Category: Obesity

Houston’s health crisis: by 2040, one in five residents will be diabetic

On By A.P.In diabetes, Houston, Kebmodee, ObesityLeave a comment

houston

Diabetes is so common in Patricia Graham’s neighbourhood that it has its own slang term. “At churches you run into people you ain’t seen in years, and they say, ‘I’ve got sugar,’” she says.

Graham does not quite have “sugar”, but when foot surgery in 2014 reduced her activity level, her blood sugar level soared. And there is a history of diabetes in her family: three of four brothers and her mother, who lost a leg to it.

So three times a week she comes to the smart, modern Diabetes Awareness and Wellness Network (Dawn) centre in Houston’s third ward, a historically African American district near downtown. Used by about 520 people a month, Dawn is in effect a free, city-run gym and support group for diabetics and pre-diabetics: a one-stop shop for inspiration, information and perspiration. Last Friday Graham, 68, was there for a walking session.

Not that she or the half-dozen other participants went anywhere. This was walking on the spot to pulsating music. Had the class stepped outside they would have enjoyed perfect conditions for a stroll: a blue sky and a temperature of 21C. If they had worked up an appetite, a soul food restaurant was only a 15-minute walk away, serving celebrated (if not exactly sugar-free) food that belies its unpromising location in a standard shopping mall on a busy road next to a dialysis centre.

But most of Houston is not built for walking, even on a sunny January day. There’s the constant traffic belching fumes that linger in the humid air; the uneven sidewalks that have a pesky habit of vanishing halfway along the street; the sheer distances to cover in this elongated, ever-expanding metropolis. Walking can feel like a transgressive act against Houston’s car-centric culture of convenience – and its status as the capital of the north American oil and gas industry.

It’s one reason why Houston regularly finishes top, or close, in surveys that crown “America’s fattest city”. Unsurprisingly, it has a diabetes problem as outsized as its residents’ waistlines. By 2040, one in five Houstonians is predicted to have the disease.

According to data from pharmaceutical company Novo Nordisk, the prevalence of type 2 diabetes in the city is 9.1% – with an estimated one in four of these being undiagnosed. Almost a third of adult Houstonians self-describe as obese, according to a 2010-11 survey. Without action, the number of people with diabetes is projected to nearly treble by 2040 to 1.1 million people, with diabetes-related costs soaring from $4.1bn in 2015 to $11.4bn by 2040.

Graham is alarmed by the damage diabetes is wreaking on her community. “I was talking to my friends and saying, so many of the people we grew up with got diabetes and lost limbs,” she says. “It’s not even so much the seniors any more, it’s the young people. But it doesn’t scare them. They act like they’re not afraid.”

Another Dawn member, Verne Jenkins, was diagnosed three years ago. “I had picked up a bit of weight that I shouldn’t have,” says the 63-year-old. “I knew what to eat, I knew what I was doing, I just got out of control.”

Jenkins loves to bake but has cut back on carbs, red meat, salt and sugar, abstaining from one of her guilty pleasures, German chocolate cake. Not that it’s easy in a city with so much choice: “All these wonderful restaurants, all these different kinds of cuisines, of course you’re going to try some. I imagine it leads to our delinquency,” she says.

Graham has watched her diet since she was in her 20s. “I eat pretty good,” she said. “‘She eats like white folks’ – that’s what they tell me!”

Time poverty

Diabetes is a major cause of death, blindness, kidney disease and amputations in the US. While federal researchers announced last year that the rate of new diabetes cases dropped from 1.7 million in 2009 to 1.4 million in 2014, in Texas the percentage of diagnosed adults rose from 9.8% in 2009 to 11% in 2014.

Houston, America’s fourth-largest city, is one of five participating in the Cities Changing Diabetes programme, along with Mexico City, Copenhagen, Tianjin and Shanghai. Vancouver and Johannesburg are soon to join the project, which attempts to understand, publicise and combat the threat through cultural analysis.

“The majority of people with diabetes live in cities,” says Jakob Riis, an executive vice-president at Novo Nordisk, one of the lead partners in the programme alongside the Steno Diabetes Center and University College London. “We need to rethink cities so that they are healthier to live in … otherwise we’re not really addressing the root cause of the problem.”

One of the programme’s key – and perhaps surprising – findings, however, is that assessing the risk of developing diabetes is not as simple as dividing the population according to income and race. The problem is broad – much like Houston itself.

The view stretches for miles from Faith Foreman’s eighth-floor office next to the Astrodome, the famous old indoor baseball stadium. It’s an impressive sight, but for someone tasked with tackling the city’s diabetes epidemic, also a worrying one: the sheer scale of the urban sprawl is part of the problem. The threat of the disease has expanded along with the city.

A low cost of living and a strong jobs market helped Houston become one of the fastest growing urban areas in the US. In response, the city loosened its beltways. Its third major ring road is under construction, with a northwestern segment set to open soon that is some 35 miles from downtown.

Once completed, the Grand Parkway – whose northwestern segment has just opened – will boast a circumference of about 180 miles. That is far in excess of the 117 miles of the M25, although about 14 million people live inside the boundary of London’s orbital motorway, more than twice as many as reside in the Houston area.

Large homes sprout in the shadow of recently opened sections, promising cheap middle-class living with a heavy cost: a commute to central Houston of up to 90 minutes each way during rush hour, with minimal public transport options.
“A lot of time in Houston is spent in a car,” says Foreman, assistant director of Houston’s Department of Health and Human Services. This informs one of the Cities Changing Diabetes study’s most notable findings: that “time poverty” is among the risk factors in Houston for developing type 2 diabetes.

This means that young, relatively well-off people can also be considered a vulnerable population segment, even though they might not fit the traditional profile of people who may develop type 2 diabetes – that is, aged over 45, with high blood pressure and a high BMI, and perhaps disadvantaged through poverty or a lack of health insurance.

“You generally think of marginalised, lower income communities in poverty as your keys to health disparities but I think what we learned from our data in Houston is that we now have to expand the definition of what vulnerable is and what at-risk means. Just because we live in an urban environment, we may all indeed be vulnerable,” says Foreman.

In other words, not only its residents’ dietary choices but the way Houston is constructed as a city appears to be contributing to its diabetes problem, so tackling the issue requires architects as well as doctors; more sidewalks as well as fewer steaks.

Urban isolation is a key challenge, says David Napier of UCL, the lead academic for Cities Changing Diabetes. “Houston is growing so quickly and also expanding geographically at such a rapid rate. When you look at how difficult it is for people just to get out and walk, or walk to work; the fact that so many people commute long distances, spend a lot of time eating out – they have a number of obstacles to overcome,” he says.

A city with notoriously lax planning regulations is now making a conscious effort to put more care into its built environment, with more public transport, expanded bike trails, better parks and denser, more walkable neighbourhoods all evident in recent years, even as the suburbs continue to swell.

Foreman’s agency has more input when officials gather to map out the future city. “That is something that has been a big change over the last two or three years in Houston,” she says. “We are at the table and we are working with city planning to make those decisions.”

But prevention is a vital focus as well as treatment. Along with his team, Stephen Linder of the University of Texas’ school of public health – the local academic lead for Houston’s Cities Changing Diabetes research – gathered data on 5,000 households in Harris County, which includes much of the Houston area.

“One way to approach this project wasn’t to focus on diabetes itself but rather to look at some of the preconditioned social factors that seemed to generate the patterns of living that then led to the clinical signs that would designate people as being prediabetic,” he says from his office at the Texas Medical Center near downtown Houston – the world’s largest medical complex.

“These were people who had neither disadvantage nor biological risk factors. They tended to be the youngest group and would normally escape any kind of assessment – we called them the ‘time-pressured-young’. They’re the ones who did the long commutes; they’re the ones whose perception was they could not manage their day’s worth of stuff, that they have no time for anything.”

For this group, obesity is so prevalent in Houston that it distorts an understanding of what a healthy weight is, Linder found. “Their perception of their health was affected by their peers as opposed to other sorts of references. If all of their peers were overweight then in a relative sense they were fine. The judgments were about one’s peers and not relative to any sort of expert standard,” he says.

Three neighbourhoods were identified as having the highest concentration of people vulnerable to developing diabetes, and a Dallas-area research company, 2M, conducted detailed interviews with 125 residents. One place was particularly surprising: Atascocita, a desirable middle-class area near a large lake and golf courses, about 30 miles north of downtown.

Houston has become, according to a 2012 Rice University study, the most ethnically diverse large metropolitan area in the US. But this cosmopolitan air – one of the qualities sought by any place seeking to become a globally renowned city – may also unwittingly be contributing to the diabetes crisis, the study found.

Some in Atascocita, Linder said, “emphasised this sense of change and transition in their neighbourhoods, that that was a source of stress for them and that they were resistant to making changes in their own lives given the flux that was around them. Because that group happened to be older, even though they were economically secure they did have some other chronic diseases and they satisfied our biorisk characteristics.

“We call them concerned seniors. They weren’t making changes because there was too much else going on for them. And so if we were to say to them ‘you’ve got to change your diet’, they’d say ‘no, I can’t handle any more changes’.”

This matters since food portions are no exception to the “everything’s bigger in Texas” cliche, while Houston’s location near Mexico and the deep south, its embrace of the Lone Star state’s love of barbecued red meat and its enormous variety of restaurants serving international cuisine combine to unhealthy effect.

“The food that had a traditional aspect to it tended not to be the healthiest food – southern food that’s fried and lots of butter and lots of starch, then there’s African American soul food and then there’s Hispanic heavy fat, prepared tamales and the like, and so we found people kind of gravitated to what the UCL people called nourishing traditions,” Linder said.

“People used food as not only a reinforcement of tradition and ritual but also as a way of connecting socially. You’ve moved here from somewhere else, it’s a way to reinforce your identity, it’s a real cultural asset to have, but in a biological sense it’s not the best thing.”

For Linder, one lesson is that generalised advice about healthy eating that has long been part of diabetes awareness efforts may not be effective locally, given the complexity and variety of Houston’s neighbourhoods and the social factors that make populations vulnerable to diabetes.

“It does make the task of dietary change a much more complex one than the simple messages about changing your diet, eat more fruit and vegetables, get more colour on your plate would suggest. Those things bounce off, it’s not a useful set of interventions then for that particular group who rely on these nourishing traditions and find some solace in the change around them,” he said.

Foreman agrees that a targeted approach is vital. “How do you change diabetes in Houston? One neighbourhood at a time, in a sense, but at the same time you have bigger things that you can change systemwide in policies and how you work together collaboratively,” she said. “But then as you narrow it and get more granular it is neighbourhood, and what works in one neighbourhood may or may not work in another.”

Patricia Graham is hoping that the Dawn programme expands to other parts of the city to combat the dangerous union of unhealthy traditional food with a modern convenience culture. “Everything is food, and I mean lots of it and all the time,” she said. “Some people don’t know how to cook without grease or butter. That’s just the way we learn.”

http://www.theguardian.com/cities/2016/feb/11/houston-health-crisis-diabetes-sugar-cars-diabetic?CMP=oth_b-aplnews_d-1

Thanks to Kebmodee for bringing this to the It’s Interesting community.

Discovery of fat breakdown trigger opens door for new obesity treatments

On By A.P.In brain, Medicine, metabolism, ObesityLeave a comment

While it’s known that the brain is responsible for instructing our fat stores to break down and release energy as we need it, scientists haven’t yet been able to pin down exactly how this process plays out. Leptin, a hormone produced by our fat cells, travels to the brain to regulate appetite, metabolism and energy, but it hasn’t been clear what communication was coming back the other way. New research has now uncovered this missing link for the first time, revealing a set of nerves that connect with fat tissue to stimulate the process in a development that could lead to new types of anti-obesity treatments.

The leptin hormone was identified around 20 years ago as a regulator of the body’s metabolism. Low levels of the hormone serve to boost one’s appetite and slow metabolism, while conversely, high leptin levels dull the appetite and facilitate better fat breakdown. Using a combination of techniques, a research team led by Ana Domingos from Portugal’s Instituto Gulbenkian de Ciência were able to shed light on how leptin behaves when sending signals back to the fat by finding the nerves that meet with white fat tissue to prompt its breakdown.

“We dissected these nerve fibers from mouse fat, and using molecular markers identified these as sympathetic neurons,” explains Domingos. “When we used an ultra sensitive imaging technique, on the intact white fat tissue of a living mouse, we observed that fat cells can be encapsulated by these sympathetic neural terminals.”

But to determine the extent of these neurons’ role in obesity, the team carried out further research on mice. The rodents were genetically engineered so that these neurons could be switched on and off through optogenetics, where brain cells are made to behave differently by exposing them to light. Optogenetics is an emerging technique we have seen explored as a means of treating blindness and altering our pain threshold, among other things.

Domingos’ team found that flicking the switch on the neurons locally triggered the release of a neurotransmitter called norepinephrine, which in turn flooded the fat cells with signals that brought about fat breakdown. The team report that without these sympathetic neurons, leptin was not able to stimulate fat breakdown on its own. Therefore the findings suggest that these sympathetic neurons offer a potential target for obesity treatments other than leptin, which the brains of many obese people have a resistance to.

“This result provides new hopes for treating central leptin resistance, a condition in which the brains of obese people are insensitive to leptin,” says Domingos.

The team’s research was published in the journal Cell.

http://www.gizmag.com/neural-mechanism-fat-breakdown-anti-obesity-therapies/39601/

Losing Weight May Require Some Serious Fun

On By A.P.In Exercise, Medicine, mental health, metabolism, Nature, ObesityLeave a comment

If you are aiming to lose weight by revving up your exercise routine, it may be wise to think of your workouts not as exercise, but as playtime. An unconventional new study suggests that people’s attitudes toward physical activity can influence what they eat afterward and, ultimately, whether they drop pounds.

For some time, scientists have been puzzled — and exercisers frustrated — by the general ineffectiveness of exercise as a weight-loss strategy. According to multiple studies and anecdotes, most people who start exercising do not lose as much weight as would be expected, given their increased energy expenditure. Some people add pounds despite burning hundreds of calories during workouts.

Past studies of this phenomenon have found that exercise can increase the body’s production of appetite hormones, making some people feel ravenous after even a light workout and prone to consume more calories than they expended. But that finding, while intriguing, doesn’t fully explain the wide variability in people’s post-exercise eating habits.

So, for the new study, published in the journal Marketing Letters, French and American researchers turned to psychology and the possible effect that calling exercise by any other name might have on people’s subsequent diets.

In that pursuit, the researchers first recruited 56 healthy, adult women, the majority of them overweight. The women were given maps detailing the same one-mile outdoor course and told that they would spend the next half-hour walking there, with lunch to follow.

Half of the women were told that their walk was meant to be exercise, and they were encouraged to view it as such, monitoring their exertion throughout. The other women were told that their 30-minute outing would be a walk purely for pleasure; they would be listening to music through headphones and rating the sound quality, but mostly the researchers wanted them to enjoy themselves.

When the women returned from walking, the researchers asked each to estimate her mileage, mood and calorie expenditure.

Those women who’d been formally exercising reported feeling more fatigued and grumpy than the other women, although the two groups’ estimates of mileage and calories burned were almost identical. More telling, when the women sat down to a pasta lunch, with water or sugary soda to drink, and applesauce or chocolate pudding for dessert, the women in the exercise group loaded up on the soda and pudding, consuming significantly more calories from these sweets than the women who’d thought that they were walking for pleasure.

A follow-up experiment by the researchers, published as part of the same study, reinforces and broadens those findings. For it, the researchers directed a new set of volunteers, some of them men, to walk the same one-mile loop. Once again, half were told to consider this session as exercise. The others were told that they would be sightseeing and should have fun. The two groups covered the same average distance. But afterward, allowed to fill a plastic bag at will with M&M’s as a thank-you, the volunteers from the exercise group poured in twice as much candy as the other walkers.

Finally, to examine whether real-world exercisers behave similarly to those in the contrived experiments, the researchers visited the finish line of a marathon relay race, where 231 entrants aged 16 to 67 had just completed laps of five to 10 kilometers. They asked the runners whether they had enjoyed their race experience and offered them the choice of a gooey chocolate bar or healthier cereal bar in consideration of their time and help. In general, those runners who said that their race had been difficult or unsatisfying picked the chocolate; those who said that they had fun gravitated toward the healthier choice.

In aggregate, these three experiments underscore that how we frame physical activity affects how we eat afterward, said Carolina O.C. Werle, an associate professor of marketing at the Grenoble School of Management in France, who led the study. The same exertion, spun as “fun” instead of “exercise,” prompts less gorging on high-calorie foods, she said.

Just how, physiologically, our feelings about physical activity influence our food intake is not yet known, she said, and likely to be bogglingly complex, involving hormones, genetics, and the neurological circuitry of appetite and reward processing. But in the simplest terms, Dr. Werle said, this new data shows that most of us require recompense of some kind for working out. That reward can take the form of subjective enjoyment. If exercise is fun, no additional gratification is needed. If not, there’s chocolate pudding.

The good news is that our attitudes toward exercise are malleable. “We can frame our workouts in different ways,” Dr. Werle said, “by focusing on whatever we consider fun about it, such as listening to our favorite music or chatting with a friend” during a group walk.

“The more fun we have,” she concluded, “the less we’ll feel the need to compensate for the effort” with food.

http://well.blogs.nytimes.com/2014/06/04/losing-weight-may-require-some-serious-fun/?_php=true&_type=blogs&_r=0

Protecting new neurons reduces depression caused by stress, and may lead to a new class of molecules to treat depression.

On By A.P.In Angela Walker, anorexia, antidepressant, Anxiety, Carver College of Medicine, Depression, Iowa, Iowa City, Jeffrey Zigman, Medicine, mental health, mental illness, Molecular Psychiatry, Neurology, Neuropsychiatric Disease, Neuroscience, Obesity, P7C3, P7C3A20, psychiatrist, Psychiatry, Science, The Brain, University of Iowa, University of Iowa Hospitals and Clinics, University of Texas1 Comment

Scientists probing the link between depression and a hormone that controls hunger have found that the hormone’s antidepressant activity is due to its ability to protect newborn neurons in a part of the brain that controls mood, memory, and complex eating behaviors. Moreover, the researchers also showed that a new class of neuroprotective molecules achieves the same effect by working in the same part of the brain, and may thus represent a powerful new approach for treating depression.

“Despite the availability of many antidepressant drugs and other therapeutic approaches, major depression remains very difficult to treat,” says Andrew Pieper, associate professor of psychiatry and neurology at the University of Iowa Carver College of Medicine and Department of Veterans Affairs, and co-senior author of the study.

In the new study, Pieper and colleagues from University of Texas Southwestern Medical Center led by Jeffrey Zigman, associate professor of internal medicine and psychiatry at UT Southwestern, focused on understanding the relationship between depression, the gut hormone ghrelin, and the survival of newborn neurons in the hippocampus, the brain region involved in mood, memory, and eating behaviors.

“Not only did we demonstrate that the P7C3 compounds were able to block the exaggerated stress-induced depression experienced by mice lacking ghrelin receptors, but we also showed that a more active P7C3 analog was able to complement the antidepressant effect of ghrelin in normal mice, increasing the protection against depression caused by chronic stress in these animals,” Zigman explains.

“The P7C3 compounds showed potent antidepressant activity that was based on their neurogenesis-promoting properties,” Pieper adds. “Another exciting finding was that our experiments showed that the highly active P7C3 analog acted more rapidly and was more effective [at enhancing neurogenesis] than a wide range of currently available antidepressant drugs.”

The findings suggest that P7C3-based compounds may represent a new approach for treating depression. Drugs based on P7C3 might be particularly helpful for treating depression associated with chronic stress and depression associated with a reduced response to ghrelin activity, which may occur in conditions such as obesity and anorexia nervosa.

Future studies, including clinical trials, will be needed to investigate whether the findings are applicable to other forms of depression, and determine whether the P7C3 class will have antidepressant effects in people with major depression.

The hippocampus is one of the few regions in the adult brain where new neurons are continually produced – a process known as neurogenesis. Certain neurological diseases, including depression, interfere with neurogenesis by causing death of these new neurons, leading to a net decrease in the number of new neurons produced in the hippocampus.

Ghrelin, which is produced mainly by the stomach and is best known for its ability to stimulate appetite, also acts as a natural antidepressant. During chronic stress, ghrelin levels rise and limit the severity of depression caused by long-term stress. When mice that are unable to respond to ghrelin experience chronic stress they have more severe depression than normal mice.

In the new study, Pieper and Zigman’s team showed that disrupted neurogenesis is a contributing cause of depression induced by chronic stress, and that ghrelin’s antidepressant effect works through the hormone’s ability to enhance neurogenesis in the hippocampus. Specifically, ghrelin helps block the death of these newborn neurons that otherwise occurs with depression-inducing stress. Importantly, the study also shows that the new “P7C3-class” of neuroprotective compounds, which bolster neurogenesis in the hippocampus, are powerful, fast-acting antidepressants in an animal model of stress-induced depression. The results were published online April 22 in the journal Molecular Psychiatry.

Potential for new antidepressant drugs

The neuroprotective compounds tested in the study were discovered about eight years ago by Pieper, then at UT Southwestern Medical Center, and colleagues there, including Steven McKnight and Joseph Ready. The root compound, known as P7C3, and its analogs protect newborn neurons from cell death, leading to an overall increase in neurogenesis. These compounds have already shown promising neuroprotective effects in models of neurodegenerative disease, including Parkinson’s disease, amyotrophic lateral sclerosis (ALS), and traumatic brain injury. In the new study, the team investigated whether the neuroprotective P7C3 compounds would reduce depression in mice exposed to chronic stress, by enhancing neurogenesis in the hippocampus.

http://now.uiowa.edu/2014/04/protecting-new-neurons-reduces-depression-caused-stress

University of Iowa scientists show that ingredient in green tomatoes (tomatidine) may build bigger muscles

On By A.P.In Carver College of Medicine, Christopher Adams, Connectivity Map, fried green tomatoes, Iowa, Iowa City, Journal of Biological Chemistry, Medicine, muscle, muscle bulk, muscle growth, muscle wasting, Obesity, Science, tomatidine, University of Iowa, University of Iowa Hospitals and Clinics1 Comment

A new study has found that a compound in green tomatoes, tomatidine, not only boosts muscle growth and strength, it protects against muscle wasting caused by illness, injury or aging. A research team at the University of Iowa found that healthy mice given supplements containing tomatidine grew bigger muscles, became stronger and could exercise longer. Even better, the mice did not gain any weight due to a corresponding loss of fat, suggesting that the compound may also have potential for treating obesity. Nice bonus.

The research team used a systems biology tool called the Connectivity Map to identify tomatidine and discovered it stimulated growth of cultured human muscle cells. (The same screening method previously identified a compound in apple peel as a muscle-boosting agent – but green tomatoes were found to be even more potent.) In fact, the team discovered that tomatidine generates changes in gene expression that are essentially opposite to the changes that occur in muscle cells when people are affected by muscle atrophy.

“Green tomatoes are safe to eat in moderation. But we don’t know how many green tomatoes a person would need to eat to get a dose of tomatidine similar to what we gave the mice,” study chief Dr. Christopher Adams said in a statement “We also don’t know if such a dose of tomatidine will be safe for people, or if it will have the same effect in people as it does in mice. We are working hard to answer these questions, hoping to find relatively simple ways that people can maintain muscle mass and function, or if necessary, regain it.”

The end goal is “science-based supplements,” or even simply incorporating tomatidine “into everyday foods to make them healthier.”

Muscle atrophy, or muscle-wasting, is a significant health issue. It can be caused by aging, injury, cancer or heart failure and makes people weak and fatigued, prohibits physical activity and predisposes them to falls and fractures. It affects more than 50 million Americans annually, including 30 million elderly.

Exercise can help but it’s not enough and is not an option for those who are ill or injured, Adams said.

The findings were published April 9 in the Journal of Biological Chemistry.

http://www.laweekly.com/squidink/2014/04/15/green-tomatoes-may-build-bigger-muscles

New sweetener from the tequila plant may treat diabetes and weight loss

On By A.P.In agavins, American Chemical Society, Centro de Investigación y de Estudios Avanzados, Diabetes, diabetes, Dr. Rajadhyaksha, Food, GLP-1, glucagon-like peptide-1, Guanajuato, Health, Hunger, insulin, Medicine, Mercedes G. López, Mexico, Obesity, Obesity, ScienceLeave a comment

Could a new sugar substitute actually lower blood sugar and help you lose weight? That’s the tantalizing – but distant – promise of new research presented at the American Chemical Society (ACS) this week.

Agavins, derived from the agave plant that’s used to make tequila, were found in mouse studies to trigger insulin production and lower blood sugar, as well as help obese mice lose weight.

Unlike sucrose, glucose, and fructose, agavins aren’t absorbed by the body, so they can’t elevate blood glucose, according to research by Mercedes G. López, a researcher at the Centro de Investigación y de Estudios Avanzados, Biotechnology and Biochemistry Irapuato, in Guanajuato, Mexico.

And by boosting the level of a peptide called GLP-1 (short for glucagon-like peptide-1), which triggers the body’s production of insulin, agavins aid the body’s natural blood sugar control. Also, because agavins are type of fiber, they can make people feel fuller and reduce appetite, López’s research shows.

“We believe that agavins have a great potential as light sweeteners since they are sugars, highly soluble, have a low glycemic index, and a neutral taste, but most important, they are not metabolized by humans,” read the study abstract. “This puts agavins in a tremendous position for their consumption by obese and diabetic people.”

The caveat: The research was conducted in mice, and more study is necessary before we’ll know whether agavins are effective and safe in humans. In other words, we’re a long way from agavins appearing on grocery store shelves.

That said, with almost 26 millions of Americans living with diabetes and another 2 million diagnosed each year, a sweetener that lowered blood sugar levels rather than raised them would be quite a useful discovery. Not to mention the potential for a sugar substitute with the potential to help people lose weight.

In the study, titled “Agavins as Potential Novel Sweeteners for Obese and Diabetic People”, López added agavins to the water of mice who were fed a standard diet, weighing them and monitoring blood sugar levels every week. The majority of the mice given the agavin-supplemented water had lower blood glucose levels, ate less, and lost weight compared with other mice whose water was supplemented with glucose, sucrose, fructose, agave syrup, and aspartame.

Unlike other types of fructose, Agavins are fructans, which are long-chain fructoses that the body can’t use, so they are not absorbed into the bloodstream to raise blood sugar. And despite the similarity in the name, agavins are not to be confused with agave nectar or agave syrup, natural sweeteners that are increasingly popular sugar substitutes. In these products the fructans are broken down into fructose, which does raise blood sugar – and add calories.

López has been studying fructans for some time, and has published previous studies showing that they have protective prebiotic effects in the digestive tract and contribute to weight loss in obese mice.

A 2012 study by another team of researchers published in Plant Foods for Human Nutrition found that fructans boosted levels of the beneficial probiotics lactobacillus and bifidus. And like many types of fiber, agavins also lower levels of cholesterol and triglycerides in the blood.

But the news isn’t all good; a 2011 literature review of human studies of the relationship between fructans (not agavins specifically) and blood sugar found that of 13 randomized studies of fructans, only three documented positive results. It remains to be seen whether – as López argues – agavins are distinct from other fructans in their action.

The downside: Agavins are don’t taste as sweet as other forms of sugar such as sucrose, fructose and glucose. And not everyone can tolerate them; like other types of fiber they have the potential to cause digestive problems.

http://www.forbes.com/sites/melaniehaiken/2014/03/17/new-sweetener-from-the-tequila-plant-may-aid-diabetes-weight-loss/

Thanks to Dr. Rajadhyaksha for bringing this to the attention of the It’s Interesting community.

As World’s Kids Get Fatter, Doctors Turn to the Knife

On By A.P.In Aayed Alqahtani, American Society for Metabolic and Bariatric Surgery, bariatric surgery, Daifailluh al-Bugami, Evan Nadler, Journal of Family and Community Medicine, King Saud University, Kirk Reichard, Medicine, Middle East, Obesity, Pete Cuomo, Saudi Arabia, Saudi Journal of Obesity, Shirley S. Wang, Wall Street Journal, weight loss, WHO, World Health Organization1 Comment

Daifailluh al-Bugami was just a year old when his parents noticed that his lips turned blue as he slept at night. It was his weight, doctors said, putting pressure on his delicate airways.

Now Daifailluh is 3, and at 61 pounds he is nearly double the typical weight of a child his age. So the Bugamis are planning the once unthinkable: To have their toddler undergo bariatric surgery to permanently remove part of his stomach in hopes of reducing his appetite and staving off a lifetime of health problems.

That such a young child would be considered for weight-loss surgery—something U.S. surgeons generally won’t do—underscores the growing health crisis here and elsewhere in the Middle East. Widespread access to unhealthy foods, coupled with sedentary behavior brought on by wealth and the absence of a dieting and exercise culture, have caused obesity levels in Saudi Arabia and many other Gulf states to approach or even exceed those in Western countries.

While solid national data are hard to come by, some experts say that obesity has turned into a serious health problem for Saudi children, with an estimated 9.3% of school-age youths meeting the World Health Organization’s body-mass-index criteria for obesity, according to research published in 2013 in the Saudi Journal of Obesity. About 18% of school-age children in the U.S. were considered obese in 2010, according to the Centers for Disease Control and Prevention.

Daifailluh’s doctor, Aayed Alqahtani, is a leading advocate of a radical approach to the problem. Patients travel to him from across the country and the Gulf region. Over the past seven years, he has performed bariatric surgery on nearly 100 children under the age of 14, which experts on the procedure believe is the largest number performed by one doctor on young children.

Dr. Alqahtani’s work is being watched amid a global debate about the appropriate age for bariatric surgery. In the U.S., the minimum is generally considered 14. The World Health Organization, in a 2012 report on pediatric bariatric surgery, concluded that there is a dearth of data available on the long-term outcomes of the procedure in children and that a “conservative approach” is necessary until long-term studies are conducted.

Bariatric surgery has been embraced as an effective and relatively safe procedure for morbidly obese adults. The concern with children revolves mostly around nonsurgical risks, such as how the abrupt change in nutrition could affect long-term brain development and sexual maturation.

Dr. Alqahtani says the decision to operate on Daifailluh is a difficult one because of his age. But after nearly two years of consultation with the clinic, Daifailluh’s obesity-related medical problems haven’t gotten any better. “We should not deprive our patients from bariatric surgery based on their age alone,” the surgeon says. “If they have [medical] conditions that threaten their lives, then we should not deny the bariatric surgery.”

The worsening obesity problem here also is manifesting itself in other ways. Some 20% of the Saudi adult population has Type 2 diabetes, a condition linked to obesity, according to the International Diabetes Federation, compared with 8.3% in the U.S., according to the CDC. The cost of diabetes treatment in Saudi Arabia is expected to rise to $2.4 billion in 2015, more than triple that spent in 2010, according to a recent study in the Journal of Family and Community Medicine.

Obesity, particularly among women, has become rampant across much of the Middle East, particularly in oil-rich Gulf nations. In Kuwait, almost half of adult women are considered obese, while 44% of Saudi women and 45% of Qatari women meet the criteria, according to the International Association of the Study of Obesity. Experts says Saudis, in particular, are more likely to carry certain genes linked to obesity.

Saudi lifestyle and parenting practices may exacerbate the problem, according to doctors at weight-loss clinics. Nannies or cooks are often employed, so parents may not know what their children are eating. Saudis often are coaxed to eat large quantities of food when visiting relatives and friends.

In Riyadh, physical activity is limited, particularly for girls, and high temperatures and few green spaces make walking difficult. School gym classes generally take place just once a week. Western-style fast food is abundant, particularly at the air-conditioned malls frequented by children and families.

Bariatric surgery has become an accepted treatment among obese Saudi adults and is paid for by the government. An estimated 11,000 bariatric surgeries were performed on Saudis in 2012, according to Dr. Alqahtani.

The surgery, of which there are several types, generally reduces the size of the stomach and, with some techniques, rearranges the digestive path to bypass much of the intestines. Some types are reversible but generally considered less effective. After the surgery, patients must eat very small meals—ideally for the rest of their lives. Many studies have shown that adults, on average, lose over 50% of their body weight after surgery.

Increasingly, youngsters are heading to the operating room here, where parents see no other options. These days, Dr. Alqahtani performs surgery on three to four youths a week.

“I have seen in my clinic patients who cannot sleep lying down—they sleep sitting—because of sleep apnea, and their age is 10 years, sometimes 5 years,” says Dr. Alqahtani, a professor in the college of medicine and an obesity specialist at King Saud University.

Pediatric surgeons in the U.S. say they also are facing demands from families to operate on younger patients. Thomas Inge, surgical director of the Surgical Weight Loss Program for Teens at Cincinnati Children’s Hospital, says he will be operating on a 12-year-old later this month. He says that as younger and younger children are referred for consideration of surgery, care teams will need to carefully weigh the pros and cons.

Evan Nadler, a pediatric surgeon at Children’s National Medical Center in Washington, D.C., is considering doing the operation on two young children. He and the family of a 7-year-old D.C. boy have agreed that surgery likely is the best option, he says. The family of an 8-year-old from the Middle East has decided to wait until their daughter is older and can better understand the surgery, he says.

Many doctors say they aren’t ready to follow Dr. Alqahtani yet. Kirk Reichard, chairman of the pediatric-surgery committee for the American Society for Metabolic and Bariatric Surgery, notes that there are no data to show that surgery doesn’t affect young children’s long-term sexual maturation or cognitive functioning. The brain, particularly in growing children, is sensitive to nutrition and needs enough energy to mature properly. Nutrition also has the potential to affect hormones linked to sexual maturation.

Dr. Alqahtani says he has seen evidence of normal growth following the procedure in his under-14 patients, many of whom are now four years postsurgery.

“We will certainly use his experience to inform us in some ways, but [Dr. Alqahtani’s work] won’t take the place of trials,” says Dr. Reichard.

One of the main criticisms from some weight-loss experts about performing the surgery on those under 14 is that changes in diet and exercise can prevent further weight gain. In addition, says Dr. Reichard, “there are a lot of other therapies short of surgery that can be helpful in managing” related medical conditions.

Saudi Arabia’s Dr. Alqahtani says he requires his child patients to enroll in a weight-loss program for at least six months because patients able to lose even a bit tend to have better outcomes after surgery. But he says that by the time families come to him, their children have such substantial health problems it is generally too late for diet and exercise alone.

Dr. Alqahtani was trained as a surgeon at McGill University in Montreal and at a minimally invasive surgery center in Denver. When he returned home to Riyadh in 2002, he says, he was inundated with pediatric patients so obese they were suffering from advanced stages fatty liver disease, diabetes and sleep apnea, a disorder in which patients repeatedly stop breathing for short periods during sleep—all diseases typically not seen until middle age.

Om Abdullah Asiri says she tried to help her 11-year-old son lose weight by restricting his eating at home. But he would eat fast food while out with his friends and plays videogames for hours on end, she says. “I can’t control him outside the home,” she says.

He grew to 250 pounds. His body-mass index—a calculation that uses weight and height to estimate percentage of body fat—was 61. A BMI of 40 or above is the most severe obesity category, according to the World Health Organization.

Ms. Asiri traveled with her son, Abdullah, from their home in Abha, more than 600 miles south of Riyadh, to see Dr. Alqahtani for the operation. Lying on a hospital bed the day before his surgery, Abdullah said he is “happy and ready” for the surgery.

His mother says surgery is the best solution for Abdullah, who has high blood pressure, fatty liver, hip pain and severe sleep apnea. Afterward, he won’t have a choice but to eat better, she says. “The surgery will make him change.” She says he dreams of playing soccer with his friends.

The procedure Dr. Alqahtani performs is called the gastric sleeve, which slices off a portion of the stomach but leaves the rest of the digestive tract intact. It is gaining in popularity because of its good weight-loss results and minimal side effects. The operation, conducted through tiny incisions in the abdomen, takes him just 30 minutes.

One recent morning, he operated on a 20-year-old, two 17-year-olds, a 12-year-old, then Abdullah, who was then 10.

Complications can include bleeding in about 10% of cases, and leaking and blood clots in 1% to 2%. Dr. Alqahtani says he has had only two leaks in 1,700 cases, neither in children.

Dr. Alqahtani says each of his pediatric patients has lost at least some weight, and nearly three-quarters have lost more than 50% of their initial body weight. Abdullah has lost close to 50 pounds since his surgery about two months ago, according to his 29-year-old brother, Ahmad.

Dr. Alqahtani says about 90% of his patients have seen medical conditions such as diabetes and hypertension clear up, according to a paper scheduled for publication in the journal Surgery for Obesity and Related Diseases. He published outcomes on 108 children in the peer-reviewed Annals of Surgery journal in 2012.

Recovery involves a six-week transition diet starting with clear liquids and puréed food. Patients eventually can resume solid foods at much-reduced quantities. At first, patients feel full after just 1 to 2 spoonfuls of food, though they gradually can eat more as their stomachs stretch.

Some bariatric-surgery experts have raised questions about whether children are capable of maintaining the restrictive lifetime diet after surgery or whether they will sabotage the procedure when they become teenagers and have a greater autonomy to eat what they want. Some experts question whether parents should make such a drastic and permanent decision for a child.

The decision has been excruciating for the family of Daifailluh, the toddler from Ta’if. Daifailluh was referred to Dr. Alqahtani’s clinic about two years ago after difficulty breathing sent him to the intensive-care unit at a hospital in his hometown. Doctors there determined the toddler was seriously overweight. His mother, Hessa Salem al-Bugami, says she tried to improve his diet but didn’t have good guidance until she came to Dr. Alqahtani’s clinic, a trip of nearly 500 miles from Ta’if. “I feel like I failed,” she says.

At first, the family wanted Daifailluh to lose weight without the operation. Ms. Bugami says her son has always had an “open appetite” and never refuses food. She says she feeds him brown bread and boiled chicken and rice, and limits his portions, hiding the rest of the food. But his obesity hasn’t improved, she says.

Daifailluh will cry and sometimes throw temper tantrums when he wants food, she says. She has tried distracting him with toys, locking the two of them in a room to play for so long she ended up missing her own meal.

“When he starts crying, it’s hard not to give him any of the food, to make the crying stop,” she says. “I feel like I work really hard, but it’s just too much on me.”

Daifailluh, who was hospitalized again for pulmonary problems, is waiting for a surgery date, which will come if he gets final medical clearance from Dr. Alqahtani.

The entire family is worried about the surgery, particularly the effects of anesthesia and whether the surgery will reduce his appetite too much. Ms. Bugami also worries that her son will regain the weight when he leaves the house eventually and is no longer under her watch.

But that is a concern for another day. “Right now is the most scary situation,” she says.

Write to Shirley S. Wang at shirley.wang@wsj.com

http://online.wsj.com/news/articles/SB10001424052702304851104579360992538215578?mg=reno64-wsj&url=http%3A%2F%2Fonline.wsj.com%2Farticle%2FSB10001424052702304851104579360992538215578.html

Thanks to Pete Cuomo for bringing this to the attention of the It’s Interesting community.

How Exercise Beefs Up the Brain

On By A.P.In Alzheimer's disease, Barbara Hempstead, BDNF, Boston, brain derived neurotrophic factor, brown fat, Bruce Spiegelman, Cell Metabolism, Christiane Wrann, Dementia, diabetes, Dr. Rajadhyaksha, Exercise, FNDC5, Harvard Medical School, hippocampus, irisin, Karolinska Institute in Sweden, Medicine, Nature, neurologist, Neurology, Neuropsychiatric Disease, Neuroscience, neuroscientist, neurotrophin, Obesity, Parkinson's disease, PGC-1α, Pontus Boström, Science, The Brain, Weill Cornell Medical College, white fatLeave a comment

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New research explains how abstract benefits of exercise—from reversing depression to fighting cognitive decline—might arise from a group of key molecules.

While our muscles pump iron, our cells pump out something else: molecules that help maintain a healthy brain. But scientists have struggled to account for the well-known mental benefits of exercise, from counteracting depression and aging to fighting Alzheimer’s and Parkinson’s disease. Now, a research team may have finally found a molecular link between a workout and a healthy brain.

Much exercise research focuses on the parts of our body that do the heavy lifting. Muscle cells ramp up production of a protein called FNDC5 during a workout. A fragment of this protein, known as irisin, gets lopped off and released into the bloodstream, where it drives the formation of brown fat cells, thought to protect against diseases such as diabetes and obesity. (White fat cells are traditionally the villains.)

While studying the effects of FNDC5 in muscles, cellular biologist Bruce Spiegelman of Harvard Medical School in Boston happened upon some startling results: Mice that did not produce a so-called co-activator of FNDC5 production, known as PGC-1α, were hyperactive and had tiny holes in certain parts of their brains. Other studies showed that FNDC5 and PGC-1α are present in the brain, not just the muscles, and that both might play a role in the development of neurons.

Spiegelman and his colleagues suspected that FNDC5 (and the irisin created from it) was responsible for exercise-induced benefits to the brain—in particular, increased levels of a crucial protein called brain-derived neurotrophic factor (BDNF), which is essential for maintaining healthy neurons and creating new ones. These functions are crucial to staving off neurological diseases, including Alzheimer’s and Parkinson’s. And the link between exercise and BDNF is widely accepted. “The phenomenon has been established over the course of, easily, the last decade,” says neuroscientist Barbara Hempstead of Weill Cornell Medical College in New York City, who was not involved in the new work. “It’s just, we didn’t understand the mechanism.”

To sort out that mechanism, Spiegelman and his colleagues performed a series of experiments in living mice and cultured mouse brain cells. First, they put mice on a 30-day endurance training regimen. They didn’t have to coerce their subjects, because running is part of a mouse’s natural foraging behavior. “It’s harder to get them to lift weights,” Spiegelman notes. The mice with access to a running wheel ran the equivalent of a 5K every night.

Aside from physical differences between wheel-trained mice and sedentary ones—“they just look a little bit more like a couch potato,” says co-author Christiane Wrann, also of Harvard Medical School, of the latter’s plumper figures—the groups also showed neurological differences. The runners had more FNDC5 in their hippocampus, an area of the brain responsible for learning and memory.

Using mouse brain cells developing in a dish, the group next showed that increasing the levels of the co-activator PGC-1α boosts FNDC5 production, which in turn drives BDNF genes to produce more of the vital neuron-forming BDNF protein. They report these results online today in Cell Metabolism. Spiegelman says it was surprising to find that the molecular process in neurons mirrors what happens in muscles as we exercise. “What was weird is the same pathway is induced in the brain,” he says, “and as you know, with exercise, the brain does not move.”

So how is the brain getting the signal to make BDNF? Some have theorized that neural activity during exercise (as we coordinate our body movements, for example) accounts for changes in the brain. But it’s also possible that factors outside the brain, like those proteins secreted from muscle cells, are the driving force. To test whether irisin created elsewhere in the body can still drive BDNF production in the brain, the group injected a virus into the mouse’s bloodstream that causes the liver to produce and secrete elevated levels of irisin. They saw the same effect as in exercise: increased BDNF levels in the hippocampus. This suggests that irisin could be capable of passing the blood-brain barrier, or that it regulates some other (unknown) molecule that crosses into the brain, Spiegelman says.

Hempstead calls the findings “very exciting,” and believes this research finally begins to explain how exercise relates to BDNF and other so-called neurotrophins that keep the brain healthy. “I think it answers the question that most of us have posed in our own heads for many years.”

The effect of liver-produced irisin on the brain is a “pretty cool and somewhat surprising finding,” says Pontus Boström, a diabetes researcher at the Karolinska Institute in Sweden. But Boström, who was among the first scientists to identify irisin in muscle tissue, says the work doesn’t answer a fundamental question: How much of exercise’s BDNF-promoting effects come from irisin reaching the brain from muscle cells via the bloodstream, and how much are from irisin created in the brain?

Though the authors point out that other important regulator proteins likely play a role in driving BDNF and other brain-nourishing factors, they are focusing on the benefits of irisin and hope to develop an injectable form of FNDC5 as a potential treatment for neurological diseases and to improve brain health with aging.

http://news.sciencemag.org/biology/2013/10/how-exercise-beefs-brain

Thanks to Dr. Rajadhyaksha for bringing this to the attention of the It’s Interesting community.

New research suggests diet soda may do more harm than good

On By A.P.In acesulfame potassium, American Beverage Association, artificial sweetener, aspartame, Diabetes, diet soda, Equal, heart disease, insulin, Medicine, Melina Jampolis, neotame, NutraSweet, Obesity, Purdue University, saccharin, Splenda, Stroke, sucralose, SugarTwin, Sunett, Susan Swithers, Sweet One, Sweet'N Low, Trends in Endocrinology & MetabolismLeave a comment

soda

Diet soda drinkers have the same health issues as those who drink regular soda, according to a new report published Wednesday.

Purdue University researchers reviewed a dozen studies published in past five years that examined the relationship between consuming diet soda and health outcomes for the report, published as an opinion piece in the journal Trends in Endocrinology & Metabolism. They say they were “shocked” by the results.

“Honestly, I thought that diet soda would be marginally better compared to regular soda in terms of health,” said Susan Swithers, the report’s author and a behavioral neuroscientist and professor of psychological sciences. “But in reality it has a counterintuitive effect.”

Artificial sweeteners in diet soda fulfill a person’s craving for a sweet taste, without the calories. But that’s the problem, according to researchers. Think of it like crying wolf.

Fake sugar teases your body by pretending to give it real food. But when your body doesn’t get the things it expects to get, it becomes confused on how to respond.

“You’ve messed up the whole system, so when you consume real sugar, your body doesn’t know if it should try to process it because it’s been tricked by the fake sugar so many times,” says Swithers.

On a physiological level, this means when diet soda drinkers consume real sugar, the body doesn’t release the hormone that regulates blood sugar and blood pressure.

Diet soda drinkers also tend to pack on more pounds than those who don’t drink it, the report says.

“The taste of sweet does cause the release of insulin, which lowers blood sugar , and if carbohydrates are not consumed, it causes a drop in blood sugar, which triggers hunger and cravings for sugar,” says CNN diet and fitness expert Dr. Melina Jampolis.

The artificial sweeteners also dampen the “reward center” in your brain, which may lead you to indulge in more calorie-rich, sweet-tasting food, according to the report.

The American Beverage Association says the report was “an opinion piece, not a scientific study.

“Low-calorie sweeteners are some of the most studied and reviewed ingredients in the food supply today,” the association said in a statement. “They are safe and an effective tool in weight loss and weight management, according to decades of scientific research and regulatory agencies around the globe.”

Diet soda’s negative effects are not just linked to weight gain, however, the report says.

It found that diet soda drinkers who maintained a healthy weight range still had a significantly increased risk of the top three killers in the United States: diabetes, heart disease and stroke.

“We’ve gotten to a place where it is normal to drink diet soda because people have the false impression that it is healthier than indulging in a regular soda,” says Swithers. “But research is now very clear that we need to also be mindful of how much fake sugar they are consuming.”

There are five FDA-approved artificial sweeteners: acesulfame potassium (Sunett, Sweet One), aspartame (Equal, NutraSweet), neotame, saccharin (SugarTwin, Sweet’N Low), and sucralose (Splenda).

“Saccharin was one of the first commercially-available artificially sweeteners, and it’s actually a derivative of tar,” says Swithers.

Even natural sweeteners like Stevia, which has no calories and is 250 times sweeter than regular sugar, are still processed extracts of a natural plant and may have increased health risks.

“Just because something is natural does not always mean that it is safer,” says Jampolis.

There more studies and research that need to be done. But in the meantime, experts say: Limit consumption.

“No one is saying cut it out completely,” says Swithers. “But diet soda should be a treat or indulgence just like your favorite candy, not an everyday
thing.”

Study: Diet soda may do more harm than good

Samoa airline introduces pay-by-weight pricing

On By A.P.In airlines, American Samoa Visitors Bureau, Ana Faapouli, Chris Langton, David Vaeafe, Obesity, Palanitina Toelupe, Samoa, Samoa air, U.S. Department of Transportation, WHO, World Health OrganizationLeave a comment

Fat-Guy-300x260

A tiny Samoa airline is giving passengers a big reason to lose weight: Tickets sold not by the seat, but by the kilogram. Samoa Air is pricing its first international flights based on the weight of its passengers and their bags. Depending on the flight, each kilogram (2.2 pounds) costs 93 cents to $1.06. That means the average American man weighing 195 pounds with a 35-pound bag would pay $97 to go one-way between Apia, Samoa, and Pago Pago, American Samoa. Competitors typically charge $130 to $140 roundtrip for similar routes.

The weight-based pricing is not new to the airline, which launched in June. It has been using the pricing model since November, but in January the U.S. Department of Transportation approved its international route between American Samoa and Samoa. The airline’s chief executive, Chris Langton, said that “planes are run by weight and not by seat, and travelers should be educated on this important issue. The plane can only carry a certain amount of weight and that weight needs to be paid. There is no other way.”

Langton, a pilot himself, said when he flew for other airlines, he brought up the idea to his bosses to charge by weight, but they considered weight as too sensitive an issue to address. “It’s always been the fairest way, but the industry has been trying to pack square pegs into round holes for many years,” he said.

Travelers in the region already are weighed before they fly because the planes used between the islands are small, said David Vaeafe, executive director of the American Samoa Visitors Bureau. Samoa Air’s fleet includes two nine-passenger planes for commercial routes and a three-passenger plane for an air taxi service. Langton said passengers who need more room will be given one row on the plane to ensure comfort.

The new pricing system would make Samoa Air the first to charge strictly by weight, a change that Vaeafe said is, “in many ways… a fair concept for passengers. For example, a 12- or 13-year-old passenger, who is small in size and weight, won’t have to pay an adult fare, based on airline fares that anyone 12 years and older does pay the adult fare,” he said.

Vaeafe said the pricing system has worked in Samoa but it’s not clear whether it will be embraced by travelers in the U.S. territory. Langton said the airline has received mixed responses since it began promoting the pricing on its website and Facebook. Langton said some passengers have been surprised, but no one has refused to be weighed yet. He said he’s given away a few free flights to some regular customers who lost weight, and that health officials in American Samoa were among the first to contact the airline when the pricing structure was announced.

“They want to ride on the awareness this is raising and use it as a medium to address obesity issues,” he said.

Islands in the Pacific have the highest rates of obesity in the world. According to a 2011 report by the World Health Organization, 86 percent of Samoans are overweight, the fourth worst among all nations. Only Samoa’s Pacific neighbors Nauru, the Cook Islands and Tonga rank worse. In comparison, the same study found that 69 percent of Americans are overweight, 61 percent of Australians, and 22 percent of Japanese. Samoa ranked just as poorly in statistics measuring those who are obese, or severely overweight.

Samoa’s Director General of Health, Palanitina Toelupe, said the airline’s plans could be a good way to promote weight loss and healthy eating. “It’s a very brave idea on their part,” she said. She added that flying on the airline may become too expensive for some large people and that the charging system could only ever be a small part of a larger strategy on weight issues. She said she’d be interested in meeting with the airline to discuss working together.

Ana Faapouli, an American Samoa resident who frequently travels to Samoa, said the pricing scheme will likely be profitable for Samoa Air. “Samoa Air is smart enough to find ways to benefit from this service as they will be competing against two other airlines,” Faapouli said.

http://www.cbsnews.com/8301-505145_162-57577683/samoa-airline-introduces-pay-by-weight-pricing/