrew Johnson, Heekyung Chung, Rafael Mayoral, Michael Maris, Jachelle M Ofrecio, Sayaka Taguchi, Min Lu, all at UC San Diego.

This research was funded, in part, by the National Institute of Diabetes and Digestive and Kidney Diseases (DK033651, DK074868, DK063491, DK09062), the Eunice Kennedy Shriver National Institute of Child Health and Human Development, and Merck Inc.

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Study taps into healthy drink choices


Low-quality water in rural immigrant communities could be prompting kids to drink sugary beverages.

The water study is part of a five-year project investigating whether community-based intervention can help prevent childhood obesity.

By Jeannette Warnert, ANR

Having established a link between obesity and sugary beverages, doctors and nutritionists recommend that children instead drink plain tap water. In virtually all of the United States and California, tap water is the best drink available for good health.

However, a team of UC Cooperative Extension and UC Davis scientists have found that low-quality tap water in some rural immigrant communities could be an obstacle to making this healthy dietary change.

The study was conducted in conjunction with a five-year research and outreach project underway in Firebaugh and San Joaquin, small communities in the San Joaquin Valley with high Mexican-American populations. The researchers are investigating whether a community-based intervention – involving nutrition education, a monthly voucher of $25 to purchase fruit and vegetables, and a physical activity program – can help prevent childhood obesity in Californians of Mexican descent living in low-income rural communities. UC Agriculture and Natural Resources and UC Davis were recipients of a $4.8 million National Institute for Food and Agriculture grant to carry out this research.

Twenty-seven mothers in the study shared with the researchers whether they use tap water and gave their perceptions of tap water quality. In addition, the researchers assessed local water quality by the frequency of violations reported by Cal EPA and contaminant-level data from the California Department of Public Health.

Contamination concerns

All 27 mothers said they avoid drinking tap water due to unpleasant taste, dirty or yellow appearance, excessive iron or general “contamination.” Most of the women rely instead on bottled, and to a lesser extent, home filtered water for drinking and cooking.

“This cost is an extra burden for these families, many of whom have limited incomes,” said Lucia Kaiser, UC Cooperative Extension specialist in the Department of Nutrition at UC Davis.

The mothers shared in interviews that at least 38 percent of their children aged 3 to 8 years old drank sugar-sweetened beverages – such as soda, energy drinks, powered drink mixes or fruit punch – more than two or three times per week.

“The children may be drinking sugar-sweetened beverages so frequently because of real or perceived low quality of water coming from their taps,” Kaiser said. “I’m not surprised. One time I was in our Firebaugh office and turned on the tap and the water came out brown. “

Two state-regulated water systems serve the majority of people in Firebaugh and San Joaquin. The rest rely on at least 11 small public or private systems. All of the 13 systems have had monitoring violations in the last 12 years. Two have had reporting violations, indicating that they either did not test for contaminants or did not report their findings.

Seeking solutions

The mothers’ perception that tap water was unappealing or contaminated was confirmed when the researchers took a close look at regulatory analyses reports from previous years. There were low-levels of arsenic detected, which fell above the benchmark for safe drinking water in the U.S. The analyses also detected high levels of manganese and iron, which are considered secondary contaminants and do not have enforceable limits set by the EPA. However, the World Health Organization has set health benchmarks for manganese, which were exceeded in some samples.

“The neurotoxic effects of manganese and chronic exposure to low levels of arsenic warrant further study,” Kaiser said. “Even if it’s not dangerous, the high level of manganese and iron can give the water an off taste.”

Regardless, removing the contaminants may not matter if perceptions and drinkability are not improved. A possible solution is better communication.

“A simple step could be sending easy-to-understand water quality reports to all residents,” Kaiser said. “Sending reports to renters in addition to property owners and in Spanish as well as English will help raise awareness about the safety of local tap water.”

The study was funded in part by the UC Davis Center for Poverty Research, which developed a two-page policy brief outlining the research findings. UC Davis doctoral student Caitlin French was the main author. Other contributors, in addition to Kaiser, were postdoctoral researcher Rosa Gomez-Camacho, UC Cooperative Extension nutrition, family and consumer sciences advisor Cathi Lamp and UC Davis nutrition professor Adela de la Torre.

In the policy brief, the authors included some additional suggestions to address the issue:

  • Increase state funds to agencies working to identify who is at risk in order to bring more water systems into compliance
  • Provide subsidies for home water filters
  • Provide subsidies to private well owners in exchange for testing reports
  • Step up outreach to owners of targeted private water systems in known problem areas
  • Provide funding for additional research to inform outreach messages about substituting tap water for sugar-sweetened beverages

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Researchers find novel signaling pathway involved in appetite control


Study could lead to new treatments for obesity.

By Tim Stephens, UC Santa Cruz

A new study has revealed important details of a molecular signaling system in the brain that is involved in the control of body weight and metabolism. The study, published today (Jan. 19) in Nature, provides a new understanding of the melanocortin pathway and could lead to new treatments for obesity.

Co-author Glenn Millhauser, a distinguished professor of chemistry and biochemistry at UC Santa Cruz, said the findings are very exciting and have broad biomedical implications. “We are getting to the real molecular features of what’s controlling this important signaling system in the brain,” Millhauser said.

The study, led by researchers at Vanderbilt University, focused on a receptor embedded in the membranes of nerve cells called the melanocortin-4 receptor, or MC4R. It belongs to a class of receptors known as G-protein coupled receptors (GPCRs), which typically act like on-off switches, signaling over short time frames, according to Roger Cone, who led the study at Vanderbilt.

“This finding identifies a molecular mechanism for converting an on-off switch into a rheostat,” Cone said. “This could help explain slow, sustained biological processes that also are mediated by GPCRs, such as tanning or weight regain after dieting.”

Millhauser’s lab has done extensive research on proteins that bind to the MC4R receptor, such as agouti-related protein (AgRP). AgRP is a potent appetite stimulant. Its role in regulating energy balance is to suppress metabolism and increase feeding when the body needs to put on weight and store energy, Millhauser said. His lab has developed modified versions of the AgRP protein that alter its activity. In the new study, the modified proteins from Millhauser’s lab helped researchers identify a previously unsuspected effect of AgRP.

Millhauser’s previous studies have shown that a single dose of AgRP given to laboratory animals can stimulate daily food intake for up to 10 days. This observation didn’t fit with the traditional “on-off” signaling model for the receptor it binds to, MC4R. G-protein coupled receptors can only take so much stimulation before they shut down, and this phenomenon, called desensitization, often happens rapidly.

Cone’s lab discovered a companion protein — a potassium channel in the membrane called Kir7.1 — that couples to the MC4R receptor and acts independently from G-protein signaling. The researchers found that AgRP induces MC4R to open the potassium channel, which “hyperpolarizes” and inhibits neurons that are involved in blocking appetite.

“Moreover, with modifications to AgRP discovered previously by our lab, we can increase or decrease this coupling of the receptor to the potassium channel,” Millhauser said. “These concepts could ultimately lead to new generations of therapeutics for treating metabolic disorders, including obesity, anorexia, and cachexia, the wasting condition that often occurs in cancer treatment.”

Co-author Rafael Palomino, a graduate student and NIH Fellow in Millhauser’s lab, did the protein synthesis and purification work for the study. The first author is Masoud Ghamari-Langroudi at Vanderbilt. Other contributors include Jerod Denton and Robert Matthews at Vanderbilt and Helen Cox at King’s College, London. This research was supported by the National Institutes of Health.

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Cooler temperatures may trigger body’s energy-burning brown fat


Study sheds light on type of fat that has drawn increased attention from researchers.

By Sarah Yang, UC Berkeley

Those who overindulged during the holidays may want to get a shot of cold air to kick-start some extra fat-burning activity for the new year.

Researchers at UC Berkeley found that exposure to cold temperatures increases levels of a newly discovered protein that is critical for the formation of brown fat, the type of fat in our bodies that generates heat. With extended exposure to chilly air, the protein, called transcription factor Zfp516, also helps the more abundant white fat in our bodies – the kind that stores excess energy – become more similar to brown fat in its ability to burn energy.

The researchers found that mice with boosted levels of the Zfp516 protein gained 30 percent less weight than control mice when both groups were fed a high-fat diet.

The new findings, published online today in the journal Molecular Cell, shed light on a type of fat that has drawn increased attention from researchers in the past five years.

“Knowing which proteins regulate brown fat is significant because brown fat is not only important for thermogenesis, but there is evidence that brown fat may also affect metabolism and insulin resistance,” said principal investigator Hei Sook Sul, UC Berkeley professor of nutritional science and toxicology. “If you can somehow increase levels of this protein through drugs, you could have more brown fat, and could possibly lose more weight even if eating the same amount of food.”

White fat, brown fat, good fat, bad fat

Unlike white fat, which stores excess energy, brown fat burns energy to keep us warm. Brown fat gets its hue from relatively high levels of mitochondria, the cell’s power station. In humans, brown fat was thought to be present only in infants, but stores of it were recently discovered in adults around such vital areas as the heart, brain, neck and spinal cord.

The study authors said that because we generally live our lives in controlled, ambient temperatures, our need for brown fat has decreased over time.

“It has been noted that outdoor workers in northern Finland who are exposed to cold temperature have a significant amount of brown fat when compared to same-aged indoor workers, but overall, the percentage of brown fat in adults is small compared to white fat,” said Sul. “We also know that obese people have lower levels of brown fat.”

The UC Berkeley team discovered that the Zfp516 protein activates uncoupling protein 1 (UCP1), found only in the mitochondria of brown fat and involved in the generation of heat.

“The amount of UCP1 produced by brown-like fat cells will be lower than that of classical brown fat, but since 90 percent of the fat in our bodies consists of white fat, finding a way to make that tissue more brown-like could have a significant impact,” said Sul.

Making white fat into brown-like fat

When the researchers disabled the gene for Zfp516 in mouse embryos, the embryos did not develop any brown fat. In another experiment, researchers found that mice with higher levels of Zfp516 protein were able to convert more white fat tissue into brown-like fat when exposed to cold air. After four hours in a room kept at 4 degrees Celsius (39.2 degrees Fahrenheit), the body temperature of the mice with the overexpressed Zfp516 protein was, on average, 1 degree Celsius (1.8 degrees Fahrenheit) higher than a control group of mice with normal levels of the protein.

“That difference in body temperature is huge for the mice,” said study co-lead author Jon Dempersmier, a Ph.D. student in nutritional science and toxicology. “The brown-like fat, the kind converted from white fat tissue, is inducible by cold. Classical brown fat, the kind in babies and prevalent in rodents, always has a ton of UCP1 and mitochondria in order to perform thermogenesis.”

The mice with overexpressed Zfp516 protein also gained less weight than their unaltered littermates after both groups ate a high-fat diet for four weeks.

“This suggests that the transgenic mice were protected from diet-induced obesity,” said Sul. “This protein could become an important target for research into the treatment and prevention of obesity and obesity-related diseases.”

The study authors noted that there’s an active area of research in the relationship between brown fat and diabetes. Higher levels of brown fat are associated with greater sensitivity to insulin. Resistance to insulin leads to Type 2 diabetes.

The researchers noted that there are many steps between discovering the protein in mice and determining whether it can be useful in humans, but they said that having a clear target is an important development.

“Brown fat is active, using up calories to keep the body warm,” said Dempersmier. “It’ll burn fat, it’ll burn glucose. So the idea is that if we can harness this, we can try to use this in therapy for weight loss and for diabetes.”

The National Institutes of Health helped support this research.

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Immune cells in brain respond to fat in diet, causing mice to eat


UCSF study indicates that microglia may play key role in shaping the brain’s response to diet.

By Jeffrey Norris, UC San Francisco

Immune cells perform a previously unsuspected role in the brain that may contribute to obesity, according to a new study by UC San Francisco researchers.

When the researchers fed mice a diet high in saturated milk fats, microglia, a type of immune cell, underwent a population explosion in the brain region called the hypothalamus, which is responsible for feeding behavior.

The researchers used an experimental drug and, alternatively, a genetic approach to knock out these microglia, and both strategies resulted in a complete loss of microglia-driven inflammation in the hypothalamus. Remarkably, doing so also resulted in the mice eating less food each day than did their untreated counterparts, without any apparent ill effects.

Furthermore, removing microglia from mice only reduced food intake when the content of saturated fat from milk in their diets was high. It had no effect on mice fed a low-fat diet or a diet high in other types of fat, including olive oil or coconut oil.

UCSF postdoctoral fellow Martin Valdearcos Contreras, Ph.D., first author on the paper, published in the Dec. 11 issue of Cell Reports, discovered that when mice consumed large amounts of saturated fats, the fat entered their brains and accumulated in the hypothalamus.

According to the senior scientist for the study, Suneil Koliwad, M.D., Ph.D., an assistant professor of medicine at the UCSF Diabetes Center, the microglia sense the saturated fat and send instructions to brain circuits in the hypothalamus. These instructions are important drivers of food intake, he said.

Microglia are primarily known for causing inflammation in the brain in response to infection or injury, but the new study indicates that they also play a key role in shaping the brain’s response to diet, according to Koliwad.

Outside the brain — in fat tissue, the liver, and muscles — other immune cells, called macrophages, trigger inflammation in response to “diet-induced obesity,” Koliwad said. This inflammation is implicated in triggering insulin resistance, a late stage event on the road to type 2 diabetes.

However, overeating causes microglia to accumulate much more quickly in the hypothalamus than macrophages accumulate in peripheral tissues, Koliwad said. But until now, the effects of this microglial build-up were unknown.

“As opposed to classically defined inflammation, in which immune cells build up in tissues where environmental insults have created disarray, microglial activation in the brain may be a part of a normal physiological process to remodel brain function in response to changes in the composition of food intake,” Koliwad said.

“When the intake of saturated fats is chronically high, this microglial sensory network may be hijacked, and this has the potential to mediate increased food consumption and promote more rapid weight gain.

“Targeting microglia may therefore be a novel way to control food intake in the face of consumption of a fat-rich diet, something that is quite common in today’s world,” he said.

The research was funded by the National Institutes of Health and by the UCSF Diabetes Family Fund.

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Obese children’s brains are more responsive to sugar


UC San Diego study detects brain differences in children as young as 8.

By Christina Johnson, UC San Diego

A new study led by researchers at the UC San Diego School of Medicine finds that the brains of obese children literally light up differently when tasting sugar.

Published online in International Journal of Obesity, the study does not show a causal relationship between sugar hypersensitivity and overeating, but it does support the idea that the growing number of America’s obese youth may have a heightened psychological reward response to food.

This elevated sense of “food reward” – which involves being motivated by food and deriving a good feeling from it – could mean some children have brain circuitries that predispose them to crave more sugar throughout life.

“The take-home message is that obese children, compared to healthy weight children, have enhanced responses in their brain to sugar,” said first author Kerri Boutelle, Ph.D., professor in the Department of Psychiatry and founder of the university’s Center for Healthy Eating and Activity Research (CHEAR).

“That we can detect these brain differences in children as young as 8 years old is the most remarkable and clinically significant part of the study,” she said.

For the study, the UC San Diego team scanned the brains of 23 children, ranging in age from 8 to 12, while they tasted one-fifth of a teaspoon of water mixed with sucrose (table sugar). The children were directed to swirl the sugar-water mix in the mouth with their eyes closed, while focusing on its taste.

Ten of the children were obese and 13 had healthy weights, as classified by their body mass indices. All had been pre-screened for factors that could confound the results. For example, they were all right-handed and none suffered from psychiatric disorders, such as anxiety or ADHD. They also all liked the taste of sucrose.

The brain images showed that obese children had heightened activity in the insular cortex and amygdala, regions of the brain involved in perception, emotion, awareness, taste, motivation and reward.

Notably, the obese children did not show any heightened neuronal activity in a third area of the brain – the striatum – that is also part of the response-reward circuitry and whose activity has, in other studies, been associated with obesity in adults.

The striatum, however, does not develop fully until adolescence. The researchers said one of the interesting aspects of the study is that the brain scans may be documenting, for the first time, the early development of the food reward circuitry in pre-adolescents.

“Any obesity expert will tell you that losing weight is hard and that the battle has to be won on the prevention side,” said Boutelle, who is also a clinical psychologist. “The study is a wake-up call that prevention has to start very early because some children may be born with a hypersensitivity to food rewards or they may be able to learn a relationship between food and feeling better faster than other children.”

According to studies, children who are obese have an 80 to 90 percent chance of growing up to become obese adults. Currently about one in three children in the U.S. is overweight or obese.

To learn more CHEAR and its weight management programs for children, call (855) 827-3498 or email chear@ucsd.edu.

Co-authors include Christina Wierenga, UC San Diego and Veterans Affairs San Diego Healthcare System; Amanda Bischoff-Grethe, Andrew James Melrose and Emily Grenesko-Stevens, UC San Diego; and Martin Paulus, Laureate Institute for Brain Research, Tulsa, Oklahoma.

Funding for the study was provided, in part, by National Institutes of Health (grants R01DK094475, R01 DK075861, K02HL112042, MH046001, MH042984, MH066122, MH001894 and MH092793).

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Related link:
UCSF sugar science initiative launched

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Cloudy water, even if it is safe, affects rural immigrants’ health


UC Davis researchers examine connection between water quality, childhood obesity.

Cloudy tap water may have a greater effect for California’s rural immigrants than merely leaving behind a bad taste, according to a new policy brief released by the Center for Poverty Research at the University of California, Davis.

Researchers looked at the connection between water quality and childhood obesity in two poor immigrant communities in California’s Central Valley — San Joaquin and Firebaugh. Poor-quality tap water, or even a perception that the water is bad, combined with environmental factors such as lack of access to healthy foods and nutrition education, likely contribute to health disparities in these communities, the study finds.

“If the tap water that comes out looks dirty or has a poor taste, they’re not going to have a lot more confidence in the drinking system here,” said Lucia Kaiser, a UC Cooperative Extension specialist in the Department of Nutrition at UC Davis and the study’s co-principal investigator. “The immigrant populations in these communities come from Mexico, where they may have experienced unsafe drinking water in rural areas,” she said.

Kaiser interviewed 27 mothers from these communities after giving a class on the health effects of sugar-sweetened beverages. Most of the women reported relying on purchased and, to a lesser extent, home-filtered water for drinking and cooking. Kaiser said that the additional cost represents an extra burden on these low-income families.

“In these communities, more than a third can’t afford to put enough food on their table, and now they have to buy drinking water, too. Every expense really matters,” said Kaiser.

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