Category Archives: Obesity in America

The overweight and obesity stigma is alive and well and provable with research

2CE809F300000578-3253766-image-a-1_1443547359971These days our society strives to be as kind and gentle as possible … well, sort of. Unfortunately, it’s pretty well known that our political correctness flies right out the window when it comes to the overweight and obese population. The overweight and obesity stigma isn’t going away any time soon. It’s already hard enough to be part of these populations … these aren’t easy lives. asks you to imagine for a minute throwing in the negative assumptions of others around you into that mix. It’s not a happy equation. For those that say that the negative stereotyping doesn’t exist, you might want to take a look at this information from a new study.

A blogger’s weight affects her or his credibility with readers seeking food advice, according to a Cornell study published online and in a forthcoming print issue of the journal Health Communication.

The study revealed that when a blogger is overweight, as shown in the blogger’s photo, readers are far more skeptical of the information that blogger provides when compared with a thin blogger’s recommendations, even when the content is exactly the same.

The findings are increasingly important as more than half of smartphone users report that they use their device to look up health-related information, making the internet one of the top places people get informed about health issues.

“When we search for health information online, there are a lot of related cues that can bias our perceptions in ways that we may not be consciously aware of,” said Jonathon Schuldt, assistant professor of communication and lead author of the study.

“Awareness of these biases could help us better navigate health information online,” he said. It could also help us “avoid being swayed by nutritional information simply because it is posted by someone who is thin rather than heavy,” he added.
But the study also suggests that “weight bias and prejudice — which are so rampant in our society — can spill over and affect not only the inferences we make about people, but also objects that are associated with them,” Schuldt said.

In one experiment, 230 subjects were randomly assigned to one of two groups. They were all shown photos of the same 10 meals — including black bean and cheese quesadillas, chopped salad with croutons, sliced beef with vegetables and so on. With each photo was also a thumbnail photo depicting the supposed author of the blog post. Participants were then asked to judge how healthy the meal was overall on a scale of one to seven.

The only thing that differed between the two groups was the thumbnail photo of the blogger, which was a real picture of the same person before and after weight loss. The researchers found that when the photo of the overweight woman accompanied the meal, “our participants perceived those meals to be less healthy” than the same meal presented with a photo of a thin blogger.

“People appear to assume that if a heavier person is recommending food, it is probably richer and less healthy,” Schuldt said.

In a second experiment, the researchers also included calorie and fat content information next to the image of the food and above the thumbnail of the blogger. “What we found is that even when we provided nutrient information that is much more relevant to the food’s health quality, people are still strongly influenced by the body weight of the recommender,” Schuldt said.

The researchers even went so far as to vary the fat and calorie content, so that some subjects saw a healthy nutritional label and others saw a label with approximately double the calorie content and triple the fat. They found that this increase in fat and calories influenced impressions to a similar extent as the heavy vs. thin blogger, all else being equal.

“When we dramatically increased the fat and calorie content, it had just as much impact as when we said the food was posted by a heavy person,” Schuldt said.

So there you have it. The overweight and obesity stigma is a very real thing. Let’s extend our kind and gentle society to EVERYONE who needs those considerations.

It doesn’t matter who you are, fast food consumption affects you the same way it affects everyone else.

KFC_Bandung_Supermall-300x199For years, we’ve all heard certain myths regarding fast food consumption. Among those myths are that low-income families are consuming more fast food than those with higher incomes. We’ve also been told that those who are overweight and obese are eating more fast food than those who maintain a healthy weight. We’ve also come to believe that folks who live in a “food desert,” or an area where there is limited access to fresh foods are consuming more fast food. These ideas have always made sense to us, but perhaps they shouldn’t have.

We may make fast food out to be worse than it is, according to a new report from the Centers for Disease Consumption of fast food has been linked to weight gain in adults, as well as associated with higher caloric intake and poorer diet quality among children and adolescents, said researchers from the CDC’s National Center for Health Statistics, Division of Health and Nutrition Examination Surveys (NHNES). These effects have seemed more prominent among low-income families, as well as individuals who are overweight and obese, where there’s less access to fresh food, also known as a food desert. And yet, the CDC doesn’t find this to be the case.

Analyzing the data collected from the NHNES in 2011-2012 — a cross-sectional survey designed to monitor the heath and nutritional status of the U.S. population — the CDC reported “no significant difference was seen by poverty status in the average daily percentage of calories consumed from fast food among children and adolescents aged 2 to 19.” Similarly, “the average daily percentage of calories consumed from fast food did not vary significantly by weight status.” As The Atlantic first put it, the level of fast food consumption based on poverty and weight status was “pretty even.”

There were, however, some trends among age and race groups. Adolescents aged 12 to 19 consumed twice the average daily percentage of calories from fast food than did younger children, and overall, non-Hispanic Asian children and adolescents consumed fewer calories from fast food compared to non-Hispanic white, non-Hispanic Black, and Hispanic children and adolescents. The CDC noted that previous studies have shown that acculturation to the U.S. lifestyle plays an important role in the adoption of unhealthy behaviors, including but not limited to fast food consumption.

The Atlantic added these findings may dispel the idea that fast food is a primary cause of obesity in the U.S. The magazine cited a fast food ban passed in South Los Angeles, where the obesity rate was higher, failed to slow the epidemic. In fact, it seemed to speed up obesity levels.

That’s not to say the CDC is giving everyone a pass to load up on fast food; studies do show fast food items are spiked with potentially harmful antibiotics, fat, sodium, and sugar. But what they are finding is that everyone eats fast food, so the obesity rate among low-income families could very well be fueled by another type of food. The Atlantic pointed a finger at the general cheap access Americans have to sugar foods. As Medical Daily previously reported, sugary drinks in particular have been shown to weave “a complicated web of disease and increased risk of death” not just in the U.S., but around the world.

While the findings may dispel the belief that fast food is a key culprit in the obesity crisis in America, they also point to the idea that too many of us are eating it, no matter where we live, no matter our socioeconomic status, no matter our weight. wants us to all get on the bandwagon and stay away from fast food!

New hope in the fight against obesity

150819211106_1_540x360We’re constantly reading about new research discovering more information regarding the obesity epidemic. There are always new developments that seem to offer promising new insights into controlling and reversing obesity for the millions that suffer with this debilitating disease. It’s rare that we hear further news surrounding any of the research that’s being done. is hopeful that the news we’re showcasing today will be something that we continue to find reports on well into the future.

Obesity is one of the biggest public health challenges of the 21st century. Affecting more than 500 million people worldwide, obesity costs at least $200 billion each year in the United States alone, and contributes to potentially fatal disorders such as cardiovascular disease, type 2 diabetes, and cancer.

But there may now be a new approach to prevent and even cure obesity, thanks to a study led by researchers at MIT and Harvard Medical School and published today in the New England Journal of Medicine. By analyzing the cellular circuitry underlying the strongest genetic association with obesity, the researchers have unveiled a new pathway that controls human metabolism by prompting our adipocytes, or fat cells, to store fat or burn it away.

“Obesity has traditionally been seen as the result of an imbalance between the amount of food we eat and how much we exercise, but this view ignores the contribution of genetics to each individual’s metabolism,” says senior author Manolis Kellis, a professor of computer science and a member of MIT’s Computer Science and Artificial Intelligence Laboratory (CSAIL) and of the Broad Institute.

The strongest association with obesity resides in a gene region known as “FTO,” which has been the focus of intense scrutiny since its discovery in 2007. However, previous studies have failed to find a mechanism to explain how genetic differences in the region lead to obesity.

“Many studies attempted to link the FTO region with brain circuits that control appetite or propensity to exercise,” says first author Melina Claussnitzer, a visiting professor at CSAIL and instructor in medicine at Beth Israel Deaconess Medical Center and Harvard Medical School. “Our results indicate that the obesity-associated region acts primarily in adipocyte progenitor cells in a brain-independent way.”

To recognize the cell types where the obesity-associated region may act, the researchers used annotations of genomic control switches across more than 100 tissues and cell types. They found evidence of a major control switchboard in human adipocyte progenitor cells, suggesting that genetic differences may affect the functioning of human fat stores.

To study the effects of genetic differences in adipocytes, the researchers gathered adipose samples from healthy Europeans carrying either the risk or the non-risk version of the region. They found that the risk version activated a major control region in adipocyte progenitor cells, which turned on two distant genes, IRX3 and IRX5.

Follow-up experiments showed that IRX3 and IRX5 act as master controllers of a process known as thermogenesis, whereby adipocytes dissipate energy as heat, instead of storing it as fat. Thermogenesis can be triggered by exercise, diet, or exposure to cold, and occurs both in mitochondria-rich brown adipocytes that are developmentally related to muscle, and in beige adipocytes that are instead related to energy-storing white adipocytes.

“Early studies of thermogenesis focused primarily on brown fat, which plays a major role in mice, but is virtually nonexistent in human adults,” Claussnitzer says. “This new pathway controls thermogenesis in the more abundant white fat stores instead, and its genetic association with obesity indicates it affects global energy balance in humans.”

The researchers predicted that a genetic difference of only one nucleotide is responsible for the obesity association. In risk individuals, a thymine (T) is replaced by a cytosine (C) nucleobase, which disrupts repression of the control region and turns on IRX3 and IRX5. This then turns off thermogenesis, leading to lipid accumulation and ultimately obesity.

By editing a single nucleotide position using the CRISPR/Cas9 system — a technology that allows researchers to make precise changes to a DNA sequence — the researchers could switch between lean and obese signatures in human pre-adipocytes. Switching the C to a T in risk individuals turned off IRX3 and IRX5, restored thermogenesis to non-risk levels, and switched off lipid storage genes.

“Knowing the causal variant underlying the obesity association may allow somatic genome editing as a therapeutic avenue for individuals carrying the risk allele,” Kellis says. “But more importantly, the uncovered cellular circuits may allow us to dial a metabolic master switch for both risk and non-risk individuals, as a means to counter environmental, lifestyle, or genetic contributors to obesity.”

The researchers showed that they could indeed manipulate this new pathway to reverse the signatures of obesity in both human cells and mice.

In primary adipose cells from either risk or non-risk individuals, altering the expression of either IRX3 or IRX5 switched between energy-storing white adipocyte functions and energy-burning beige adipocyte functions.

Similarly, repression of IRX3 in mouse adipocytes led to dramatic changes in whole-body energy balance, resulting in a reduction of body weight and all major fat stores, and complete resistance to a high-fat diet.

“By manipulating this new pathway, we could switch between energy storage and energy dissipation programs at both the cellular and the organismal level, providing new hope for a cure against obesity,” Kellis says.

These findings are significant and impressive and point to the idea that science can achieve a cure for obesity – as well as a way to prevent it from ever happening. There are truly genetic differences between us all … and reasons why some of us become obese while others don’t. Science is finding answers at a cellular level that can help millions of people worldwide. This is something we think we’ll hear about a lot more in the future that can have far-reaching implications for health across the globe.

Can obesity be reversed?

3829063385_8e46d16540_oMany different initiatives have been undertaken to attempt to reverse obesity in affected individuals, up to and including bariatric surgery. The recent classification of obesity as a disease has encouraged research and study into effective treatments for the condition. Can obese people turn their situation around, losing weight and keeping it off?

Casting aspersions on the effectiveness of current weight management programs focused on dieting and exercise, it has been found that chances of obese people recovering normal body weight are very slim, shows research.

The chance of an obese person attaining normal body weight is one in 210 for men and one in 124 for women, increasing to one in 1,290 for men and one in 677 for women with severe obesity, the findings showed.

“Once an adult becomes obese, it is very unlikely that they will return to a healthy body weight,” said study’s first author Alison Fildes from the University College London.

The findings suggest that current weight management programs focused on dieting and exercise are not effective in tackling obesity at population level.

The research tracked the weight of 278,982 participants (129,194 men and 149,788) women using electronic health records from 2004 to 2014.

The study, published in the American Journal of Public Health, looked at the probability of obese patients attaining normal weight or a five percent reduction in body weight.

Patients who received bariatric surgery were excluded from the study.

The annual chance of obese patients achieving five percent weight loss was one in 12 for men and one in 10 for women.

For those people who achieved five percent weight loss, 53 percent regained this weight within two years and 78 percent had regained the weight within five years.

Overall, only 1,283 men and 2,245 women with a body mass index (BMI) of 30-35 reached their normal body weight, equivalent to an annual probability of one in 210 for men and one in 124 for women.

For those with a BMI above 40, the odds increased to one in 1,290 for men and one in 677 for women with severe obesity.

Weight cycling, with both increases and decreases in body weight, was also observed in more than a third of patients.

“This evidence suggests the current system is not working for the vast majority of obese patients,” Fildes said.

Finding out what will work for the majority of patients suffering from obesity is still the task at hand. fully supports the continuation of this important research. While the odds don’t look great today, we can only assume that with more research and study, we’ll discovered a combination of medication and lifestyle changes that will have a significant impact on the lives of obese men and women, and help us avoid obesity in future generations.

Obesity crisis may be bigger than we originally thought

shutterstock164062556We’ve been hearing that 30% of the population is overweight or obese for quite a while now. Thirty percent is a big enough number and certainly speaks to the prevalence of the condition of obesity. But today learned that it really may be much larger than that.

New estimates have revealed the extent of one of the biggest public health problems facing the US, as a research letter reports that more than two-thirds of Americans are either overweight or obese.

The authors of the research letter, published in JAMA Internal Medicine, are Dr. Graham A. Colditz and Lin Yang of the Washington University School of Medicine, St. Louis, MO.

Their paper describes an analysis of the most recent data taken from the National Health and Nutrition Examination Survey (NHANES, 2007-12) to calculate the prevalence of overweight and obesity.

Researchers had conducted a similar study around 20 years ago, analyzing data taken from 1988-1994 to work out the chronic disease burden associated with body mass index (BMI). The findings of that study were used to inform clinical practice and prevention strategies.

“Compared with 1988-1994, the distribution of the population’s weight status has increased in the past 20 years,” write the authors of the new research letter. “The rising trends in overweight and obesity warrant timely attention from health policy and health care system decision makers.”

In the new analysis, overweight was defined as a BMI between 25.0 and 29.9. Obesity was defined as a BMI of 30.0 and above and was divided into three different classes. BMIs of 30.0-34.9 were defined as class 1, BMIs of 35.0-39.9 were class 2 and BMIs of 40 and above were class 3.

Data were obtained for 15,208 men and women aged 25 and above in a sample representative of over 188 million adults. The researchers estimated that around 36.3 million men (39.96%) and 28.9 million women (29.74%) were overweight, with around 31.8 million men (35.04%) and 35.9 million women (36.84%) obese.

These findings make alarming reading when considering that overweight and obesity are associated with numerous chronic health conditions, including type 2 diabetes, heart disease and stroke. There is also a financial cost to the problem; the American Heart Association (AHA) estimates that obesity costs $190 billion each year in weight-related medical bills.

Such is the scale of the problem that a Gallup Poll conducted in November 2013 found that obesity was considered to be the third most urgent health problem facing the US, behind cost and access but ahead of cancer and heart diseases, the two leading causes of death in the country.

Dr. Donna H. Ryan – professor and associate executive director for clinical research at the Pennington Biomedical Research Center at Louisiana State University in Baton Rouge – suggests a number of possible triggers for the obesity epidemic.

These suggestions include changes to sleep patterns, increased availability of food and more sedentary lifestyles fueled by the decreased physical demands of many jobs and increased “screen time” with the use of televisions, computers and smartphones.

“Population-based strategies helping to reduce modifiable risk factors such as physical environment interventions, enhancing primary care efforts to prevent and treat obesity, and altering societal norms of behavior are required,” state the authors.

Dr. Ryan believes that society must learn to treat obesity as a disease rather than a consequence of a lack of willpower, becoming more accepting of people with the condition:

“If you have not had a friend, family member or colleague who has struggled with their weight and particularly if you haven’t tried to lose weight yourself, then it’s easy for you to ascribe negative stereotypical traits to overweight and obese people. It’s a lot like alcohol and drug addiction. Our society is more accepting of these conditions as a disease and less so for obesity.”

Previously, Medical News Today reported on a study finding that stepping on the scales daily and tracking the results on a chart is an effective way of losing weight and keeping it off.

We’ve been referring to obesity as a disease medically. But we know that in the minds of the population it isn’t necessarily viewed as other diseases. Instead, as the article states, obesity is looked upon more as a lack of willpower — some sort of a character flaw. It involves shame and sometimes shunning. It’s time to rethink our views in order to arrive at solutions for this tremendous health crisis.

Fructose and weight gain. Turns out not all sugar is sugar after all.

Fructose-in-the-firing-line-Study-warns-of-weight-gain-and-increased-body-fat-compared-to-glucose_strict_xxlWe all remember those ads from the Corn Refiner’s Association for “corn sugar” — high fructose corn syrup. In an effort to gain consumer acceptance of high fructose corn syrup, the CRA ran a television advertisement proclaiming that “sugar is sugar.” The concept didn’t fly very well with consumers (or with lawyers for that matter). Since that time, high fructose corn syrup has been linked with weight gain — and new studies seem to be proving the idea out more and more.

In the last 40 years, fructose, a simple carbohydrate derived from fruit and vegetables, has been on the increase in American diets. Because of the addition of high-fructose corn syrup to many soft drinks and processed baked goods, fructose currently accounts for 10 percent of caloric intake for U.S. citizens. Male adolescents are the top fructose consumers, deriving between 15 to 23 percent of their calories from fructose–three to four times more than the maximum levels recommended by the American Heart Association.

A recent study at the Beckman Institute for Advanced Science and Technology at the University of Illinois found that, matched calorie for calorie with the simple sugar glucose, fructose causes significant weight gain, physical inactivity, and body fat deposition.

The paper, “Fructose decreases physical activity and increases body fat without affecting hippocampal neurogenesis and learning relative to an isocaloric glucose diet,” was published in Scientific Reports.

“The link between increases in sugar intake, particularly fructose, and the rising obesity epidemic has been debated for many years with no clear conclusions,” said Catarina Rendeiro, a postdoctoral research affiliate at the Beckman Institute for Advanced Science and Technology and lead author on the study. “The reality is that people are not only consuming more fructose through their diets, but also consuming more calories in general.

“One of the key questions is whether an increase in fructose intake contributes to obesity in the absence of excessive calorie intake.”

The researchers, under the direction of Justin Rhodes of Beckman’s NeuroTech Group and professor of psychology at Illinois, studied two groups of mice for two-and-a-half months: one group was fed a diet in which 18 percent of the calories came from fructose, mimicking the intake of adolescents in the United States, and the other was fed 18 percent from glucose.

“The important thing to note is that animals in both experimental groups had the usual intake of calories for a mouse,” said Rendeiro. “They were not eating more than they should, and both groups had exactly the same amount of calories deriving from sugar, the only difference was the type of sugar, either fructose or glucose.”

The results showed that the fructose-fed mice displayed significantly increased body weight, liver mass, and fat mass in comparison to the glucose-fed mice.

“In previous studies, the increases in fructose consumption were accompanied by increases in overall food intake, so it is difficult to know whether the animals put on weight due to the fructose itself or simply because they were eating more,” Rhodes said.

Remarkably, the researchers also found that not only were the fructose-fed mice gaining weight, they were also less active.

“We don’t know why animals move less when in the fructose diet,” said Rhodes. “However, we estimated that the reduction in physical activity could account for most of the weight gain.”

“Biochemical factors could also come into play in how the mice respond to the high fructose diet,” explained Jonathan Mun, another author on the study. “We know that contrary to glucose, fructose bypasses certain metabolic steps that result in an increase in fat formation, especially in adipose tissue and liver.”

The precise mechanisms are still being investigated, but one thing is certain: high intake of fructose by itself adds pounds.

“We designed this study based on the intake of fructose by adolescents in the United States,” said Rhodes. “Our study suggests that such levels of fructose can indeed play a role in weight gain, favor fat deposition, and also contribute to physical inactivity. Given the dramatic increase in obesity among young people and the severe negative effects that this can have on health throughout one’s life, it is important to consider what foods are providing our calories.” knows that everyone in our community counts high-fructose corn syrup among the top ingredients they avoid. Not all sugar is just sugar for our bodies. Fructose isn’t the same as cane sugar and studies like this are illustrating the facts regarding the subject.

Finding it tough to take off those extra pounds? It may have more to do with your biology than your willpower.

150511162918_1_540x360Did you ever wonder how two people can follow the same exact diet, strictly adhere to it, and end up with two completely different sets of results? Some people do seem to have an easier time taking off weight than others. We’ve heard people say that it’s “in their genes,” but for those who can’t seem to get the weight off, it’s really not enough information to help them. Especially for obese people desperately trying to shed pounds, that simple statement does nothing to help them find out what they need to focus on to make a diet work for them.

For the first time in a lab, researchers at the National Institutes of Health found evidence supporting the commonly held belief that people with certain physiologies lose less weight than others when limiting calories. Study results published May 11 in Diabetes.

Researchers at the Phoenix Epidemiology and Clinical Research Branch (PECRB), part of the NIH’s National Institute of Diabetes and Digestive and Kidney Diseases, studied 12 men and women with obesity in the facility’s metabolic unit. Using a whole-room indirect calorimeter — which allows energy expenditure to be calculated based on air samples — researchers took baseline measurements of the participants’ energy expenditure in response to a day of fasting, followed by a six-week inpatient phase of 50 percent calorie reduction. After accounting for age, sex, race and baseline weight, the researchers found that the people who lost the least weight during the calorie-reduced period were those whose metabolism decreased the most during fasting. Those people have what the researchers call a “thrifty” metabolism, compared to a “spendthrift” metabolism in those who lost the most weight and whose metabolism decreased the least.

“When people who are obese decrease the amount of food they eat, metabolic responses vary greatly, with a ‘thrifty’ metabolism possibly contributing to less weight lost,” said Susanne Votruba, Ph.D., study author and PECRB clinical investigator. “While behavioral factors such as adherence to diet affect weight loss to an extent, our study suggests we should consider a larger picture that includes individual physiology — and that weight loss is one situation where being thrifty doesn’t pay.”

Researchers do not know whether the biological differences are innate or develop over time. Further research is needed to determine whether individual responses to calorie reduction can be used to prevent weight gain.

“The results corroborate the idea that some people who are obese may have to work harder to lose weight due to metabolic differences,” said Martin Reinhardt, M.D., lead author and PECRB postdoctoral fellow. “But biology is not destiny. Balanced diet and regular physical activity over a long period can be very effective for weight loss.”

More than one-third of American adults are obese. Complications from obesity can include heart disease, type 2 diabetes and certain types of cancer, some of the leading causes of preventable death.

“What we’ve learned from this study may one day enable a more personalized approach to help people who are obese achieve a healthy weight,” said NIDDK Director Griffin P. Rodgers, M.D. “This study represents the latest advance in NIDDK’s ongoing efforts to increase understanding of obesity.”

The study does seem to suggest that for obese people, dieting needs to be individually focused. Perhaps staying on a specific eating regimen for six months may work for some, but others will need a year long program. Perhaps specific foods need to be included for some and not for others. And exercise may fall into that same category.

Obesity doesn’t appear to be a one-size-fits-all diagnosis. It affects health in different ways for different people. understands that it makes sense that reversing obesity in specific individuals can require more than a one-size-fits-all approach. That’s probably true for the non-obese population as well. Find what works for your body and your lifestyle and stick to it as long as it’s necessary to shed the pounds you want to see gone. All of us should keep in mind that the best diet isn’t a diet at all, it’s a lifestyle. A healthy, balanced approach to nutritious foods helps us all maintain ideal weight and avoid weight-related health problems.

Obesity and Inflammation … new insights into obesity-related metabolic conditions

1263-obese-woman-eating-enormous-burger_0Metabolic conditions caused by obesity are in the news consistently. Complications like high blood pressure, Type 2 diabetes, cancer and heart disease can, in many instances, be linked with obesity. While we know the link exists, it’s been difficult to understand how these things are a direct result of excessive body fat. Understanding that obesity affects health negatively isn’t enough. Getting to the root of the problem is key to help doctors and individuals reverse the obesity crisis for generations to come.

Teams led by Nicolas Venteclef, Inserm Research Fellow (Cordeliers Research Centre, Inserm/Pierre and Marie Curie University Joint Research Unit 1138, Paris, France) and Irina Udalova (Kennedy Institute of Rheumatology, University of Oxford, UK) in collaboration with several teams, have succeeded in elucidating part of the mechanisms involved in the development of these metabolic complications associated with obesity. Results of these studies are published online in the journal Nature Medicine.

Currently, over one and a half billion people worldwide suffer from overweight or obesity. We have known for about a decade that a chronic state of inflammation is present in obese patients. This state might play a fundamental role in the development of associated metabolic diseases. This inflammation results from abnormal activity of the immune system observed both systemically (bloodstream) and locally (in metabolic organs such as the liver, muscles, pancreas and especially the adipose tissue).

Following excessive weight gain, the adipose tissue develops in an abnormal manner in the intra-abdominal region (android obesity), and becomes an important source of pro-inflammatory mediators, the “chemical messengers” that activate inflammation, with harmful metabolic consequences. This phenomenon is particularly provoked by the accumulation of pro-inflammatory macrophages in this tissue. Paradoxically, some obese subjects do not develop metabolic alterations. Indeed, when adipose tissue expansion occurs in the more superficial deposits, such as the subcutaneous adipose tissue (gynoid obesity), the risk of developing metabolic complications is reduced.

In an earlier study (Dalmas et al. Diabetes 2014), the team led by Karine Clément (Guerre-Millo and coll., UMR_S 1166, Paris, France), in collaboration with Nicolas Venteclef, had observed the importance of inflammatory and prodiabetogenic cross-talk between macrophages and lymphocytes in the visceral adipose tissue of obese patients. By characterising these macrophages, they were able to identify transcription factor IRF5 (Interferon Regulatory Factor 5) as the orchestral conductor of macrophage activation in adipose tissue in obesity.

In order to demonstrate the importance of IRF5 in obesity and type 2 diabetes, the authors generated mice lacking this factor, and then subjected them to a high-fat diet that usually induces obesity and type 2 diabetes. Surprisingly, mice deficient in IRF5 did develop obesity, but without metabolic complications, in contrast to wild-type mice expressing IRF5. This beneficial adaptation by IRF5-deficient mice can be explained by preferential storage of fat in the subcutaneous (protective) and not the intra-abdominal (harmful) region. Decoding of molecular and cellular mechanisms made it possible to show a substantial reprogramming of inflammation in the visceral adipose tissue when IRF5 is absent, which helps to limit its expansion. Indeed, in the absence of IRF5, obesity induces an immune response characterised by the presence of anti-inflammatory macrophages and reduced immune response activation. This modification induces tissue remodelling that limits the expansion of intra-abdominal adipose tissue. This allows the redistribution of lipids in the intra-abdominal cavity to the subcutaneous deposits, a less harmful form of storage for the body.

Data obtained with mice were confirmed in overweight, obese or massively obese patients, by showing significant correlation between IRF5 expression in the visceral adipose tissue and metabolic dysfunctions associated with obesity.

This pioneering study suggests that the immune system (in this case the macrophages of the adipose tissue) directly influences the accumulation of fatty matter in the visceral region, a likely target in the prevention of type 2 diabetes. For the researchers, “It is therefore crucial to decipher the different aspects of inflammation in order to better understand the multifactorial diseases associated with obesity, such as type 2 diabetes.”

The approach implemented in this study encapsulates translational research, which is aimed at developing effective therapies for patients by establishing a fruitful dialogue between clinicians and researchers, in order to produce robust results that are supported by mouse models while being relevant to humans.

Obesity and inflammation appear to go hand in hand. Scientists are beginning to understand exactly how obesity affects the body which will eventually yield treatments, not simply for the metabolic difficulties that plague the obese population, but hopefully for the treatment of obesity as a disease. is hopeful that research like this will not only result in successful treatments, but also add to a different understanding of obesity as a health condition. By removing the stigma attached to obesity in society and creating an understanding of the disease of obesity, we’re more likely to move in the right direction for everyone.

Scientists block obesity-related protein in mice and stop fat formation

150506133621_1_540x360We’ve known for a while that where a person develops fat in their body is very significant in the determination of obesity-related health issues. Belly fat is bad fat and puts people at a higher risk for diseases like type 2 diabetes as well as other metabolic issues. A new study out of Oxford University looked at how blocking one protein in mice might change the course of obesity-related conditions.

By changing mouse genes to block a protein associated with obesity, Oxford University scientists have prevented fat from forming around the animals’ internal organs, even when the animals eat an unhealthy diet. The study in Nature Medicine found that these genetically engineered mice also retained their sensitivity to insulin (normally blunted by obesity), despite gaining weight.

Visceral fat deposits around internal organs in the stomach are particularly harmful: they are associated with insulin resistance, type-2 diabetes and heart disease. The study, conducted in close collaboration with researchers at the at the French Institute of Health and Medical research (INSERM) in Paris, shows that changing the pattern of fat deposition from around the stomach to under the skin starts a chain of events which result in insulin sensitivity being maintained, reducing the chances of type-2 diabetes.

Researchers already know that visceral fat attracts special M1-type macrophages (immune cells that attack infections and damaged cells). These M1-type macrophages produce harmful proteins that promote insulin resistance. ‘We’ve previously found that a protein called interferon regulatory factor-5 (IRF-5) seems to push macrophages to change from a more ‘peaceful’, M2-type to the more aggressive M1-type’, said Professor Irina Udalova at the Kennedy Institute of Rheumatology at Oxford University, ‘so we wondered if ‘deleting’ IRF-5 might have a beneficial effect’.

To test this idea, the two research teams fed the mice that were lacking the gene coding for IRF-5 with a healthy diet or a high-fat one. The mice with genetic changes were no different from standard lab mice when both the groups ate the healthy diet. Both groups of mice gained weight when they ate the high-fat diet. However, the mice with the altered gene piled on the fat under the skin, rather than around the internal organs in their stomach. The size of the fat cells in the stomach was also smaller in these mice, because there was more collagen (a ‘scaffolding’ protein that provides the structure for many parts of the body) deposits, holding the fat cells in.

‘The mice without IRF-5 still got fat, but what was different was where they deposited this fat. We know that people who put on fat around their belly have a higher risk of developing obesity-related illnesses such as type-2 diabetes, compared to people who put on weight around their thighs. But we can’t change the pattern of fat deposition in people, which we can now do in these mice. So this turned out to be an excellent way of testing if changing the pattern of fat deposition actually changes the factors that lead to type-2 diabetes’, said Professor Udalova.

The researchers tested this idea by giving the mice a very sweet drink, containing glucose. They then tracked how quickly the glucose was broken down by insulin. Obesity can make the body less sensitive to insulin, which means that it takes longer for the glucose to disappear from the blood stream. This loss of sensitivity can eventually lead to type-2 diabetes. Despite being fatter, the mice without IRF-5 did better than the standard mice on this glucose challenge test.

Researchers at INSERM also found that IRF-5 levels were elevated in fatty tissue from very obese people, especially in their visceral fat. A gene analysis of this group of people found that the higher the levels of IRF-5, the lower the levels of another protein produced by macrophages, transforming growth factor beta (TGFbeta). By mimicking the environment in fatty tissue in a test-tube, the researchers also found that artificially increasing the levels of IRF-5 in cells from thin people reduced the levels of TGFbeta, similar to what was found in the obese people. The researchers think that reducing IRF-5 levels sets off a chain of events, starting with increased TGFbeta levels. Increased TGFbeta in turn leads to more collagen being deposited, which results in ‘remodelling’ of abdominal fat deposits, and the release of other chemicals that maintain insulin sensitivity.

‘We found that the mice without IRF-5 were essentially healthy, despite being significantly fatter. Blocking IRF-5′s activity may however have other side-effects, such as increasing allergies. So more work is needed to understand if changing levels of IRF-5 (by using new drugs to target the protein) in humans would be a good way of treating the problem of obesity and obesity associated metabolic diseases. But the results show very clearly that where you get fat matters a lot’, said Professor Udalova.

We can’t genetically engineer human beings — at least not just yet, thankfully. But this information certainly raises the idea that science may come up with a way to block the protein in humans, thus redirecting the course of obesity related disease. is certainly encouraged by the findings. We still do believe that a healthy, balanced diet beginning in childhood would do everyone a world of good. The before-the-fact solution is easier, less expensive and ultimately healthier than treating obesity after it has already occurred.

Diet and exercise may not be the cure for obesity

obesity is fairly certain that most people think that the best thing to do for obesity is to establish a healthy, low-calorie diet and a consistent exercise schedule. It only makes sense that diet and exercise would be the key ingredients in reversing the condition. Sometimes, though, the things that may appear to make the most sense could, in fact, be counterintuitive to the problem.

According to a new research done by Johns Hopkins Bloomberg School of Public Health, diet and exercise might not be enough to cure obesity. The researchers are asking the physicians to look for their biological mechanisms, which makes it harder for obese people to lose weight. According to Christopher Ochner, an assistant Professor of Pediatrics and Psychiatry at the Icahn School of Medicine at Mount Sinai in New York, “When people diet, the body thinks that it’s starving, so several biological mechanisms kick in to encourage people to eat more so that they gain the weight back”. He then added, “For example, the body slows down the rate at which it burns calories in order to conserve fat, and there are changes in brain signaling that make people more attracted to high-calorie foods”.

In the statement Ochner also stated that, “These mechanisms originally evolved to help humans survive when food was scarce, but the problem is that those same mechanisms kick in if somebody is 400 lbs. and trying to lose 40 lbs”. Ochner noted, “In people who have been obese for many years. Body weight seems to become biologically ‘stamped in’ and defended”.

He suggested that doctors should consider before giving advice to these people about losing weight by dieting and exercising as these methods are not going to work for them. But researchers are also saying that the current biological treatment for obesity is expensive and there are no proven data about the long term effectiveness of this treatment is available. Over the long term till to date an operation on the stomach and intestine is the only treatment for obesity that has been shown to be effective.

Ochner said, “We don’t have enough treatments to address our underlying biology [of obesity]. We would like to see other, safer, more widely available treatments”.

We should all be concerned with the quality of our diet and making sure we get enough exercise. But it does seem that diet and exercise have their limits in terms of extensive weight loss. While weight loss surgery has certainly become more successful and, thus, more common, it remains serious surgery with many risks. We’ll be watching for the introduction of other obesity treatments in addition to better diet and exercise.