Mediterranean diet may help stave off cognitive decline for older adults

150511124849_1_540x360We’ve been hearing more and more regarding the health benefits of the Mediterranean diet. FoodFacts.com has always considered this diet as more of a lifestyle choice as it was born from the lifestyle of the Mediterranean population. Rich in vegetables, fruits, grains, and lean proteins (mostly fish), the diet allows for a wide variety of healthy food choices that offer both flavor and variety. The health benefits are truly impressive and we keep learning that there are new ones linked to Mediterranean-style eating. Here is another new addition to that already-impressive list.

Supplementing the plant-based Mediterranean diet with antioxidant-rich extra virgin olive oil or mixed nuts was associated with improved cognitive function in a study of older adults in Spain but the authors warn more investigation is needed, according to an article published online by JAMA Internal Medicine.
Emerging evidence suggests associations between dietary habits and cognitive performance. Oxidative stress (the body’s inability to appropriately detoxify itself) has long been considered to play a major role in cognitive decline.

Previous research suggests following a Mediterranean diet may relate to better cognitive function and a lower risk of dementia. However, the observational studies that have examined these associations have limitations, according to the study background.

Emilio Ros, M.D., Ph.D., of the Institut d’Investigacions Biomediques August Pi Sunyer, Hospital Clinic, Barcelona, and Ciber Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Madrid, and coauthors compared a Mediterranean diet supplemented with olive oil or nuts with a low-fat control diet.

The randomized clinical trial included 447 cognitively healthy volunteers (223 were women; average age was nearly 67 years) who were at high cardiovascular risk and were enrolled in the Prevencion con Dieta Mediterranea nutrition intervention.

Of the participants, 155 individuals were assigned to supplement a Mediterranean diet with one liter of extra virgin olive oil per week; 147 were assigned to supplement a Mediterranean diet with 30 grams per day of a mix of walnuts, hazelnuts and almonds; and 145 individuals were assigned to follow a low-fat control diet.

The authors measured cognitive change over time with a battery of neuropsychological tests and they constructed three cognitive composites for memory, frontal (attention and executive function) and global cognition. After a median of four years of the intervention, follow-up tests were available on 334 participants.

At the end of the follow-up, there were 37 cases of mild cognitive impairment: 17 (13.4 percent) in the Mediterranean diet plus olive oil group; eight (7.1 percent) in the Mediterranean diet plus nuts group; and 12 (12.6 percent) in the low-fat control group. No dementia cases were documented in patients who completed study follow-up.

The study found that individuals assigned to the low-fat control diet had a significant decrease from baseline in all composites of cognitive function. Compared with the control group, the memory composite improved significantly in the Mediterranean diet plus nuts, while the frontal and global cognition composites improved in the Mediterranean diet plus olive oil group.

The authors note the changes for the two Mediterranean diet arms in each composite were more like each other than when comparing the individual Mediterranean diet groups with the low-fat diet control group.

“Our results suggest that in an older population a Mediterranean diet supplemented with olive oil or nuts may counter-act age-related cognitive decline. The lack of effective treatments for cognitive decline and dementia points to the need of preventive strategies to delay the onset and/or minimize the effects of these devastating conditions. The present results with the Mediterranean diet are encouraging but further investigation is warranted,” the study concludes.

If you’re interested in trying to follow a Mediterranean diet, it’s fairly simple to do and there are resources all over the internet that can help you. Mediterranean-style eating emphasizes vegetables, fruits and grains supplemented with fish and some other lean proteins in small amounts. It allows for flexible menus — you won’t be eating the same meals repeatedly. It also allows for tremendous flavors and doesn’t ignore your desire to eat well at the expense of being healthy. And most importantly, it’s really not a diet. It doesn’t have a beginning and an end. It’s really an eating style that’s simple to incorporate into your life. It’s definitely worth a look.

http://www.sciencedaily.com/releases/2015/05/150511124849.htm

Fast food marketing influences teenage boys far more than teenage girls

child eating beefburgerParents of teenagers understand just how different teenage boys and girls can be. But regardless of the gender of your teenager, at some point during these important years, we begin to relinquish a small amount of our decision making for them to them. The way they choose to dress and wear their hair come to mind immediately. Their food choices are another area where our teenagers begin to rely on themselves more and more. Even though they may be home for dinner every night, they are all spending more and more time away from us, with their friends at school and sports activities. Regardless of how much we’ve emphasized healthy eating, they have plenty of opportunity to fall in love with junk food. Our teenagers are subjected to a constant barrage of messaging from fast food and junk food on a daily basis.

Despite our knowledge of its scant nutritional value and questionable degree of quality, fast food does have its appeal. When it’s sweet, it’s really sweet; when it’s salty, it’s really salty; when it’s fatty, it’s really fatty; and hey, it’s cheap. We are all born innocent and then learn to love and accept concepts like Fourthmeal and Chicken Fries. Sometimes, it feels like a burger chain or taco stop just “gets you.”

A new survey, however, finds that fast food and junk food marketing is more likely to hit you just right if you’re a “dude”—namely, a teenage boy—than if you’re a young lady. The most recent findings of the Australian national survey of the dietary and behavioral habits of its high schoolers says so, anyway.

The study included data from nearly 9,000 students at 196 different secondary schools gathered in 2012 and 2013, and was released by Australia’s Cancer Council and the National Heart Foundation. Researchers found that 46 percent of the nation’s teenage boys regularly eat fast food, compared to 34 percent of girls, and that 63 percent of the boys often gorged on salty snacks.

But more interesting is the fact that the teenage boys were markedly more susceptible to the allures of junk food advertising that integrated giveaways, contests, or influencers, such as celebrities and pro athletes. Perhaps as a result, the boys were more likely to be overweight or obese than their female counterparts, despite engaging in more sports and other physical activities.

Almost one-third of boys are likely to buy a food or drink if it’s tied to an actor or sports personality that they like, versus just 19 percent of girls, and 40 percent of teenage boys will patronize a fast-food chain if they are offering a special product or giveaway.

This might not come as such a shock to everyone. If anything, it kind of just affirms the archetype of the stoned high school senior whose car floor is littered with stale French fries, or a cluster of chubby 17-year-old gamers eating dollar tacos in their parents’ basement while taking turns playing GTA 5.

But Kathy Chapman, speaking on behalf of the Cancer Council, tells the Australian Associated Press that the huge budgets of fast-food companies are enabling them to thoroughly and knowingly infiltrate the programming primarily watched by teenagers, and that “a barrage of increasingly sophisticated junk food marketing is undermining teenage boys’ longer-term health, highlighting the urgent need for measures to protect them.”
“Mass-media advertising works,” she adds.

But working out—rather than lounging in the plastic booth of a fast-food joint all day—might be the crucial kicker there.

Yes, advertising works. Of course consumers will deny ever being influenced by television, radio, print and the web. But whatever you see, hear, or read is in your mind somewhere and connections are drawn between those ads and your purchases. If you’ve ever taken an eight-year-old to a grocery store, you know it can turn into a series of requests from your child for products they’ve seen advertised. The same is certainly true for teenagers — just in different places, involving different foods and beverages. FoodFacts.com thinks it makes perfect sense that food marketing is affecting boys differently than girls. By the time a girl reaches her teenage years, other forms of marketing have affected her. She’s concerned about her clothes, how they fit and what she looks like. Unfortunately, that can be detrimental in different ways. Teenage boys are always hungry. And without those “girlish” concerns, can become prey to junk food marketing much more easily.

While we can’t be with our teenagers 24/7, we can make sure that when they are at home, we continue to inform and educate them. The habits we instill will make a difference and will help them make healthier choices.

http://munchies.vice.com/articles/teenage-boys-are-more-susceptible-to-the-lure-of-fast-food-than-girls

Does who you eat with affect how much you eat?

food_0It’s an interesting question. Do our dining companions influence our consumption? Are there friends or family members we sit down for a meal with somehow affecting the amount of food we consume during any given meal? A new study from UNSW Australia says the answer is “Yes!”

This psychological effect, known as social modelling, leads people to eat less than they normally would if alone when their companion consumes a small amount of food.

Study lead author, Associate Professor Lenny Vartanian of the UNSW School of Psychology, says that in social situations the appropriate amount of food to eat can be unclear.

“Internal signals like hunger and feeling full can often be unreliable guides. In these situations people can look to the example of others to decide how much food they should consume,” he says.

Associate Professor Vartanian and his colleagues analysed the results of 38 studies in which the amount of food that people ate in company was measured. The results are published in the journal Social Influence.

“The research shows that social factors are a powerful influence on consumption. When the companion eats very little, people suppress their food intake and eat less than they normally would if alone,” he says.

“If the social model eats a large amount, people have the freedom to eat their normal intake, or even more if they want.”

The effect is observed in many different situations: with healthy and unhealthy snack foods, during meals, when the diner has been deprived of food for up to day, and among children, and it occurs independent of people’s body weight.

“It even occurs when the companion is not physically present and diners are simply given a written indication of what that other person ate,” says Associate Professor Vartanian.

The effect appears to be stronger in women than men, and this may be because women tend to be more concerned about how they are viewed by others when they are eating.

“Or the explanation could be more mundane, that undergraduate males participating in the research are over-enthusiastic about an offer of free food,” he says.

The research shows that the modelling effect is stronger in older children than in younger children, which also suggests that relying on external rather than internal cues for how much to eat is a learnt behaviour.

“Media reports usually focus on how portion size affects how much we eat, but this modelling effect deserves as much attention, because of its big impact on people’s ability to regulate their intake of food,” says Associate Professor Vartanian.

The next time any of us at FoodFacts.com enjoys a meal out with a friend or family member, we may not be thinking so much about the far-too-big portion size we’re being served. We may actually spend some time observing the eating patterns of our dining partners. Perhaps by staying aware of those, we’ll actually be able to control our own consumption. It’s an interesting concept and one we might be able to apply on an immediate level as part of our healthy lifestyles!

http://www.sciencedaily.com/releases/2015/05/150511095612.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

Another reason to stay away from fast food: new book claims fast food kills the gut bacteria that help you stay slim

fastfood (1)When we hear the word bacteria, our first inclination is to think of illness and things we should stay away from. Standing water, for instance, could be “crawling with bacteria.” Gas station bathrooms, uncleaned countertops, sticky seats in restaurants and bars are generally related in our minds to “nasty bacteria.” Bacteria gets a bad rap — and sometimes it should. There are harmful bacteria, but there are also beneficial bacteria. Those should be residing in our gut. What happens when those beneficial bacteria are killed off? What can cause that to happen?

While highly processed ingredients and huge portions typically aren’t doing you any favors, new information says they can also kill off the beneficial gut bacteria that help burn calories.

The findings are the result of research into the links between gut bacteria and health conducted by genetic epidemiology professor Tim Spector of King’s College London.

He found that diets composed of a relatively small number of ingredients, most of which are highly processed, are toxic to these bacteria. In fact, many of them can die off within days of beginning such a diet.

Spector will elaborate on the research in his upcoming book, “The Diet Myth: The Real Science Behind What We Eat,” which focuses on the role that a diverse diet plays in fostering a healthy microbes in the human body.

In one study discussed in the book, Spector enlisted his 23-year-old son, Tom, who agreed to spend 10 days eating nothing but McDonald’s chicken nuggets, fries, burgers and Coca-Cola.

“Before I started my father’s fast food diet there were about 3500 bacterial species in my gut, dominated by a type called firmicutes,” the younger Spector, a genetics student told The Australian.

“Once on the diet I rapidly lost 1,300 species of bacteria and my gut was dominated by a different group called bacteroidetes. The implication is that the McDonald’s diet killed 1,300 of my gut species,” he said.

This discovery suggested to his father that many cases of obesity may not simply be due to overeating.

“Microbes get a bad press, but only a few of the millions of species are harmful and many are crucial to our health,” Professor Spector told The Australian.

“What is emerging is that changes in our gut microbe community , or microbiome, are likely to be responsible for much of our obesity epidemic, and consequences like diabetes, cancer and heart disease,” he said. “It is clear that the more diverse your diet, the more diverse your microbes and the better your health at any age.”

Previous studies made similar findings: Professor Rob Knight of the University of Colorado Boulder, who collaborates with Spector, famously showed that transferring gut bacteria from obese humans to mice could make the rodents gain weight.

Spector’s book claims that the diversity of microbes in the human body has decreased almost a third over the last century. But there’s also good news: Foods like dark chocolate, garlic, coffee and Belgian beer may help increase gut microbes.

Some of these claims cannot be independently verified, as the noted study isn’t published publicly nor readily available in a peer-reviewed journal. In addition, while mouse studies have found links between gut microbes, dietary changes and obesity, the evidence remains less clear in humans. As Robert Knight of the University of Colorado wrote in a recent review in the British Journal of Nutrition: “It remains a challenge to identify the key pathogenic microbiota and to establish a causal (rather than associative) relationship between specific microbes or community states and a given physiological or disease phenotype.”

In large part, the idea that fast food (and highly processed ingredients of all kinds) kills beneficial gut bacteria and throws bodies out of balance, inviting excessive weight gain is a theory. It is, however, a theory on which FoodFacts.com would like to see more credible studies done. While we’re at it, we’d like to see those studies include more than fast food. We think that other highly processed foods — foods from boxes and cans — should be studied as well. Let’s remember the big coincidence surrounding the obesity crisis. It’s a relatively new phenomenon that corresponds directly with the infiltration of highly processed foods in our diets over the last 30 years or so. Our grocery shelves are lined with unnecessary highly-processed everything, fast food is available everywhere (in some areas, every few blocks) and most people aren’t taking the time to cook actual food. It does seem that we’ve traded our health for convenience, with encouragement from food manufacturers and fast food chains. While we wait for further study and exploration, let’s all remember that real food doesn’t have any ingredient list — real food IS the ingredient list. Protein, produce, grains, nuts, seeds, beans … we all know what they are. Go to the grocery store and buy ingredients.

http://www.pbs.org/newshour/rundown/junk-food-kills-helpful-gut-bacteria-study-finds/

Craving snacks late at night? Blame your brain

150505121418_1_540x360We’ve all been there. It’s late. You’re watching television. Somehow, you find yourself in front of your open refrigerator or freezer or snack drawer or cabinet. “Just a little something,” you think to yourself. But inexplicably that “little something” doesn’t seem to be enough. And that is how pints of ice cream can “disappear” after 11 p.m.

What’s going on with that?

Researchers at BYU have shed new light on why you, your friends, neighbors and most everyone you know tend to snack at night: some areas of the brain don’t get the same “food high” in the evening.

In a newly published study, exercise sciences professors and a neuroscientist at BYU used MRI to measure how people’s brains respond to high- and low-calorie food images at different times of the day. The results showed that images of food, especially high-calorie food, can generate spikes in brain activity, but those neural responses are lower in the evening.

“You might over-consume at night because food is not as rewarding, at least visually at that time of day,” said lead author Travis Masterson. “It may not be as satisfying to eat at night so you eat more to try to get satisfied.”

The study, which appears in academic journal Brain Imaging and Behavior, also reports that participants were subjectively more preoccupied with food at night even though their hunger and “fullness” levels were similar to other times of the day.

Masterson, who carried out the research for his master’s thesis under faculty advisor James LeCheminant, said the intent was to better understand if time of day influences neural responses to pictures of food.

The researchers teamed up with BYU neuroscientist Brock Kirwan to use functional MRI to monitor the brain activity of study subjects while they viewed images of food. The participants viewed 360 images during two separate sessions held one week apart–one during morning hours and one during evening hours.

Subjects looked at images of both low-calorie foods (vegetables, fruits, fish, grains) and high-calorie foods (candy, baked goods, ice cream, fast food). As expected, the researchers found greater neural responses to images of high-calorie foods. However, they were surprised to see lower reward-related brain reactivity to the food images in the evening.

“We thought the responses would be greater at night because we tend to over-consume later in the day,” said study coauthor Lance Davidson, a professor of exercise sciences. “But just to know that the brain responds differently at different times of day could have implications for eating.”

Nevertheless, researchers noted that the study is preliminary and additional work is needed to verify and better understand the findings. The next research steps would be to determine the extent that these neural responses translate into eating behavior and the implications for weight management.

Masterson, who is heading to Penn State University to work on his PhD in the fall, said the study has helped him pay better attention to how food makes him feel both in the morning and the evening. And as for his late-night eating habits?

“I tell myself, this isn’t probably as satisfying as it should be,” he said. “It helps me avoid snacking too much at night.”

FoodFacts.com wonders if a greater understanding of our brains can actually help us stave off late night cravings. Can we talk ourselves out of late-night snacking? Or perhaps, at least, help ourselves understand that the “little something” we want would actually be enough for us earlier in the day? We’re not sure. But the weekend is coming and we’re going to quietly put those pints of ice cream back in our freezer and test this out!

http://www.sciencedaily.com/releases/2015/05/150505121418.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

Real progress: Panera Bread commits to removing over 150 controversial ingredients by 2016

635660908535487026-XXX-CEO-Profile-Panera-Ron-Shaich-2Panera Bread just made everyone at FoodFacts.com happier than we’ve ever been about fast casual dining. They’ve committed to the removal of over 150 controversial ingredients from their menu items by 2016.

We’ve been saying the same thing over and over, every time a fast food or fast casual chain commits to using antibiotic-free chicken, or the removal of a single ingredient due to consumer demand. It’s nice, but just one thing isn’t going to change the perception of an increasingly health-conscious consumer. It has to be bigger than that.

Panera Bread got the real message and they’re doing something about it.

Last week the chain began using only “clean” salad dressings — dressings free from artificial sweeteners, colors, flavors and preservatives. That’s already great news, but it’s much bigger than that. The list of ingredients slated for removal could come directly from the FoodFacts.com controversial ingredient list. You can find the full list here: https://www.panerabread.com/panerabread/documents/panera-no-no-list-05-2015.pdf.

Among the real standouts for us are the removal of aspartame, artificial colors, artificial flavors, caramel color, high fructose corn syrup, partially hydrogenated oils and propylene glycol from their foods. The list goes on though and you should really check it out.

This is a stunning move by Panera Bread and one that challenges every other fast casual and fast food chain. If Panera Bread can find a way to remove just about every ingredient we want to avoid from their menu (we don’t see natural flavor and carrageenan on their list), it’s really impossible to imagine that other chains can’t accomplish the same thing while still offering food that’s appealing and affordable to their consumers.

With this statement, Panera Bread proves that no chain has an excuse. It’s time for the rest of the fast casual and fast food giants to follow their lead.

https://www.panerabread.com/panerabread/documents/panera-no-no-list-05-2015.pdf
http://www.usatoday.com/story/money/2015/05/04/panera-panera-bread-fast-food-restaurants-dining-artificial-additives/26696823/

Taco Bell’s new Chipotle Chickstar almost makes a Big Mac look good

Screen Shot 2015-05-04 at 1.11.15 PMAnother new one from Taco Bell proves that fast food chicken sandwiches can, in fact, be a poorer nutritional choice than a fast food burger. This time we have Chipotle Chickstars.

It’s basically a chicken sandwich wrapped in a tortilla that’s grilled. The website describes it this way, “A warm, soft, flour tortilla filled with new premium all-white-meat crispy chicken that’s marinated in bold Mexican spices, rolled in a crunchy corn tortilla coating, and crisped to perfection combined with creamy chipotle sauce, real cheddar cheese, lettuce, and tomatoes and then wrapped up and grilled for maximum portability.” Sounds innocent enough, doesn’t it?

Let’s see what we can find out about this “unique” new chicken sandwich …

Nutrition Facts:
Calories:                 760
Fat:                          43 grams
Saturated Fat:       8 grams
Sodium:                 1650 mg

WOW. There is no one eating this chicken sandwich who should be thinking that it’s better than other alternatives being served. You could actually consume less calories from a Big Mac at McDonald’s than from the Chipotle Chickstar — not to mention fat and sodium.

What about the ingredients?

CRISPY CHICKEN Chicken White Meat, Water, Seasoning [Maltodextrin, Salt, Sodium Phosphate, Tomato Powder, Sugar, Vinegar Solids, Yeast Extract, Onion Powder, Citric Acid, Chicken Broth, Sunflower Oil, Garlic Powder, Jalapeno Juice Solids, Chicken Powder, Gum Arabic, Chicken Fat, Acetic Acid, Modified Corn Starch, Smoke Flavor, and Grill Flavor (from Sunflower Oil)], Salt, Rice Starch, and Sodium Phosphate. BREADED WITH: Wheat Flour, Tortilla Pieces (Corn, Vegetable Oil {Corn, Soybean, and/or Sunflower Oil], Dextrose, Salt, Dried Yeast, Roasted Barley Flour, Annatto Extract (color). BATTERED WITH: Water, Bleached Wheat Flour, Hydrogenated Cottonseed Oil, Salt, Leavening (Sodium Acid Pyrophosphate, Sodium Bicarbonate, Monocalcium Phosphate), Spices, Disodium, Inosinate and Disodium Guanylate, Dried Onion, and Dried Garlic. PREDUSTED WITH: Bleached Wheat Flour, Hydrogenated Cottonseed Oil, Salt, Leavening (Sodium Acid Pyrophosphate, Sodium Bicarbonate, Monocalcium Phosphate), Spices, Disodium, Inosinate and Disodium Guanylate, Dried Onion, and Dried Garlic. CONTAINS: Wheat CHIPOTLE SAUCE Soybean Oil, Water, Egg Yolk, Distilled Vinegar, Sour Cream (Cream, Modified Corn Starch, Gelatin, Lactic Acid, Guar Gum, Mono & Di Glycerides, Disodium Phosphate, Citric Acid, Artificial Flavor), Chili Peppers, Salt, Sugar, Chipotle Peppers, Garlic Including Dehyrated, Natural Flavors Including Smoke Flavor, Potassium Sorbate and Sodium Benzoate Added As Preservatives, Xanthan Gum, Onion*, Mustard Seed, Propylene Glycol Alginate, Maltodextrin, Corn Starch, Jalapeno Peppers*, Calcium Disodium EDTA To Protect Flavor, Canola and Sesame Oil. *Dehydrated CONTAINS EGG, MILK CHEDDAR CHEESE Cultured Pasteurized Milk, Salt, Enzymes, Annatto (Color), Anti-Caking Agent. CONTAINS MILK LETTUCE Iceberg Lettuce TOMATO Tomatoes TORTILLA Enriched Bleached Wheat Flour (Flour, Niacin, Reduced Iron, Thiamine Mononitrate, Riboflavin, Folic Acid), Water, Vegetable Shortening (Soybean Oil, Hydrogenated Soybean Oil), Contains less than 2% of the following: Sugar, Salt, Leavening (Sodium Bicarbonate, Sodium Acid Pyrophosphate), Fumaric Acid, Calcium Propionate and Sorbic Acid (used as preservatives), Yeast, Molasses, Dough Conditioner [Distilled Monoglycerides, Enzymes, Wheat Starch and Calcium Carbonate with Tocopherols, Ascorbic Acid, and Citric Acid (added as Antioxidants)] CONTAINS: WHEAT

FoodFacts.com feels badly for the poor innocent chicken used in this sandwich. Inherently, consumers hear chicken sandwich and automatically relate the sandwich to healthier options. Lean protein, less calories. We understand the dilemma and hope that posts like this can help make it abundantly clear that not all chicken is equal after processing and the addition of a strange and very controversial list of ingredients.

The Big Mac is NOT a healthy choice for anyone — but it’s still better than the Chipotle Chickstar from Taco Bell. And that is saying a mouthful.

http://www.tacobell.com/food/specialties/Chipotle-Chickstar