Category Archives: Obesity Crisis

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. FoodFacts.com 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.

http://zeenews.india.com/news/health/health-news/most-obese-people-likely-to-stay-fat_1632507.html

Can obesity be genetic? New inherited form of obesity identified

150630080159_1_900x600Obesity is classified as a disease. For a myriad of reasons, that classification is important to how we perceive both the condition itself and the people struggling with it. It’s also helped further research into possible causes of and treatments for obesity. And new research just made available has uncovered some significant information.

A large number of genes are involved in regulating body weight, and there are now over 30 genes known in which people with harmful changes in DNA sequence become extremely overweight. Similarly, there are a number of genes that can, when altered, cause type 2 diabetes. These conditions are inherited through families in exactly the same way as disorders such as cystic fibrosis or Huntington’s disease.

It is unclear what proportion of severe obesity and type 2 diabetes is caused by genetic disease.

Researchers at Imperial College London discovered the new defect by sequencing the DNA of an extremely obese young woman and members of her family. In addition to an increased appetite leading to severe weight problems from childhood, she had type 2 diabetes, learning difficulties, and reproductive problems.

They found that she had inherited two copies of a harmful genetic change that meant she could not make a protein called carboxypeptidase-E (CPE). This is an enzyme that is important in the proper processing of a number of hormones and brain transmitters controlling appetite, insulin and other hormones important in the reproductive system.

Studies have previously shown that CPE deficiency causes obesity, diabetes, and impaired memory in mice, but no humans with the condition have been found before. CPE deficiency is a recessive condition, so a person would need to inherit the altered genetic sequence from both parents to be affected.

The study, published in the journal PLOS ONE, was funded by the NIHR Imperial Biomedical Research Centre and Diabetes UK.

Professor Alex Blakemore from the Department of Medicine at Imperial College London, who led the study, said: “There are now an increasing number of single-gene causes of obesity and diabetes known. We don’t know how many more have yet to be discovered, or what proportion of the severely obese people in our population have these diseases — it is not possible to tell just by looking.

“These are serious disorders that affect the body’s ability to regulate hunger and fullness signals. They are inherited in the just same way as other genetic diseases and the sufferers should not be stigmatized for their condition. They should be offered genetic counselling and specialized lifelong support to allow them as healthy a life as possible.”

The patient was clinically evaluated by consultant endocrinologist Dr Tony Goldstone, who runs a specialist genetics obesity clinic at Hammersmith Hospital. The patient’s parents are cousins, giving her a relatively high likelihood of inheriting the same genetic change from both parents. She had an older brother with similar symptoms who died aged 21.

The first author Dr Sanne Alsters, also in the Department of Medicine, who carried out the genetic tests, said: “Finding a genetic cause for the patient’s problems has helped her and her family to understand and manage her condition better. We can also look at members of her family with one abnormal copy of the gene, to see they are affected in more subtle ways that could increase their risk of obesity.”

Professor Blakemore said genetic tests should be widely available for patients with severe obesity. “If people are diagnosed with a genetic condition like this one, we can look for other possible symptoms, and offer genetic advice to other family members if they want this. Diagnosis is very valuable to the patient. It helps to set realistic expectations, and can help them get the best possible treatment,” she said.

Research like this can lead to better outcomes for obese people seeking treatment. In addition to those benefits, the stigma surrounding obesity may begin to dissipate. One cannot be responsible for one’s own genetics.  FoodFacts.com is painfully aware that the perception of the obese has not changed.  Obese people can be viewed as people who don’t know when to stop eating and don’t know when to start moving.  That can truly be changed with the realization of a genetic component to the disease. Once the stigma is lifted, treatment can be much more effective.

http://www.sciencedaily.com/releases/2015/06/150630080159.htm

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 FoodFacts.com 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.

http://www.medicalnewstoday.com/articles/295734.php

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.”

FoodFacts.com 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.

http://www.sciencedaily.com/releases/2015/06/150601122540.htm

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. FoodFacts.com 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.

http://www.sciencedaily.com/releases/2015/05/150511162918.htm

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. FoodFacts.com 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.

http://www.sciencedaily.com/releases/2015/05/150507114320.htm

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. FoodFacts.com 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.

http://www.sciencedaily.com/releases/2015/05/150506133621.htm

Sugar consumption driving obesity and diabetes

sugar-obesity-webFoodFacts.com has conscientiously covered news regarding the obesity crisis for the last few years. We’ve covered junk food, fast food, processed food, white bread, chocolate, and genetics (among hundreds of other things) as links to obesity and weight gain. The research we read today though, made so much sense. That sense began with the concepts behind the study.

In the report, published Thursday in the Mayo Clinic Proceedings, a team of researchers performed a literature review to determine whether certain ingredients are much more dangerous than others when it comes to diabetes, and to challenge the idea that all calories are equal. To do so, they looked at the effects of carbohydrates from similar calories. They compared starch, pure glucose and lactose to added sugars like sucrose (table sugar) and fructose, which occurs naturally in fruit but which we mostly consume as a sweetener, such a with high-fructose corn syrup, added to food and drinks).

What they found was that the added sugars were significantly more harmful. Fructose was linked to worsening insulin levels and worsening glucose tolerance, which is a driver for pre-diabetes. It caused harmful fat storage—visceral fat on the abdomen—and promoted several markers for poor health like inflammation and high blood pressure. “We clearly showed that sugar is the principal driver of diabetes,” says lead study author James J. DiNicolantonio, a cardiovascular research scientist at Saint Luke’s Mid America Heart Institute. “A sugar calorie is much more harmful.”

DiNicolantonio and his fellow authors say current dietary guidelines are harmful since they recommend levels of sugar consumption that are unhealthy. For instance, the Institute of Medicine says added sugar can make up 25% of the total calories we consume, and the 2010 Dietary Guidelines for Americans say up to 19% of calories from added sugars is alright. That varies greatly from the American Heart Association, which recommends no more than 6 tsp of sugar a day for women 9 tsp for men. The World Health Organization has proposed that added sugar make up only 5% of a person’s daily calories.

“The studies that we looked at clearly show that once you hit 18 percent compared to just 5 percent of your total calories from sugar, there’s significant metabolic harms promoting prediabetes and diabetes,” says DiNicolantonio. “In fact, there’s a two-fold increase.”

This is not the first time sugar has been fingered as a primary culprit in American’s bad health. Other researchers are pushing the message that it’s refined carbohydrates like added sugars that are the problem.

“We need to understand that it isn’t the overconsuming of calories that leads to obesity and leads to diabetes. We need to totally change that around,” says DiNicolantonio. “It’s refined carbs and added sugars that lead to insulin resistance and diabetes, which leads to high insulin levels, which drives obesity.”

DiNicolantonio recommends major changes to combat the problem. He says the government should stop subsidizing corn which makes high fructose corn syrup so cheap and should instead subsidize healthy foods so that consumers are encouraged to make the switch from processed foods to whole foods, since it’s the processed stuff that’s putting so much sugar in our diets. He adds that in his opinion, sugar-sweetened beverages should not be sold in schools or hospitals, and perhaps the government should put warning labels on them.

Such severe changes are not likely in the immediate future, but if sugar is indeed the number on cause for diabetes among all other foods, then more needs to happen to help Americans cut back. Especially since there is no real need for added sugar in our diets.

Sugar is addicting for millions of us. And food manufacturers have fed that addiction by adding sugar to most every product in our grocery stores. We’re eating too much of it. Sure, we believe in coincidences sometimes — but not here. The tremendous rise in obesity across the globe doesn’t simply coincide with the meteoric rise in the availability of processed food, junk food, fast food and sugary beverages. They go hand in hand and it’s time to make the real changes that will allow us to reverse this life-threatening trend.

http://time.com/3687808/this-is-the-number-1-driver-of-diabetes-and-obesity/

New study debunks the concept of healthy obesity

obesity-460_784309cIn the last few weeks FoodFacts.com posted information from a study that claimed that for certain people obesity might not have long-term health implications. The concept of “healthy obesity” has become an actual theory among some researchers and some in the general population.

But now a new study shows that the idea may be quite misleading, since over time, healthy obesity often devolves into unhealthy obesity, and the markers of health naturally worsen over time. So “healthy obesity” may not be a steady state at all – it may just be a phase that will likely deteriorate in the future.

The researchers, from University College London, looked at data over a period of 20 years – longer than any study on healthy obesity had tracked health previously. Their first group consisted of 2500 people, 66 of whom were said to be “healthy obese,” based on their metabolic profiles, which included analyses of high-density lipoprotein (“good”) cholesterol, blood pressure, fasting glucose or use of diabetes medication, triglyceride (blood fats) levels, and insulin resistance.

Of those who started out in the “healthy obese” category, over the next two decades, more than half had moved into the “unhealthy obese” category – and just 6% had lost enough weight to move into the healthy non-obese category.

The researchers then looked at a larger group of participants, consisting of 389 “healthy obese.” After 10 years, 35% had become “unhealthy obese”; after 15 years, it had risen to 38%, and to 48% after 20 years. Just 10% of the original healthy obese had lost the weight to become “healthy non-obese” after 20 years. Which prompted the authors to suggest that the “natural course of healthy obesity is progression to metabolic deterioration.”

In other words, for most people, healthy obesity is just a phase that will likely give way to unhealthy obesity in the future.

This is not the first study to suggest that healthy obesity is somewhat of a myth, at least for most people. Earlier research had found that obesity of any kind, healthy or unhealthy, increases the risk of heart disease, diabetes, cancer, and early death. What’s more, even shorter-term studies than the current one have shown that the good metabolic markers of the healthy obese do tend to deteriorate with time. “A few previous studies,” author Joshua Bell tells me, “using shorter follow-up times showed about one-third of healthy obese adults progress to unhealthy obesity. And our study with at least 10 years longer follow-up, indicates that this tendency gets stronger with time, with about half making this transition after 20 years….These results indicate that healthy obesity is often just a phase.”

Some of the healthy obese participants in the current study did remain so over time – even after 20 years, about a third of the participants still had good metabolic profiles. “However,” says Bell, “the tendency for these adults to progress to unhealthy obesity gets stronger with time… Healthy obese adults tend to get worse, not better.”

The takeaway message may be that for most people, weight loss really is the best bet: Even though markers may look good now, they may not be in 10 or 20 years’ time. A small subset of people may be obese into old age, but for the majority, obesity is linked to greater risk of a number of chronic diseases and mortality over the long term.

“Adults of any size can take steps to improve health by avoiding processed foods and embedding physical activity into daily life,” says Bell. “This can reduce harmful visceral fat, build muscle, and reduce inflammation even if weight is not initially lost. Our results stress the need to take a long-term view of healthy obesity, as healthy obese adults tend to progress to ill-health over time. Healthy obesity is still a high-risk state – the harmful effects may just be delayed.”

We’re not surprised to see the release of new information that contradicts the most recent study regarding “healthy obesity.” It’s a controversial concept so it’s possible we’ll be hearing even more conflicting information. The healthiest response to obesity is reversing the condition. We don’t need more information to figure out that concept for ourselves.

http://www.forbes.com/sites/alicegwalton/2015/01/06/is-healthy-obesity-a-real-thing-not-likely-study-says/

Not all obese people are prone to metabolic issues

scaleThe effects of obesity are very well known. The biggest concerns surrounding the condition are diabetes, heart disease and stroke. For a long while, it’s been assumed that obesity and metabolic conditions go hand in hand. But new research is pointing to the idea that this may not necessarily be the case.

In a study at Washington University School of Medicine in St. Louis, researchers found that a subset of obese people do not have common metabolic abnormalities associated with obesity, such as insulin resistance, abnormal blood lipids (high triglycerides and low HDL cholesterol), high blood pressure and excess liver fat.

In addition, obese people who didn’t have these metabolic problems when the study began did not develop them even after they gained more weight.

The study involved 20 obese participants who were asked to gain about 15 pounds over several months to determine how the extra pounds affected their metabolic functions.

“Our goal was to have research participants consume 1,000 extra calories every day until each gained 6 percent of his or her body weight,” said first author Elisa Fabbrini, MD, PhD, assistant professor of medicine. “This was not easy to do. It is just as difficult to get people to gain weight as it is to get them to lose weight.”

All of the subjects gained weight by eating at fast-food restaurants, under the supervision of a dietitian. The researchers chose fast-food chain restaurants that provide rigorously regulated portion sizes and nutritional information.
Before and after weight gain, the researchers carefully evaluated each study subject’s body composition, insulin sensitivity and ability to regulate blood sugar, liver fat and other measures of metabolic health.

After gaining weight, the metabolic profiles of obese subjects remained normal if they were in the normal range when the study began. But the metabolic profiles significantly worsened after weight gain in obese subjects whose metabolic profiles already were abnormal when the study got underway.

“This research demonstrates that some obese people are protected from the adverse metabolic effects of moderate weight gain, whereas others are predisposed to develop these problems,” said senior investigator Samuel Klein, MD, the Danforth Professor of Medicine and Nutritional Science and director of Washington University’s Center for Human Nutrition.

“This observation is important clinically because about 25 percent of obese people do not have metabolic complications,” he added. “Our data shows that these people remain metabolically normal even after they gain additional weight.”

As part of the study, the researchers then helped the subjects lose the weight they had gained.

“It’s important to point out that once the study was completed, we enrolled all subjects in our weight-loss program to make sure they lost all of the weight they had gained, or more,” said Klein, who also directs the Division of Geriatrics and Nutritional Science and the Atkins Center of Excellence in Obesity Medicine.

The researchers identified some key measurements that distinguished metabolically normal obese subjects from those with problems. One was the presence of fat inside the liver. Those with abnormal metabolism accumulated fat there.

Another difference involved gene function in fat tissue. People with normal metabolism in spite of their obesity expressed more genes that regulate fat production and accumulation. And the activity of those genes increased even more when the metabolically normal people gained weight. That wasn’t true for people with abnormal metabolism.

“These results suggest that the ability of body fat to expand and increase in a healthy way may protect some people from the metabolic problems associated with obesity and weight gain,” said Klein.

He noted that obesity contributes to more than 60 different unhealthy conditions.
“We need more studies to try to understand why obesity causes specific diseases in some people but not in others,” Klein said. “Could it be genetics, specific dietary intake, physical lifestyle, emotional health or even the microbes that live in the gut?”

As they look for answers, Klein and his colleagues plan to more closely analyze fat, muscle and liver tissue and to include lean people in future studies so that the researchers can learn more about how and why some individuals are protected from metabolic problems while others are vulnerable.

While FoodFacts.com knows that it is good news that about a quarter of the obese population seem to have genetic protection from metabolic difficulties, that does leave the bulk of those afflicted at risk for serious health problems. This research and the related studies that follow will result in benefits for those who are at risk … hopefully leading to real answers with meaningful solutions.

http://www.sciencedaily.com/releases/2015/01/150102172716.htm