Starting your meal with a bowl of soup, apple or a salad will help you to lose weight

Eating soup, apple or a salad as a first course helped study participants lose weight because they consumed fewer total calories in the rest of the meal.

Dr. Barbara Rolls, a weight control researcher at Pennsylvania State University and author of "The Volumetrics Eating Plan," found that eating soup as a first course helped study participants lose weight because they consumed fewer total calories in the rest of the meal.

Rolls' theory is that the more water a food contains the more full we feel. And the lower the energy density of a food (the concentration of fat and calories) the more we can eat.

Source: detnews.com

Too much fructose can induce leptin resistance

Although previous studies have shown that being leptin resistant can lead to rapid weight gain on a high-fat, high-calorie diet, this is the first study to show that leptin resistance can develop as a result of high fructose consumption.

The study also showed for the first time that leptin resistance can develop silently, that is, with little indication that it is happening.

Source: Medical News Today

New research reveals the process by which unsaturated, or “good” fats, may actually aid in weight loss.

A recent University of California, Irvine, study shows when oleic acid, a component of healthy unsaturated fats like those found in olive oil, enters the small intestine, a hormone is released that ultimately creates a feeling of fullness. This feeling can fight off one important cause of overeating -- hunger pangs.

“People already recognize the health benefits of unsaturated fatty acids, and this is just an additional health benefit -- these nutrients produced delaying hunger,” study author Daniele Piomelli, Ph.D., Pharm.D., a professor of pharmacology at the University of California, Irvine, told Ivanhoe.

This discovery may help researchers develop drugs to boost levels or block breakdown of the hormone, called OEA, to manually fend off feelings of hunger. The discovery may also help experts determine the exact balance of fat and protein needed to best control hunger.

“One can design strategies to get a better bang for your buck, so if you eat the same amount of calories, you can design strategies whereby you will get greater control of the amount of food you eat in each individual meal as well as in delaying the hunger pangs after a meal,” Dr. Piomelli said.

Source: Ivanhoe Medical Breakthroughs

Severe obesed teenagers will be given drastic weight-loss surgery under a NSW Government strategy to fight the obesity epidemic

The Children's Hospital at Westmead is set to be the first in the State to offer taxpayer-funded gastric banding.
Doctors say the radical measure is needed to save teens with severe weight-related health conditions.

Dr Michael Kohn, of adolescent medicine at The Children's Hospital at Westmead, told The Sunday Telegraph lap-banding would be restricted to teens aged 14 and over because it was too controversial in younger children.

He said the surgery was reversible and could stall - or even resolve - severe health problems until teens could establish controlled eating patterns.

"Certainly with eating disorders, it's really about getting the young person through a critical period and developing eating patterns they can maintain,'' he said.

"I think the degree to which (our) population is overweight is not dissimilar to the US.''

Dr Kohn will formally apply to provide bariatric - or weight-loss - surgery in three weeks.

The State Government agreed it would provide funding for the surgery two months ago, with the first clinics expected to open by the end of 2008.

Publicly funded weight-loss surgery is expected to be available across the State by 2012.

Dr Kohn said some young people were developing severe lifestyle-related conditions such as pancreatitis and type 2 diabetes which needed urgent medical action.

Gastric banding costs at least $10,000 - an unaffordable amount for most parents of morbidly obese children, with statistics showing obesity levels are higher in poorer "battler'' areas of NSW.
Source: The Daily Telegraph

OEA might be useful in the treatment of obesity and other eating disorders

A fatty acid found in abundance in olive oil and other "healthy" unsaturated fats has yet another benefit: it helps keep the body satisfied to prolong the time between meals. A new study in the October Cell Metabolism, a publication of Cell Press, reveals that once this type of fat, known as oleic acid, reaches the intestine, it is converted into a lipid hormone (oleoylethanolamide, or OEA) that wards off the next round of hunger pangs.

The researchers said it may be the first description of an ingredient in food that directly provides the raw materials for a hormone's production.

The findings in rats may yield insight into the precise dietary makeup of fat and protein for optimal hunger control, the researchers said. (Protein plays in important role in limiting hunger as well, but by different means.) The newly discovered signaling pathway might also be tapped into with drugs designed to control appetite by supplementing OEA levels or blocking its breakdown. Similarly, in conditions where people don't eat enough, the researchers speculate that treatments targeting this system might improve the appetite.

Importantly, diets high in processed foods that are riddled with saturated fats might throw a wrench into this system of metabolic control, the researchers said.

" Eating is one of the most important things animals do," said Daniele Piomelli of the University of California, Irvine. "This is just one of many things that control it. That said, a system like this could be forced to inactivation by inappropriate feeding," he said, noting that saturated fats generally lack in oleic acid.

While such diets may lead people to overeat, Piomelli said it will also be of interest to see if this mechanism may be defective in some who tend to eat in excess.

Previous studies had shown that feeding stimulates cells in the intestinal lining to produce OEA, which, when administered as a drug, decreases meal frequency by engaging receptors called peroxisome proliferator-activated receptors a (PPARa).

Piomelli's team now reports that infusion of fat into the small intestine stimulates the release of OEA, whereas infusion of protein or carbohydrate does not. They also demonstrate that OEA production uses dietary oleic acid and is disrupted in mutant mice lacking the membrane fatty-acid transporter CD36. Treatments that disrupt CD36 or PPARa undermine the hunger control otherwise driven by fat.

Overall, the results suggest that activation of small-intestinal OEA release, enabled by CD36-mediated uptake of oleic acid from the diet, serves as a molecular sensor linking fat consumption to satiety. (Piomelli said satiety is perhaps best described as the opposite of hunger.)

" In conclusion," the researchers wrote, "our studies identify OEA as a key physiological signal that specifically links dietary fat ingestion to across-meal satiety. Nutritional and pharmacological strategies aimed at magnifying this lipid-sensing mechanism, such as inhibitors of OEA degradation, might be useful in the treatment of obesity and other eating disorders."

Source: Medical News Today

You can’t assume someone is unhealthy just because he’s fat

Some activists and academics, part of a growing social movement known as fat acceptance, suggest that we rethink this war — as well as our definition of health itself. Fat-acceptance activists insist you can’t assume someone is unhealthy just because he’s fat, any more than you can assume someone is healthy just because he’s slim. (They deliberately use the word “fat” as a way to reclaim it, much the way some gay rights activists use the word “queer.”) Rather, they say, we should focus on health measurements that are more meaningful than numbers on a scale. This viewpoint received a boost in August when The Archives of Internal Medicine reported that fully half of overweight adults and one-third of the obese had normal blood pressure, cholesterol, triglycerides and blood sugar — indicating a normal risk for heart disease and diabetes, conditions supposedly caused by being fat.

This is a core argument of fat acceptance: that it’s possible to be healthy no matter how fat you are and that weight loss as a goal is futile, unnecessary and counterproductive — and that fatness is nobody’s business but your own.

Many fat-acceptance activists prefer a new approach to dieting that focuses on nutrition, exercise and body image. A new book out this fall, “Health at Every Size,” by Linda Bacon, a nutritionist and physiologist at the University of California at Davis, outlines this approach, which is less about dieting than a lifestyle change that emphasizes “intuitive eating”: listening to hunger signals, eating when you’re hungry, choosing nutritious food over junk. It encourages exercise, but for its emotional and physical benefits, not as a way to lose weight. It advocates tossing out the bathroom scale and loving your body no matter what it weighs.

The philosophy is migrating slowly into mainstream programs, like a spa in Vermont that focuses on “acceptance of ourselves and our wonderful sizes.” But the spas and other programs have trouble with the bottom line of fat acceptance — rejection of weight loss as a goal. Weight Watchers, for instance, uses some of the same slogans, and while it promotes its program as “not a diet,” it still tracks weight loss down to the decimal point.

Several studies suggest that if the aim is getting healthier rather than slimmer, then in the long run the “Health at Every Size” approach works better than dieting. In 2005, Bacon led the only randomized control trial to date that tested this hypothesis physiologically. She randomly assigned half of the 78 subjects, all women, to a “Health at Every Size” group; while they lost no weight, their healthier behavior led to lower blood-pressure and cholesterol levels, which stayed low even two years later. In the weight-loss group, more than 40 percent dropped out before the six-month low-calorie diet ended, and at the two-year follow-up, the average dieter had regained all her lost weight, and the only measurement that dropped was one for self-esteem.

Scientists who study obesity at the cellular level say genetics determines people’s natural weight range, right down to the type and amount of food they crave, how much they move and where they accumulate fat. Asking how someone got to be so fat is as meaningless as asking how he got to be so tall. “The severely obese have some underlying genetic or metabolic difference we’re not smart enough to identify yet,” says Dr. Rudolph Leibel of Columbia University Medical Center. “It’s the same way that a 7-foot-tall basketball player is genetically different from me, at 5-foot-8.”

Fat has been blamed for cardiac trouble, diabetes and some forms of cancer. But fat-acceptance activists argue that the epidemiological studies that link fatness to disease often fail to adjust for non-weight-related risk factors found more often in fat populations. Poverty, minority-group status, too much fast food, a sedentary lifestyle, lack of access to health insurance or to nonjudgmental medical care, the stress of self-loathing and being part of a stigmatized group — all are more common among fat people, and all are linked to poorer health outcomes at any weight. This makes it harder to say to what extent an association between obesity and disease is due to the fatness itself or to the risk factors that tend to go along with being fat.

It remains an open question, one deserving of further scientific scrutiny, whether the health risks seen in fat populations are caused by the fat itself or by something else. Only then can we really know how to effectively wage the war on obesity — or if such a war even needs to be waged.

Source: NY Times

Inflammation may be a player in the development of obesity

Obesity is known to increase inflammation throughout the body. The new study -- published in tomorrow's edition of Cell -- shows that inflammation may be a player, and not an innocent bystander, in the development of obesity.

The researchers -- based at the University of Wisconsin-Madison and the University of California, San Diego -- focused on two things:

The hypothalamus, a brain region that regulates the body's energy balance.
A "master switch" of inflammation -- called IKK beta/NF kappa B -- that's usually turned off.
In lab tests on mice, that "master switch" of inflammation turned on in the hypothalamus of mice on a high-fat diet. "Chronic overnutrition" flipped on the inflammation switch, the researchers note.

With that master switch turned on in the hypothalamus, the mice gained weight and became resistant to insulin (a hormone that controls blood sugar) and leptin (a hormone involved in feeling full).

Next, the scientists used genetic engineering to flip that master switch off in the hypothalamus of other mice. Those mice were "significantly protected" from becoming obese, even on a high-fat diet, the researchers write.

Still, you wouldn't want to turn that master switch off forever, because inflammation is one of the body's tools for fighting infection.

Figuring out how to selectively control that switch in the hypothalamus might be a new strategy for curbing obesity and related diseases, the researchers conclude. In the meantime, the time-tested methods of a healthier diet and a more active lifestyle are still the cornerstones of managing weight. Easier said than done? Health care professionals can help with the process.

Source: WebMD