The number of people affected by dementia worldwide is estimated to double over the next 20 years from the current number of about 36 million people, the authors provide as background information in the article. AD is the most common form of dementia. The authors write that data suggest an association between insulin resistance and inflammation, hallmarks for type 2 diabetes, and development of dementia. “An additional potential factor that may contribute to the onset of AD and all-cause dementia is adiponectin. Adiponectin is a hormone derived from visceral fat, which sensitizes the body to insulin, has anti-inflammatory properties, and plays a role in the metabolism of glucose and lipids.”

Thomas M. van Himbergen, Ph.D., from the Lipid Metabolism Laboratory, Human Nutrition Research Center on Aging, Tufts University, Boston, and colleagues measured levels of glucose, insulin, and glycated albumin, as well as C reactive protein, lipoprotein associated phospholipase A2, and adiponectin in the plasma of patients at the 19th biennial examination (1985 – 1988) of the Framingham Heart Study.

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Study finds another potential risk factor for developing dementia and Alzheimer’s disease in women

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“The brain is the body’s only organ that needs a constant supply of glucose to survive, so it makes sense that it would have some say over how much glucose is produced,” said study leader Meredith Hawkins, M.D., professor of medicine and director of the Global Diabetes Initiative at Einstein. “This role for the brain was demonstrated in earlier Einstein studies in rodents, but there was considerable controversy over whether the results could be applied to humans. We hope this study helps to settle the matter.”

In an earlier study in rodents, Einstein researchers showed that activation of potassium channels in the brain’s hypothalamus sends signals to the liver that dampen its production of glucose. Those findings, published in Nature in 2005, challenged the conventional thinking that blood sugar production by the liver (the body’s glucose factory) is regulated only by the pancreas (which makes insulin to metabolize glucose). But carefully performed studies on dogs, conducted at Vanderbilt University, failed to replicate the results, suggesting the Einstein findings in rodents might not be relevant to higher mammals, including humans.

The current Einstein study, involving people, was aimed at resolving this controversy. Ten nondiabetic subjects were given oral diazoxide, a drug that activates potassium channels in the hypothalamus. (The drug is not used to treat diabetes.) Hormone secretion by the pancreas was controlled to ensure that any change in sugar production would only have occurred through the drug’s effect on the brain. After the researchers administered the drug, blood tests revealed that patients’ livers were producing significantly less glucose than before.

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Einstein study indicates brain plays role in regulating blood sugar in humans

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The research, led by Umut Ozcan, MD, in the Division of Endocrinology at Children’s, is reported in the October issue of Nature Medicine, published online September 4.

“This finding is completely contrary to the general dogma in the diabetes field that low-grade inflammation in obesity causes insulin resistance and type 2 diabetes,” says Ozcan. “For 20 years, this inflammation has been seen as detrimental, whereas it is actually beneficial.”

Ozcan’s team previously showed that obesity places stress on the endoplasmic reticulum (ER), a structure in the cell where proteins are assembled, folded and dispatched to do jobs for the cell. This so-called “ER stress” impairs the body’s response to insulin in maintaining appropriate blood glucose levels, and is a key link between obesity and type 2 diabetes. Last year, Ozcan and colleagues showed that a protein that relieves ER stress, called XBP1s, cannot function in obese mice. Earlier this year, they showed that activating XBP1s artificially in the liver normalized high blood sugar in obese, insulin-resistant type 2 diabetic mice (as well as lean, insulin-deficient type 1 diabetic mice).

The new study shows that a second protein triggered by inflammatory signals, p38 MAPK, chemically alters XBP1s, enhancing its activity — and that without these alterations, XBP1s cannot function to maintain normal glucose levels. The study further showed that obese mice have reduced p38 MAPK activity, and that re-activating p38 MAPK in the liver reduced their ER stress, increased insulin sensitivity and glucose tolerance, and significantly reduced blood glucose levels.

Together, the findings suggest that either increasing p38 MAPK activity — despite its being an inflammatory signal — or increasing XBP-1 activity by other means could represent new therapeutic options for diabetes.

The study also suggests a new model for understanding type 2 diabetes, in which obesity may interfere with the ability of people’s cells to respond to inflammatory signals. “It may be that inflammatory pathways are not working optimally and there could be a resistance to cytokines which mediates the inflammation,” Ozcan says. “This could be a paradigm shift for the field.”

The researchers also raise a possible down side in using p38 MAPK inhibitors to treat inflammatory diseases such as Crohn’s disease, psoriasis and asthma. “These therapeutic approaches should … be evaluated within the context of our results, and in light of the possibility that inhibition of XBP1s activity also decreases the ability of the cell to cope with the inflammatory conditions,” they write.

The study (doi:10.1038/nm.2449) was supported by the National Institutes of Health and the Timothy Murphy funds provided to the Division of Endocrinology, Children’s Hospital Boston. Jaemin Lee, Ph.D., and Cheng Sun, Ph.D., were co-first authors on the paper.

SOURCE Children’s Hospital Boston

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“The study had three objectives: we wanted to look at the effect of metformin on exercise in people with type 2 diabetes, examine the effect of exercise on metformin concentrations in the body, and finally to look at the effects of metformin and exercise on glucose control, which is essential for people with diabetes,” says Boulé, whose study – a randomized, double-blind, crossover study – involved a multi-disciplinary team of researchers from five faculties at the U of A.

Ten men and women between 30 and 65 with type 2diabetes, but not taking glucose-lowering medication or insulin for their condition were recruited into the study. Participants were randomly assigned to take metformin or a placebo for the first 28 days of the study, then crossed over so those taking the placebo received metformin and vice versa for a second 28 day period. On days 27 and 28, participants spent six hours in the exercise physiology lab and performed different tests, including approximately 40 minutes of exercise on day 28.

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Metformin and exercise combination less effective for glucose control

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“The ongoing assumption was that if you have a mixture of different sized particles in a liquid, the faster-settling particles will end up on the bottom,” said Darrell Velegol, professor of chemical engineering. “We found that in many cases it doesn’t matter how fast they settle. The particles keep jostling until they reach the low-energy state.”

Another known mechanism for settling is the Brazil nut effect, where dry particles eventually sort themselves out with the larger particles on the top — the way the Brazil nuts are always found on the top of the can of mixed nuts. This mechanism, however, does not apply to particles in liquids.

Velegol, working with César González Serrano, former graduate student, and Joseph J. McDermott, graduate student, found that settling speeds were not the determining characteristics of settling mixtures, but that the particles on the bottom are the ones in the lowest energy state. They reported their results in today’s (July 24) online issue of Nature Materials.

“Sedimentation is an old field, and it’s taken us a long time to figure it out,” said Velegol.

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But what if other cells in the body could be coaxed into becoming pancreatic beta cells? Could we potentially cure diabetes?

Researchers from UCLA’s Larry L. Hillblom Islet Research Center have taken an important step in that direction. They report in the April issue of the journal Developmental Cell that they may have discovered the underlying mechanism that could convert other cell types into pancreatic beta cells.

While the current standard of treatment for diabetes — insulin therapy — helps patients maintain sugar levels, it isn’t perfect, and many patients remain at high risk of developing a variety of medical complications. Replenishing lost beta cells could serve as a more permanent solution, both for those who have lost such cells due to an immune assault (Type 1 diabetes) and those who acquire diabetes later in life due to insulin resistance (Type 2).

“Our work shows that beta cells and related endocrine cells can easily be converted into each other,” said study co-author Dr. Anil Bhushan, an associate professor of medicine in the endocrinology division at the David Geffen School of Medicine at UCLA and in the UCLA Department of Molecular, Cell and Developmental Biology.

It had long been assumed that the identity of cells was “locked” into place and that they could not be switched into other cell types. But recent studies have shown that some types of cells can be coaxed into changing into others — findings that have intensified interest in understanding the mechanisms that maintain beta cell identity.

The UCLA researchers show that chemical tags called “methyl groups” that bind to DNA — where they act like a volume knob, turning up or down the activity of certain genes — are crucial to understanding how cells can be converted into insulin-secreting beta cells. They show that DNA methylation keeps ARX, a gene that triggers the formation of glucagon-secreting alpha cells in the embryonic pancreas, silent in beta cells.

Deletion of Dnmt1, the enzyme responsible for DNA methylation, from insulin-producing beta cells converts them into alpha cells.

These findings suggest that a defect in beta cells’ DNA methylation process interferes with their ability to maintain their “identity.” So if this “epigenetic mechanism,” as the researchers call it, can produce alpha cells, there may be an analogous mechanism that can produce beta cells that would maintain blood sugar equilibrium.

“We show that the basis for this conversion depends not on genetic sequences but on modifications to the DNA that dictates how the DNA is wrapped within the cell,” Bhushan said. “We think this is crucial to understanding how to convert a variety of cell types, including stem cells, into functional beta cells.”

According to the American Diabetes Association, 25.8 million children and adults in the U.S. — 8.3 percent of the population — have diabetes.

The National Institute of Diabetes and Digestive and Kidney Diseases, the Juvenile Diabetes Research Foundation, and the Helmsley Trust funded this study.

Additional co-authors of the study are Sangeeta Dhawan, Senta Georgia, Shuen-ing Tschen and Guoping Fan, all of UCLA.

Source material reprinted from the UCLA

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Much of the extra medical costs come from prescription drugs and outpatient care. Young people with the highest medical costs were treated with insulin, and included all those with type 1 diabetes and some with type 2 diabetes. People with type 1 diabetes cannot make insulin anymore and must receive insulin treatment. Some people with type 2 diabetes also are treated with insulin, because their bodies do not produce enough to control blood glucose (sugar).

Children and adolescents who received insulin treatment had annual medical costs of $9,333, compared to $5,683 for those who did not receive insulin, but did take oral medications to control blood glucose.

“Young people with diabetes face medical costs that are six times higher than their peers without diabetes,” said Ann Albright, Ph.D., R.D., director of CDC’s Division of Diabetes Translation. “Most youth with diabetes need insulin to survive and the medical costs for young people on insulin were almost 65 percent higher than for those who did not require insulin to treat their diabetes.”

The study examined medical costs for children and teens aged 19 years or younger who were covered by employer-sponsored private health insurance plans in 2007, using the MarketScan Commercial Claims and Encounters Database. The estimates were based on administrative claim data from nearly 50,000 youth, including 8,226 with diabetes.

Medical costs for people with diabetes, the vast majority of whom are adults, are 2.3 times higher than costs for those without diabetes, according to CDC’s National Diabetes Fact Sheet, 2011. Authors of the Diabetes Care study suggest that the difference in medical costs associated with diabetes may be greater for youth than for adults because of higher medication expenses, visits to specialists and medical supplies such as insulin syringes and glucose testing strips.

Among youth with diabetes, 92 percent were on insulin, compared to 26 percent of adults with diabetes. Insulin is a hormone produced by the pancreas that helps convert blood glucose into energy. Without adequate insulin, blood glucose levels rise and can eventually lead to serious health complications, including heart disease, kidney failure, blindness, nerve damage and amputation of feet and legs.

Source: CDC

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Dogs are susceptible to type 1, insulin-dependent diabetes. Affected animals are unable to utilize sugar in their bloodstream because their bodies do not produce enough insulin, a hormone that helps cells turn sugar into energy. Veterinarians treat animals with this type of diabetes similarly to the way humans are treated, with insulin injections and a low-carbohydrate diet.

Amy DeClue, assistant professor of veterinary internal medicine, and Charles Wiedmeyer, assistant professor of veterinary clinical pathology, have been studying the use of a “continuous glucose monitor” (CGM) on animals since 2003. A CGM is a small flexible device that is inserted about an inch into the skin, to constantly monitor glucose concentrations.

“Continuous glucose monitoring is much more effective and accurate than previous glucose monitoring techniques and has revolutionized how veterinarians manage diabetes in dogs,” said DeClue. “The CGM gives us a complete view of what is happening in the animal in their natural setting. For example, it can show us if a pet’s blood glucose changes when an owner gives treats, when the animal exercises or in response to insulin therapy.”

CGMs have become more commonly used in dogs with diabetes that are not responding well to conventional treatment. The monitor provides detailed data for glucose concentrations throughout the course of three days in a dog’s usual environment, so veterinarians can make better treatment decisions. Previously, veterinarians would have created an insulin regimen based on a glucose curve by taking blood from the animal in the veterinary hospital every two hours over the course of a single day. The glucose curve was often inaccurate due to increased stress from the animals being in an unnatural environment.

Dogs show clinical signs of diabetes similar to humans.  Clinical signs include increased urination, thirst, hunger and weight loss. Typically, no direct cause is found for diabetes in dogs, but genetic disposition and obesity are thought to play a role in causing diabetes, according to DeClue. Just like people, dogs suffering with diabetes must be medically managed or complications can arise.

“Typically, dogs that are treated properly for diabetes go on to live a long, full life,” said Wiedmeyer. “Actually, dogs with diabetes are similar to young children with diabetes but somewhat easier to manage.  Dogs will eat what their owners give them at the same time each day and they won’t ask for a cupcake at a friend’s birthday party. With tools like the continuous glucose monitor to assist with disease management, the outlook is very good for a dog with diabetes.”

In the future Wiedmeyer projects that the device will become smaller and less invasive. In addition, he hopes device manufacturers develop a device that would monitor blood sugar levels remotely.

DeClue and Wiedmeyer’s most recent article on methods for monitoring and treating diabetes in dogs was published in the journal, Clinic in Laboratory Medicine.

Source: University of Missouri

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Now, researchers at UCLA have discovered a possible molecular mechanism behind coffee’s protective effect. A protein called sex hormone–binding globulin (SHBG) regulates the biological activity of the body’s sex hormones, testosterone and estrogen, which have long been thought to play a role in the development of type 2 diabetes. And coffee consumption, it turns out, increases plasma levels of SHBG.

Reporting with colleagues in the current edition of the journal Diabetes, first author Atsushi Goto, a UCLA doctoral student in epidemiology, and Dr. Simin Liu, a professor of epidemiology and medicine with joint appointments at the UCLA School of Public Health and the David Geffen School of Medicine at UCLA, show that women who drink at least four cups of coffee a day are less than half as likely to develop diabetes as non-coffee drinkers.

When the findings were adjusted for levels of SHBG, the researchers said, that protective effect disappeared.

The American Diabetes Association estimates that nearly 24 million children and adults in the U.S. — nearly 8 percent of the population — have diabetes. Type 2 diabetes is the most common form of the disease and accounts for about 90 to 95 percent of these cases.

Early studies have consistently shown that an “inverse association” exists between coffee consumption and risk for type 2 diabetes, Liu said. That is, the greater the consumption of coffee, the lesser the risk of diabetes. It was thought that coffee may improve the body’s tolerance to glucose by increasing metabolism or improving its tolerance to insulin.

“But exactly how is elusive,” said Liu, “although we now know that this protein, SHBG, is critical as an early target for assessing the risk and prevention of the onset of diabetes.”

Earlier work by Liu and his colleagues published in the New England Journal of Medicine had identified two mutations in the gene coding for SHBG and their effect on the risk of developing type 2 diabetes; one increases risk while the other decreases it, depending on the levels of SHBG in the blood.

A large body of clinical studies has implicated the important role of sex hormones in the development of type 2 diabetes, and it’s known that SHBG not only regulates the sex hormones that are biologically active but may also bind to receptors in a variety of cells, directly mediating the signaling of sex hormones.

“That genetic evidence significantly advanced the field,” said Goto, “because it indicated that SHBG may indeed play a causal role in affecting risk for type 2 diabetes.”

“It seems that SHBG in the blood does reflect a genetic susceptibility to developing type 2 diabetes,” Liu said. “But we now further show that this protein can be influenced by dietary factors such as coffee intake in affecting diabetes risk — the lower the levels of SHBG, the greater the risk beyond any known diabetes risk factors.”

For the study, the researchers identified 359 new diabetes cases matched by age and race with 359 apparently healthy controls selected from among nearly 40,000 women enrolled in the Women’s Health Study, a large-scale cardiovascular trial originally designed to evaluate the benefits and risks of low-dose aspirin and vitamin E in the primary prevention of cardiovascular disease and cancer.

They found that women who drank four cups of caffeinated coffee each day had significantly higher levels of SHBG than did non-drinkers and were 56 percent less likely to develop diabetes than were non-drinkers. And those who also carried the protective copy of the SHBG gene appeared to benefit the most from coffee consumption.

When the investigators controlled for blood SHBG levels, the decrease in risk associated with coffee consumption was not significant. This suggests that it is SHBG that mediates the decrease in risk of developing type 2 diabetes, Liu said.

And there’s bad news for decaf lovers. “Consumption of decaffeinated coffee was not significantly associated with SHBG levels, nor diabetes risk,” Goto said. “So you probably have to go for the octane!”

Other authors of the study included Brian Chen, of UCLA, and Julie Buring, JoAnn Manson and Yiqing Song, of Brigham and Women’s Hospital and Harvard Medical School. Funding was provided by the National Institutes of Health. No conflicts of interest were reported by the authors.

Source material reprinted from the UCLA

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TORC 2 activates a protein called Akt, which plays a crucial role in how cells respond to insulin, said Kazuo Shiozaki, professor of microbiology in the College of Biological Sciences at UC Davis and senior author on the paper.

Normally, insulin triggers fat and muscle cells to take up sugar from the blood. Patients with type II diabetes make plenty of insulin, but their cells do not respond to it properly. Akt plays a role in the series of steps between insulin exposure and sugar uptake; specifically, it causes proteins that take sugar from the blood to move to the cell surface. Mice that lack the gene for Akt develop diabetes-like symptoms.

“We know that Akt is a key player in diabetes, so we are trying to work upstream from there,” Shiozaki said.

Akt also controls cell growth in early embryos and can promote the growth of cancer cells, he added.

Since TORC 2 was first identified in 2005 as a regulator of Akt, researchers have been trying to identify how it is activated, Shiozaki said. The complex appears to be very similar across organisms ranging from humans to yeast.

Shiozaki and colleagues Hisashi Tatebe, Susumu Morigasaki, Shinichi Murayama and Cui Tracy Zeng studied TORC 2 in a yeast. They found that a protein called Ryh1, when bound to another molecule called guanosine triphosphate, is needed to activate TORC 2.

Yeast strains that had a defective form of Ryh1 were more sensitive to temperature or other stressful conditions.

Ryh1 is very similar to a human protein, Rab6. The researchers found that human Rab6 could to some extent replace yeast Ryh1 as an activator of TORC 2 in defective yeast strains.

Rab6 belongs to a class of proteins better known for moving other proteins around within cells. This suggests that Rab6 might play a dual role in insulin signaling, Shiozaki said.

“Our discovery suggests that the early and late steps in insulin response are closely linked to each other,” Shiozaki said.

Co-authors Tatebe, Morigasaki and Murayama also hold positions at the Nara Institute of Science and Technology, Japan. The work was funded by grants from the National Institutes of Health, the University of California Cancer Research Coordinating Committee, and the Japan Society for the Promotion of Science. Morigasaki is an international research fellow of the Nara Institute of Science and Technology Global Center of Excellence Program, funded by the Ministry of Education, Culture, Sports, Science and Technology of Japan.

Source: UC Davis

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Insulin resistance, or the stage before diabetes, happens when insulin, a hormone in the body, becomes less effective in lowering blood sugar.

“Type 2 diabetes and Alzheimer’s disease are two epidemics growing at alarming levels around the world,” said study author Kensuke Sasaki, MD, PhD, with Kyushu University in Fukuoka, Japan. “With the rising obesity rates and the fact that obesity is related to the rise in type 2 diabetes, these results are very concerning.”

The study involved 135 people with an average age of 67 from Hisayama, Japan. The participants had several diabetes glucose tests to measure blood sugar levels. They were also monitored for symptoms of Alzheimer’s disease over the next 10 to 15 years. During that time, about 16 percent developed Alzheimer’s disease.

After the participants died, researchers examined their autopsied brains for the physical signs of Alzheimer’s disease, called plaques and tangles. While 16 percent had symptoms of Alzheimer’s disease while alive, a total of 65 percent had plaques.

The study found that people who had abnormal results on three tests of blood sugar control had an increased risk of developing plaques. Plaques were found in 72 percent of people with insulin resistance and 62 percent of people with no indication of insulin resistance. However, the study did not find a link between diabetes factors and tangles in the brain.

“Further studies are needed to determine if insulin resistance is a cause of the development of these plaques,” said Sasaki. “It’s possible that by controlling or preventing diabetes, we might also be helping to prevent Alzheimer’s disease.”

Source: The American Academy of Neurology

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Identification of cognitive impairments as a complication of type 2 diabetes emphasizes the importance of addressing issues of inactivity and obesity, two important risk factors for the development of the disease among the young. The study appeared online in the journal Diabetologia, July 30, 2010.

“This is the first study that shows that children with type 2 diabetes have more cognitive dysfunction and brain abnormalities than equally obese children who did not yet have marked metabolic dysregulation from their obesity, ” says Antonio Convit, MD, professor of Psychiatry and Medicine at NYU Langone Medical Center and the Nathan S. Kline Institute for Psychiatric Research.  “The findings are significant because they indicate that insulin resistance from obesity is lowering children’s cognitive performance, which may be affecting their ability to perform well in school.”

Researchers studied 18 obese adolescents with type 2 diabetes and compared them to equally obese adolescents from the same socioeconomic and ethnic background but without evidence of marked insulin resistance or pre-diabetes.  Investigators found that adolescents with type 2 diabetes not only had significant reductions in performance on tests that measure overall intellectual functioning, memory, and spelling, which could affect their school performance, but also had clear abnormalities in the integrity of the white matter in their brains.

“We have previously found brain abnormalities in adults with Type 2 diabetes, but believed those changes might have been a result of vascular disease,” adds Dr. Convit.  “Now we see that subtle changes in white matter of the brain in adolescents may be a result of the abnormal physiology that accompanies type 2 diabetes. If we can improve insulin sensitivity and help children through exercise and weight loss, perhaps we can reverse these deficits.”

Co-authors of the study include P.L. Yau, W.H. Tsui, B.A. Ardekani of NYU Langone Medical Center and the Nathan S. Klein Institute for Psychiatric Research.

Source material reprinted from the NYU Newsroom

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Diabetic ketoacidosis occurs when the body is lacking insulin and burns fat for energy instead of sugar. Apart from nausea, vomiting and fatigue, patients can feel mentally sluggish. If the condition is not treated, patients may fall into a coma. The new study, published online Oct. 15 in the Journal of Pediatrics, shows that children known to have had such an episode in the past performed worse on memory tests than children with diabetes who had not had such an episode.

Diabetic ketoacidosis — and its consequences — can be avoided with proper glucose control in patients known to have diabetes, said Simona Ghetti, associate professor at the UC Davis Department of Psychology and the Center for Mind and Brain. Many cases, however, occur at the time of diagnosis of diabetes and these cases are more difficult to detect early.

“These results underscore the importance of maintaining control of known diabetes and prompt diagnosis of new cases should diabetic ketoacidosis symptoms arise,” Ghetti said.

The UC Davis researchers studied 33 children with type 1 diabetes and a history of diabetic ketoacidosis, and 29 diabetic children with no history of such an episode. They compared the children’s ability to recall events and associations, as measured by simple tests.

Children with a history of ketoacidosis performed significantly worse on the memory tests than children without a history, they found.

The results back up anecdotal accounts from parents, who complain of slight but consistent memory deficits in their children with type 1 (insulin-dependent) diabetes that are not captured by IQ measures or other typical assessments, such as school grades, Ghetti said.

Co-authors on the paper are UC Davis psychology graduate students Joshua Lee and Dana DeMaster; Nicole Glaser, associate professor of pediatrics at UC Davis; and Clare Sims, graduate student at the University of Colorado at Boulder.

The work was supported by a Young Investigator Research Award to Ghetti from the Children’s Miracle Network.

Source: UC Davis

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