Monthly Archives: January 2015
Teenage misperception of weight may lead to adult obesity

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A study due to be published Psychological Science, a journal of the Association for Psychological Science, suggests that teenagers who have a false perception of themselves as being overweight are more likely to become obese as adults.

Teens who falsely believe themselves to be overweight may be more likely to using diet pills or vomiting in an attempt to control their weight – behaviors linked with long-term weight gain. The authors of the new study, from Florida State University College of Medicine in Tallahassee, were interested in what the health outcomes might be for teenagers of a healthyweight who misperceived themselves as being overweight.

To do this, the team examined data from the National Longitudinal Study of Adolescent Health (also known as Add Health) concerning the height, weight and self-perceptions of 6,523 adolescents.

At the start of the study, the adolescents rated what they thought their weight was, on a scale ranging from 1 (“very underweight”) to 5 (“overweight”). The study participants had an average age of 16 at the start of the study and were followed-up when they were about 28 years old.

The results show that adolescents who had an inaccurate perception of themselves as being overweight had a 40% increased risk of obesity – defined as a body mass index (BMI) of 30 or more – in adulthood, compared with peers who had an accurate perception of their weight.

Although it might seem strange that healthy teens who feel that they are overweight subsequently actually become overweight, the authors suggest mechanisms that might drive this association between misperception and overall weight gain.

One theory proposed in the study is that teens who falsely believe themselves to be overweight may be more susceptible to using diet pills or vomiting in an attempt to control their weight – unhealthy behaviors that are known to be linked with weight gain over the long term.

The same psychological factors that drive the weight misperception could also cause the teens to have “lower self-regulatory abilities,” the researchers suggest. And it is also likely that weight-related stigmatization could influence this group’s weight-control behaviors, as previous studies have found that weight stigmatization is associated with obesity.

It is possible that these factors contribute to what the authors describe as a “self-fulfilling prophecy,” where teens who see themselves as overweight then fail to take the required steps to maintain a healthy weight, “because as they gain weight, they physically become what they have long perceived themselves to be.”

Boys who misperceive weight have 89% increased risk of adult obesity
A surprise finding of the research was a particularly strong association between misperceived weight and later obesity among males. The boys in the study who had a misperception of their weight had an 89% increased risk of adult obesity.

Study author Angelina Sutin says that it is not clear why the association is stronger for boys:

“It may be that girls are more attentive to their weight and may intervene earlier when they experience any weight gain. As such, the self-fulfilling prophecy may be stronger for boys than for girls. Physicians and other health care providers may also notice weight gain sooner for girls than for boys, or may be more likely to address any weight gain with girls than with boys. We were unable, however, to test exactly why there is this difference across the sexes.”

Sutin says her study proves how complex the determinants of obesity are, suggesting that a greater understanding is needed of determinants at all levels, including psychological determinants, in order to address the obesity-related challenges faced by medical practitioners and policymakers.


Research into brain control of liver lipid production could cause break in obesity and diabetes treatment

Ways of keeping the heart healthy has widened, with the discovery that the brain can help fight off hardening of the arteries.

Atherosclerosis–hardening and narrowing of the arteries–can be caused by fat build up that causes plaque deposits, and is one of the main causes of cardiovascular disease. Jessica Yue, a newly recruited researcher in the Department of Physiology in the Faculty of Medicine & Dentistry, has shown a link between how the brain can regulate fat metabolism, potentially stopping the development of this disease risk factor in obesity and diabetes.

Her findings, published this month in Nature Communications, the online version of the high-impact Nature publication, outlines how the brain can use the presence of fatty acids, which are building blocks of fat molecules, to trigger the liver to reduce its own lipid production.

“We know that when there is dyslipidemia, or an abnormal amount of fat in the bloodstream, it’s dangerous for health–largely because this can lead to obesity, obesity-related disorders such as Type 2 diabetes, and atherosclerosis,” says Yue, and that “if you can find ways to lower fats in the bloodstream, it helps to lower these chances of diabetes and cardiovascular disease as a result of this atherosclerosis.”

Yue trained at the Toronto General Research Institute under Tony Lam, where she was a recipient of fellowships from the Canadian Institutes of Health Research (CIHR) and the Canadian Diabetes Association. With her associates in Toronto and with Peter Light, professor of pharmacology in the Faculty of Medicine & Dentistry, she looked at how the infusion of oleic acid, a naturally occurring monounsaturated fatty acid, in the brain “triggers” a signal from the hypothalamus to the liver to lower its fat secretion, which Yue says is a “triglyceride-rich, very-low-density lipoprotein. Light is the co-author of Yue’s paper in Nature Communications and is the director of the Alberta Diabetes Institute (ADI), where Yue is applying for membership.

“This fat complex is the kind of lipoprotein that is dangerous when its levels in the blood are elevated because it promotes atherosclerosis,” she says.

The catch, though, is that this “trigger” doesn’t work in obesity, a setting in which blood lipid levels are usually high. “In a model of diet-induced obesity, which then leads to insulin resistance and pre-diabetes, oleic acid no longer provides the fat-lowering trigger to the liver.” Yue’s findings, though, demonstrate how this faulty signal can be bypassed, unveiling potentially other ways to trigger this same function in obese patients.

This study could potentially impact how obesity and diabetes are treated, says Yue, which is the focus of her future research.

The next steps, she says, will be to look at how the brain can sense other compounds to regulate not only liver secretion of fats, but also liver glucose production, a significant contributing factor to diabetes. As a member of the Group on Molecular and Cell Biology of Lipids and with the strength of the ADI, she feels enthusiastic and inspired by her new research environment at the University of Alberta.

“It’s a big field and it’s emerging,” says Yue about neuroscience research in the areas of metabolic disease. “Whereas the peripheral organs have gained a lot of attention in terms of how they release glucose and lipids, it’s exciting to see that within the last decade and a half that the brain now is emerging as an organ that has a lot of control over our health.”


‘Healthy’ fat tissue could be key to reversing type 2 diabetes

Preventing inflammation in obese fat tissue may hold the key to preventing or even reversing type 2 diabetes, new research has found.

Researchers from Melbourne’s Walter and Eliza Hall Institute, with colleagues from the RIKEN Institute, Japan, found they could ‘reverse’ type 2 diabetes in laboratory models by dampening the inflammatory response in fat tissue.

Dr Ajith Vasanthakumar, Dr Axel Kallies and colleagues from the institute discovered that specialised immune cells, called regulatory T cells (Tregs), played a key role in controlling inflammation in fat tissue and maintaining insulin sensitivity. The findings were published in the journal Nature Immunology.

More than 850,000 Australians are estimated to have type 2 diabetes, which is the most common type of diabetes, and its prevalence is rising. The disease is strongly linked with ‘lifestyle’ factors, such as being overweight or having high blood pressure. Long-term complications of type 2 diabetes include kidney, eye and heart disease, and there is no cure.

People with type 2 diabetes have reduced sensitivity to insulin, a hormone that normally triggers uptake of glucose by cells, and their cells no longer respond to insulin appropriately. This decrease in insulin sensitivity is thought to be a result of long-term, low-level inflammation of fat tissue in people who are obese.

Dr Vasanthakumar said Tregs acted as the guardians of the immune system, preventing the immune response from getting out-of-hand and attacking the body’s own tissues. “When Treg numbers are reduced, inflammatory diseases such as diabetes and rheumatoid arthritis can occur,” he said.

Recent studies have shown that fat tissue has its own unique type of Tregs, which disappear from fat tissue during obesity. “The fat tissue of obese people has lower numbers of Tregs than the fat tissue of people in a healthy weight range,” Dr Vasanthakumar said. “Without Tregs, inflammation-causing cell levels increase, and this rise in inflammation can lead to insulin resistance and high blood glucose levels, a classic hallmark of type 2 diabetes.”

The research team discovered a key hormone called IL-33 (interleukin-33) was able to selectively boost Treg populations in fat tissue, effectively halting the development of type 2 diabetes, or even reversing the disease in preclinical models.

“Treating fat tissues with IL-33 restored normal Treg cell levels, which reduced inflammation and decreased blood glucose levels,” Dr Vasanthakumar said. “Treatments that mimic IL-33 could have the potential to reduce obesity-related inflammation and type 2 diabetes.”

Dr Kallies said the research underscored the importance of ‘healthy’ fat tissue in maintaining a healthy body. “We can no longer think of fat tissue simply as energy storage,” Dr Kallies said.

“Fat tissue is increasingly being recognised as a crucial organ that releases hormones and regulates development. Keeping our fat tissue healthy is important for our general wellbeing, and our research highlights the important role it plays in preventing disease.”


Researchers find new links between obesity and cardiovascular disease

In a new study published in the Journal of Biological Chemistry, a research group led by James A. Hamilton, PhD, professor of Physiology, Biophysics and Radiology at Boston University School of Medicine, applied novel methods to detect binding of fatty acids to CD36 and their effect on internalization of oxidized LDL. Although other research groups have characterized a fatty acid binding site on CD36 and postulated CD36 to be a gatekeeper for fatty acid entry into cells, the Hamilton lab previously found that CD36 did not increase fatty acid translocation across the plasma membrane.

In the current study all of the common dietary fatty acid types (saturated, unsaturated, trans and polyunsaturated) were shown by a new assay to bind to CD36 at levels greater than expected for a single binding site characterized in previous studies. In cells with CD36 present in the plasma membrane, all of the fatty acids also enhanced oxidized LDL uptake, except for the fish oil fatty acid DHA. This current study adds to the possible mechanisms for fish oil benefits that are now widely recognized.

“Since obesity and type 2 diabetes are characterized by high plasma levels of fatty acids, the demonstrated enhancement of oxLDL uptake by increases in common dietary fatty acids may contribute to the pathophysiology of these diseases. Furthermore, our new results provided a link between fatty acids, CD36, and atherosclerosis and new drugs can be designed that target the exact mechanism more precisely.” added Hamilton.


‘Imaginary meal’ in a pill could be new dieting aid

Some obese individuals struggle to lose weight by following a healthy diet and regular exercise alone, which is why many turn to diet pills for a helping hand. In a new study, researchers from the Salk Institute for Biological Studies in La Jolla, CA, detail the creation of a novel diet pill that tricks the body into losing weight, potentially making it more effective than existing diet pills and likely to cause fewer side effects. Ronald Evans, director of the Gene Expression Laboratory at Salk, says the new diet pill – called fexaramine – acts like an “imaginary meal.” “It sends out the same signals that normally happen when you eat a lot of food, so the body starts clearing out space toweightloss-pic-vitatious store it. But there are no calories and no change in appetite,” he explains. When tested in obese mice, fexaramine was found to trigger fat loss, prevent weight gain, control blood sugar and reduce cholesterol and inflammation.

Evans and colleagues recently published their findings in the journal Nature Medicine. Fexaramine targets the body’s farensoid X receptor (FXR) – a protein that is involved in food digestion, fat and sugar storage and the release of bile acids from the liver. The researchers explain that when we start eating a meal, FXR is activated in preparation for food intake. Past studies from Evans and team have indicated that as well as triggering the release of bile acids to aid digestion, FXR alters blood sugar levels and switches on a fat-burning process. Some existing diet pills activate an array of pathways controlled by FXR – including the intestines, liver, kidneys and adrenal glands. Fexaramine, however, only activates the FXR pathway linked to the intestines. When taken orally, the diet pill is only absorbed in the gut and does not enter the bloodstream, meaning it is unlikely to cause the side effects typically associated with existing diet pills – such as high blood pressure, dizziness, insomnia and even heart disease. What is more, the fact that fexaramine only acts in the intestines means it is a more effective weight loss aid, according to the researchers, as the drug is not transported throughout the entire body.

Body’s response to a meal is like a relay race; we’ve learned how to trigger the first runner’ To test the effectiveness of fexaramine, Evans and colleagues gave obese mice a daily dose of the drug for 5 weeks and compared the outcomes with mice that remained untreated. The mice given fexaramine stopped gaining weight and saw a reduction in body fat, blood sugar and cholesterol. What is more, the body temperature of the treated mice increased, indicating a heightened metabolism, and some of the rodent’s white fat deposits were converted into healthier, energy-burning fats. The team says they also saw a change in the assortment of bacteria in the gut, but they note that they are unclear on what this indicates at present. Evans says fexaramine is more effective than diet pills that trigger numerous FXR pathways because it activates the mechanisms by which the body naturally responds to a meal. He explains: “When you eat, you have to quickly activate a series of responses all throughout the body. And the reality is that the very first responder for all this is the intestine. The body’s response to a meal is like a relay race, and if you tell all the runners to go at the same time, you’ll never pass the baton.

We’ve learned how to trigger the first runner so that the rest of the events happen in a natural order.”   Obesity is a major problem in the US, affecting more than a third of adults. Evans and colleagues believe fexaramine is a promising candidate to reduce obesity and the risk of its related diseases – such as type 2 diabetes – in humans. They hope the drug would be used alongside diet and lifestyle changes under the guidance of health care professionals. The team is now in the process of setting up clinical trials to assess the effectiveness of fexaramine in humans.


Metabolic syndrome linked to increased risk of endometrial cancer

Older women with metabolic syndrome may be at increased risk of endometrial cancer, regardless of whether they are overweight or obese. This is according to a new study published in the journal Cancer Epidemiology, Biomarkers & Prevention.

Metabolic syndrome is when an individual has a cluster of factors associated with increased risk of cardiovascular problems and other health conditions. These factors include abdominal obesity, high blood pressure, high cholesterol and abnormal fasting glucose. Around 34% of adults in the US have metabolic syndrome, meaning they are at increased risk of cardiovascular disease, stroke, diabetes and other metabolic-related diseases, compared with the general population. Obesity is considered a major risk factor for endometrialcancer – a form of cancer then begins in the inner lining of the uterus, called the endometrium. In the US, endometrial cancer is the most common cancer of the female reproductive organs; around 1 in 37 women will be diagnosed with the disease in their lifetime.

Past research has indicated that metabolic syndrome may also increase the risk of endometrial cancer. But according to the investigators of this latest study – including Britton Trabert, PhD, of the Division of Cancer Epidemiology and Genetics at the National Institutes of Health – it was unclear as to whether this association was down to obesity or other factors of metabolic syndrome. Metabolic syndrome increased endometrial cancer risk by 17-21%, independent of obesityWith a view to finding out, Trabert and colleagues used the SEER-Medicare Linked Database to gather information of 16,323 women aged 65 and over who had been diagnosed with endometrial cancer between 1993 and 2007, alongside 100,751 women who were free of the disease.

A diagnosis of metabolic syndrome among the women was given using criteria set by either the US National Cholesterol Education Program Adult Treatment Panel III (ATP III) or the International Diabetes Foundation. The results of the analysis revealed that women who had been diagnosed with metabolic syndrome using the ATP III criteria were 39% more likely to be diagnosed with endometrial cancer, while women diagnosed with metabolic syndrome using the International Diabetes Foundation were 109% more likely to be diagnosed with the cancer.

After accounting for overweight or obesity among the women, the researchers found that those diagnosed with metabolic syndrome under ATP III criteria were still 21% more likely to be diagnosed with endometrial cancer, while an International Diabetes Foundation diagnosis of metabolic syndrome put the women at 17% higher risk of the cancer.

In addition, the researchers identified four factors involved in metabolic syndrome – excessive weight, high blood pressure, high triglycerides and impaired fasting glucose – that raised the risk of endometrial cancer individually.

“We found that a diagnosis of metabolic syndrome was associated with higher risk of endometrial cancer, and that metabolic syndrome appeared to increase risk regardless of whether the woman was considered obese.

Although our study was not designed to evaluate the potential impact of preventing metabolic syndrome on endometrial cancer incidence, weight loss and exercise are the most effective steps a woman can take to prevent developing metabolic syndrome.”

Commenting on the team’s findings, Trabert says: