The 'Obesity Epidemic': Contagious?

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#1
Big assed piece article but I thought it worth reporducing the lot:

Catching Obesity: Identifying Viruses That May Make Us Fat

Do human adenoviruses cause obesity? Is a vaccine possible?Researcher advises: ‘Eat right, exercise, wash your hands’

BETHESDA, Md. (Jan. 30, 2006) – There is a lot of good advice to help us avoid becoming obese, such as “Eat less,” and “Exercise.” But here’s a new and surprising piece of advice based on a promising area of obesity research: “Wash your hands.”

There is accumulating evidence that certain viruses may cause obesity, in essence making obesity contagious, according to Leah D. Whigham, the lead researcher in a new study, “Adipogenic potential of multiple human adenoviruses in vivo and in vitro in animals,” in the January issue of the American Journal of Physiology-Regulatory, Integrative and Comparative Physiology published by the American Physiological Society.

The study, by Whigham, Barbara A. Israel and Richard L. Atkinson, of the University of Wisconsin, Madison, found that the human adenovirus Ad-37 causes obesity in chickens. This finding builds on studies that two related viruses, Ad-36 and Ad-5, also cause obesity in animals.

Moreover, Ad-36 has been associated with human obesity, leading researchers to suspect that Ad-37 also may be implicated in human obesity. Whigham said more research is needed to find out if Ad-37 causes obesity in humans. One study was inconclusive, because only a handful of people showed evidence of infection with Ad-37 – not enough people to draw any conclusions, she said. Ad-37, Ad-36 and Ad-5 are part of a family of approximately 50 viruses known as human adenoviruses.

Researchers now must:

  • * dentify the viruses that cause human obesity

    * devise a screening test to identify people who are infected

    * develop a vaccine

Screening test and vaccine still a long way off

The Whigham et al. study prompted an editorial in the same issue of AJP-Regulatory, Integrative and Comparative Physiology by Frank Greenway, professor in the Department of Clinical Trials, Pennington Biomedical Research Center, Louisiana State University, Baton Rouge.

“If Ad-36 is responsible for a significant portion of human obesity, the logical therapeutic intervention would be to develop a vaccine to prevent future infections,” Greenway wrote. “If a vaccine were to be developed, one would want to ensure that all the serotypes of human adenoviruses responsible for human obesity were covered in the vaccine.”

“If one could predict the potential of an adenovirus to cause human obesity by using an in vitro assay or even by animal testing, screening of the approximately 50 human adenoviruses might be accelerated, shortening the time required for vaccine formulation," Greenway wrote. “Human antibody prevalence in obese and lean human populations appears to be the only reliable method to screen adenoviruses for their potential to cause obesity in humans at the present time,” he noted.

Obesity contagion theory slow to catch on

The notion that viruses can cause obesity has been a contentious one among scientists, Whigham said. And yet, there is evidence that factors other than poor diet or lack of exercise may be at work in the obesity epidemic. “The prevalence of obesity has doubled in adults in the United States in the last 30 years and has tripled in children,” the study noted. “With the exception of infectious diseases, no other chronic disease in history has spread so rapidly, and the etiological factors producing this epidemic have not been clearly identified.”

“It makes people feel more comfortable to think that obesity stems from lack of control,” Whigham said. “It’s a big mental leap to think you can ‘catch’ obesity.” However, other diseases once thought to be the product of environmental factors are now known to stem from infectious agents. For example, ulcers were once thought to be the result of stress, but researchers eventually implicated bacteria, Helicobacter pylori, as a cause.

“The nearly simultaneous increase in the prevalence of obesity in most countries of the world is difficult to explain by changes in food intake and exercise alone, and suggest that adenoviruses could have contributed,” the study said. “The role of adenoviruses in the worldwide epidemic of obesity is a critical question that demands additional research.”

Ad-37 third virus implicated in animal obesity

The theory that viruses could play a part in obesity began a few decades ago when Nikhil Dhurandhar, now at Pennington Biomedical Research Center at LSU, noticed that chickens in India infected with the avian adenovirus SMAM-1 had significantly more fat than non-infected chickens. The discovery was intriguing because the explosion of human obesity, even in poor countries, has led to suspicions that overeating and lack of exercise weren’t the only culprits in the rapidly widening human girth. Since then, Ad-36 has been found to be more prevalent in obese humans.

In the current study, Whigham et al. attempted to determine which adenoviruses (in addition to Ad-36 and Ad-5) might be associated with obesity in chickens. The animals were separated into four groups and exposed to either Ad-2, Ad-31, or Ad-37. There was also a control group that was not exposed to any of the viruses. The researchers measured food intake and tracked weight over three weeks before ending the experiment and measuring the chickens’ visceral fat, total body fat, serum lipids, and viral antibodies.

Chickens inoculated with Ad-37 had much more visceral fat and body fat compared with the chickens infected with Ad-2, Ad-31 or the control group, even though they didn’t eat any more. The Ad-37 group was also generally heavier compared to the other three groups, but the difference wasn’t great enough to be significant by scientific standards.

The authors concluded that Ad-37 increases obesity in chickens, but Ad-2 and Ad-31 do not. “Ad-37 is the third human adenovirus to increase adiposity in animals, but not all adenoviruses produce obesity,” the study concluded.

There is still much to learn about how these viruses work, Whigham said. “There are people and animals that get infected and don’t get fat. We don’t know why,” she said. Among the possibilities: the virus hasn’t been in the body long enough to produce the additional fat; or the virus creates a tendency to obesity that must be triggered by overeating, she said.

Mass screening for these viruses is impractical right now because there is no simple blood test available that would quickly identify exposure to a suspect virus, Whigham et al. said. More work is needed to develop such a test, Whigham said.

Source, funding and disclosure

“Adipogenic potential of multiple human adenoviruses in vivo and in vitro in animals,” by Leah D. Whigham and Richard L. Atkinson of the Departments of Medicine and Nutritional Sciences at the University of Wisconsin, Madison, and Barbara A. Israel of the Department of Pathobiological Sciences, University of Wisconsin, Madison, is in the January issue of the American Journal of Physiology - Regulatory, Integrative and Comparative Physiology published by the American Physiological Society.

Research was supported by grants from the National Institute of Diabetes and Digestive and Kidney Diseases, and the Beers-Murphy Clinical Nutrition Center, University of Wisconsin. Atkinson, now at the Virginia Commonwealth University, owns all shares of Obetech LLC, a company that markets assays to detect infection with human adenovirus-36 and owns patent rights for these assays.
www.the-aps.org/press/journal/06/4.htm

--------
I was also reminded of this:

Do you know what the number one health risk in America is?
Obesity. They say we're in the middle of an obesity epidemic.
An epidemic like it is polio. Like we'll be telling our grand kids about it one day.
The Great Obesity Epidemic of 2004.
"How'd you get through it grandpa?"
"Oh, it was horrible Johnny, there was cheesecake and pork chops everywhere."
Lazyboy - Underwear goes inside the pants
 

Jerry_B

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#2
Hmm - one is reminded of what Dennis Leary had to say about obesity being casued by a virus... ;)
 

Yithian

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#4
Percentage obsese (2 to 3 stone overweight apparently):

Country % Men % Women
Finland 19 19
Russia 10.8 27.9
England 17 20
Germany 17.2 19.3
Czech Republic 16.3 20.2
Scotland 15.9 17.3
Belgium 12.1 18.4
Spain 11.5 15.2
Sweden 10 11.9
France 9.6 10.5
Denmark 10 9
Netherlands 8.4 8.3
Italy 6.5 6.3
USA 19.5 25
Australia 18 18

http://www.bbc.co.uk/health/healthy_liv ... acts.shtml
English women are doing us proud but we've quite a way to go before we reach the superleagues of the US and Russia.
 

Leaferne

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#5
Irrelevant trivia: poor women are more likely to be obese, while poor men more likely to be underweight. Works in reverse as you go up the socioeconomic scale.
 

Mythopoeika

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#6
Leaferne said:
Irrelevant trivia: poor women are more likely to be obese, while poor men more likely to be underweight. Works in reverse as you go up the socioeconomic scale.
According to that, I must be extremely wealthy. I'm 7 stones overweight.
Perhaps I should go and live in Tonga - I'd get more respect there.
 
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#7
Obesity and bacteria

Obesity and bacteria

Greedy guts?

Jan 4th 2007
From The Economist print edition


Every week seems to bring a new theory about why people are getting fatter. The latest is that intestinal microbes are partly to blame



ALTHOUGH most people prefer not to think about it, human guts are full of bacteria. And a good thing, too. These intestinal bugs help digestion, and also stop their disease-causing counterparts from invading. In return, their human hosts provide them with a warm place to live and a share of their meals. It is a symbiotic relationship that has worked well for millions of years.

Now it is working rather too well. A group of researchers led by Jeffrey Gordon, of the Washington University School of Medicine, in St Louis, has found that some types of microbes are a lot better than others at providing usable food to their hosts. In the past, when food was scarce, those who harboured such microbes would have been blessed. These days, paradoxically, they are cursed, for the extra food seems to contribute to obesity. Worse still, these once-benign microbes have even subtler effects, regulating the functioning of human genes and inducing the bodies of their hosts to lay down more fat than would otherwise be the case.


Dr Gordon's research is outlined in a paper published in this week's Proceedings of the National Academy of Sciences (PNAS) and two others published last month in Nature. In the Nature papers, he and his team reported that obese people have a different mix of gut microbes from that found in lean people—a mix that is more efficient at unlocking energy from the food they consume. Although individuals can harbour up to a thousand different types of microbes, more than 90% of these belong to one or other of two groups, called Bacteroidetes and Firmicutes. The researchers sequenced bacterial DNA from faecal samples taken from volunteers and discovered that those who were obese had a higher proportion of Firmicutes than lean people did.



Bugs in the system
This also turned out to be true in mice, and working with these rodents, the researchers discovered that the types of Firmicute found in obese animals are more efficient at converting complex polysaccharides (a form of carbohydrate that mammals have a hard time digesting by themselves) into simple, usable sugars such as glucose. In effect, the Firmicutes made more energy available from the same amount of food. The researchers were even able to make mice that had been raised in a germ-free environment fatter or thinner by colonising their guts with microbes from either obese or lean mice.

It sounds simple enough. Unfortunately, further probing showed that the story is a little more complicated, for Dr Gordon did not merely count the gut bacteria of fat and thin people—he then put some of the fat ones on a diet. As these once-obese humans lost weight over the course of a year, their mix of gut microbes changed to reflect their new, svelte status. Why this happened is not clear. It does not seem to have been a result of the composition of the diet, since the effect was the same whether people lost weight with a low-fat diet or a low-carbohydrate diet. Nevertheless, this part of the experiment suggests it is weight that determines gut biodiversity, not the other way round.

The paper published in PNAS, though, supports the idea that the bacterial mixture is cause not effect, by adding yet another element to the story. In this study, Dr Gordon took normal mice and germ-free mice, and fed both groups a “Western” diet that was high in fat and sugar. The normal mice gained weight; the germ-free mice stayed lean.

Part of the reason was that the normal mice had microbes that made more useful sugar available. But the researchers looked more closely and found that there was even more going on. By comparing the two kinds of mice, they discovered that the gut microbes in the regular mice were tinkering with their hosts' metabolisms, regulating them in at least two different ways.

First, they suppressed production by the mice's bodies of a substance called fasting-induced adipose factor. This encouraged the mice to store fat. Second, they caused lower levels of another substance, called adenosine monophosphate-activated protein kinase, which made it harder for them to burn fat that they had already accumulated. The upshot is that gut microbes not only release energy from food, they also encourage bodies to store that energy as fat and to keep the fat on.

The practical upshot of this is hard to see at the moment. But if these two suppression mechanisms could, themselves, be suppressed, that might stop people putting on weight. The findings do, however, emphasise how profound the relationship is between people and their gut bacteria. These bacteria can be thought of as an additional digestive organ. Alternatively, humans might view themselves as a sort of collective organism—a human casing surrounding a vast colony of microbes. It is just a pity that this colony is working so hard on behalf of its casing that, in an era when food comes from the supermarket rather than the savannah, the result is rather too good.

http://www.economist.com/science/displa ... id=8486096
 

tilly50

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#8
It would prove interesting if they studied the antibiotic restistance of these bacteria. If they are resistant to antibiotics commonly used for cases of childhood infections then they would begin to predominate in the gut early on in the individuals life leading to them making any other tendencies to obesity so much worse.
 

Leaferne

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I must be unusual because I don't recall ever taking antibiotics until I was in my 20s (for strep throat); I may have been given them when I had tonsillitis at age seven but then again, I don't remember being given a lot of pills at that time either. Nowadays kids seem to be on ABs all the bloody time. :?
 

JamesWhitehead

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"The paper published in PNAS, though, supports the idea that the bacterial mixture is cause not effect, by adding yet another element to the story. In this study, Dr Gordon took normal mice and germ-free mice, and fed both groups a “Western” diet that was high in fat and sugar. The normal mice gained weight; the germ-free mice stayed lean."

Eureka! There's a pill we need. Eat filth, stay slim! :?
 

rynner2

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Fat boy may be put in care

Sarah-Kate Templeton, Health Correspondent

AN eight-year-old boy who weighs 14 stone, more than three times the average for his age, may be taken into care if his mother fails to improve his diet.

Connor McCreaddie, from Wallsend, near Newcastle upon Tyne, has broken four beds and five bicycles. The family claims to have a history of intolerance to fruit or vegetables.

On Tuesday his mother and grandmother will attend a formal child protection conference to decide his future, which could lead to proceedings to take him into care.

Connor could be placed on the child protection register, along with victims of physical and sexual abuse, or on the less serious children in need register.

The intervention of social services is a landmark in the fight against youth obesity.

The boy’s mother, Nicola McKeown, said: “If Connor gets taken into care that is the worst scenario there could be. Hopefully, we will be able to work through it and come up with a good plan and he will just be put on the at-risk register or some other register. That wouldn’t be so bad because, hopefully, there will be some help for us at the end of it.”

Two specialist obesity nurses, a consultant paediatrician, the deputy head of Connor’s school, a police officer and at least two social workers are expected to be on the panel deciding what action should be taken.

One National Health Service source said: “We have attempted many times to arrange for Connor to have appointments with community and paediatric nutritionists, public health experts, school nurses and social workers to weigh and measure him and to address his diet, but the appointments have been missed.

“Taking the child into care or putting him on the child protection register is absolutely the last resort. We do not do these things lightly but we have got to consider what effect this life-style is having on his health. Child abuse is not just about hitting your children or sexually abusing them, it is also about neglect.”

The source added: “The long-term health effects of obesity such as diabetes are well known and it is concerning that Connor is more than twice the weight he should be. There has to be some parental responsibility.”

McKeown will appear on Tonight with Trevor McDonald on ITV tomorrow.

http://www.timesonline.co.uk/tol/news/u ... 434607.ece
 

filcee

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#12
rynner said:
...The family claims to have a history of intolerance to fruit or vegetables...
Not liking the taste, and being too bone idle to find a healthy alternative is not[/] an intolerance. :x

rynner said:
...The boy’s mother, Nicola McKeown, said: “If Connor gets taken into care that is the worst scenario there could be. Hopefully, we will be able to work through it and come up with a good plan and he will just be put on the at-risk register or some other register. That wouldn’t be so bad because, hopefully, there will be some help for us at the end of it.”...
Having seen her on breakfast TV this morning the help should be cookery lessons, and how to say no to her kids once in a while.
 

rynner2

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#13
"The Big Ballet"

"A comedy ballet of weighty elegance and adorable humour"

Perm, the academy's home town, is a beautiful city with over two million inhabitants in the Urals. The city boasts a long tradition of music and ballet - a first-class ballet company has been based here permanently since 1820. The training and work at the Perm Ballet Academy are decisively influenced by the works of Peter Tchaikovsky and by Serge Diaghlev, the genius of the "Ballets Russes“, who both lived in Perm.

A ballet like no other ever seen in the UK before, Amande Concerts presents The Big Ballet, an ensemble of 16 Corps de Ballet dancers, each weighing no less than 220 pounds and united in a common cause; not to lose a single pound.

From Russia's Ural mountains, the 2500 km-long region from where two of the ballet world's pre-eminent geniuses Peter I. Tchaikovsky and Serge Diaghilev also hail, The Big Ballet formed in 1994 and set out to deliberately and, above all, self-confidently challenge accepted social standards in a world where the pursuit of slenderness and beauty seems obsessive. The dancers courageously and imposingly prove that grace, elegance, charisma and nimbleness is not the demesne of the "thin", proudly presenting their voluptuous yet surprisingly sinuous and flexible figures.

These ladies enchant their audiences with three different classical and modern ballet pieces in a hilarious comedy show full of fun and astonishing choreography, proving that you shouldn't take life, or yourself, too seriously.

Enjoy the show! It will both surprise and thrill you!

http://www.thebigballet.co.uk/eng/index.html
 

crunchy5

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#14
An interesting angle on the obesity epidemic.

http://www.sciencedaily.com/releases/20 ... 140845.htm

Obesity is generally discussed in terms of caloric intake (how much a person eats) and energy output (how much a person exercises). However, according to a University of Missouri-Columbia scientist, environmental chemicals found in everyday plastics and pesticides also may influence obesity. Frederick vom Saal, professor of biological sciences in MU's College of Arts and Science, has found that when fetuses are exposed to these chemicals, the way their genes function may be altered to make them more prone to obesity and disease.


"Certain environmental substances called endocrine-disrupting chemicals can change the functioning of a fetus's genes, altering a baby's metabolic system and predisposing him or her to obesity. This individual could eat the same thing and exercise the same amount as someone with a normal metabolic system, but he or she would become obese, while the other person remained thin. This is a serious problem because obesity puts people at risk for other problems, including cancer, diabetes, cardiovascular disease and hypertension," vom Saal said.

Using lab mice, vom Saal has studied the effects of endocrine-disrupting chemicals, including bisphenol-A, which recently made news in San Francisco, where controversy has ensued over an ordinance that seeks to ban its use in children's products. In vom Saal's recent study, which he will present at the 2007 Annual Meeting of the American Association for the Advancement of Science (AAAS), he found that endocrine-disrupting chemicals cause mice to be born at very low birth weights and then gain abnormally large amounts of weight in a short period of time, more than doubling their body weight in just seven days. Vom Saal followed the mice as they got older and found that these mice were obese throughout their lives. He said studies of low-birth-weight children have shown a similar overcompensation after birth, resulting in lifelong obesity.

"The babies are born with a low body weight and a metabolic system that's been programmed for starvation. This is called a 'thrifty phenotype,' a system designed to maximize the use of all food taken into the body. The problem comes when the baby isn't born into a world of starvation, but into a world of fast food restaurants and fatty foods," vom Saal said.

More research must be done to determine which chemicals cause this effect. According to vom Saal, there are approximately 55,000 manmade chemicals in the world, and 1,000 of those might fall into the category of endocrine disrupting. These chemicals are found in common products, from plastic bottles and containers to pesticides and electronics.

"You inherit genes, but how those genes develop during your very early life also plays an important role in your propensity for obesity and disease. People who have abnormal metabolic systems have to live extremely different lifestyles in order to not be obese because their systems are malfunctioning," vom Saal said. "We need to figure out what we can do to understand and prevent this."

"Perinatal Programming of Obesity: Interaction of Nutrition and Environmental Exposures" is the title of vom Saal's AAAS presentation. Also presenting with vom Saal at the AAAS symposium are Reth Newbold of the National Institute of Environmental Health Sciences, Bruce Blumberg of the University of California-Irvine, George Corcoran of Wayne State University and James O'Callaghan of the National Institute for Occupational Safety and Health.
 

rynner2

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#15
Mexican who once weighed half a tonne leaves home for first time in five years
(Monica Rueda/AP)

Manuel Uribe, who once weighed half a tonne, left his house yesterday for the first time in five years.

Six people pushed Mr Uribe’s wheel-equipped iron bed onto the street, as a mariachi band played and a crowd gathered to see the man – thought to be the world’s heaviest – who once weighed 560kg (88st).

“The sky is beautiful and blue and what I want is to enjoy the sun,” Mr Uribe said after taking a sip from a bottle of champagne.

Unable to leave his bed for more than five years, the 6ft 3ins divorcee has lost 180kg (28st) since he began a high-protein diet a year ago. He now weighs about 380kg (60st).

To celebrate the milestone, a forklift lifted Mr Uribe’s bed onto a trailer pulled by a pickup truck and the 41-year-old former mechanic rode through the streets of San Nicolas de los Garza, a Monterrey suburb.

Dozens of reporters and photographers followed Mr Uribe as he passed the town’s plaza and church, waving at crowds of onlookers eager to get a glimpse of him.

“It fills me with joy to see he’s getting better and getting a little sun,” Mr Uribe’s neighbor Guadalupe Guerra said. “I would go crazy if I had to be inside my house for so many years.”

Mr Uribe was a chubby child, weighing more than 115kg (18st) as an adolescent. In 1992, he said his weight began ballooning further.

Since the summer of 2002, Mr Uribe has been bedridden, relying on his mother and friends to feed and clean him. He keeps a television and a computer he uses to update his Web site near his iron bed.

He drew worldwide attention when he pleaded for help on national television in January 2006. Afterwards, Italian and Spanish doctors visited and offered him gastric bypass surgery.

But Mr Uribe chose to accept help from Mexican nutritionists working with the Zone diet. He said he will stick to that diet until he reaches his goal weight of 120kg (18st).

He said: “My goal is to leave the house on my own but I know that will be a long process.” Doctors say it may take between three and four years for him to reach his goal.

The Zone diet, conceived by American nutritionist Barry Sears, advocates a 40:30:30 split of calories obtained from carbohydrates, proteins and fats respectively to promote a “hormonal balance” said to boost energy levels and cut excess weight.

Mr Uribe said: "People think that I can eat a whole cow but it's not just over-eating, it's also a hormonal problem."

He plans to start a foundation to help overweight people get medical assistance and teach them about healthy eating habits.

Guinness World of Records could not confirm Mr Uribe’s weight, but said they do not have details of any living person weighing more than 380kg on record.

Jon Brower Minnoch, of Bainbridge Island, Washington, who died in 1983 aged 42, holds the record for world’s heaviest ever man at more than 100st.

http://www.timesonline.co.uk/tol/news/w ... 487454.ece
 

crunchy5

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#16
http://www.scienceagogo.com/news/200702 ... _sys.shtml

Flame retardants, known as polybrominated diphenyl ethers (PBDEs), are found in consumer products like carpeting, upholstered furniture, computers and household appliances. In use since the 1960s, the chemicals supposedly make for safer households by retarding combustibility, but their ubiquity is now prompting questions about what other effects these additives might have.

PBDEs are so widespread that it is estimated that American consumers come into contact with up to 100 products containing PBDEs every day. Perhaps more worryingly, their persistence in the environment has been compared to the now-banned toxins PCB and DDT.

Now, researchers from the University of New Hampshire are investigating if PBDEs are in some way linked to the obesity epidemic plaguing America. "Environmental chemicals are a possible third component to the obesity epidemic, along with diet and exercise," says project leader Gale Carey. She and her co-researchers are exploring how PBDEs affect fat storage and production. "We know PBDEs are fat-soluble - they dissolve in fat tissue," says Carey. "What are they doing in the fat as they sit there? Nobody has asked that question yet."

The researchers plan to expose laboratory rats to PBDEs through pregnancy and lactation, stages Carey describes as critical windows for exposure. The team will be working at the molecular level, seeing what PBDEs do to stem cell populations and their effects on gene expression; as well as at a cellular level, exploring the insulin sensitivity of fat cells.

The preliminary data make interesting reading, suggesting that chronic exposure to PBDEs can cause fat cells to become less sensitive to insulin, which is a forerunner to developing Type II diabetes. The fat cells of growing male rats that were fed PBDEs daily for a month acted metabolically like the fat cells of obese rats, although the PBDE-fed rats weighed the same as a control group. Additionally, the researchers noted that PBDEs appear to interrupt thyroid hormone levels, which may impact caloric expenditure.

But with the research just getting underway, the scientists are duly cautious about predicting outcomes. If the findings do implicate PBDEs in obesity, Carey mused, the news would be good and bad. "From a scientific standpoint, it would be very interesting if these animals began to put on weight," she said. "But part of me hopes they don't, because these chemicals are all around".
 

rynner2

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#17
Clear obesity gene link 'found'

Scientists say they have identified the clearest genetic link to obesity yet.
They found people with two copies of a "fat" version of a gene had a 70% higher risk of obesity than those with none, and weighed 3kg (6.5lb) more.

The work in Science by the Peninsula Medical School and Oxford University studied data from about 40,000 people.

The findings suggest that although improving lifestyle is key to reducing obesity, some people may find it harder to lose weight because of their genes.

The authors say their work, funded by the Wellcome Trust, could improve understanding of obesity and eventually help prevent it, as well as an illness it is linked to.

Genome differences

Obesity is associated with an increased risk of type two diabetes, and the investigators first identified the FTO gene when looking for differences between the genomes of people with type two diabetes and people without diabetes.

People with type two diabetes were more likely to have a particular variant of the FTO gene, which was also shown to be linked to increased body weight.

The variant making people fatter differed from the other version of the FTO gene by a single mutation in the DNA sequence.

The team then looked at other studies involving 40,000 people searching for this FTO mutation, and confirmed that it was associated with body weight.

People carrying one copy of the "fat" FTO variant had a 30% increased risk of being obese compared to a person with no copies of that version.

Those carrying two copies of the variant had a 70% increased risk of being obese, and were on average 3kg (6.6lb) heavier than a similar person with no copies.

Professor Andrew Hattersley of the Peninsula Medical School said this could explain why two people can seem to eat the same things and do the same amount of exercise yet one may struggle to lose weight more than the other.

He said: "The typical message has been that if you are overweight it is due to sloth and gluttony and it is your fault.

"This work is suggesting that there is also a genetic component."

And he said although a 3kg difference in weight sounds relatively small, it is enough to make a big change in the risks of obesity.

Improving treatment

Dr Sadaf Farooqi of the Department of Clinical Biochemistry at the University of Cambridge said: "This study is important because it has yielded evidence for the first obesity susceptibility gene.

"Understanding the genetic susceptibility to weight gain will make an important contribution to the prevention and treatment of obesity."

The team does not yet know exactly what the FTO gene does or how the different variants work to influence body weight.

But they hope further research to understand the gene may lead to the unravelling of the basic biology of obesity.

Dr Mark Walport, director of the Wellcome Trust, said this could have very helpful consequences for public health as about one in six white Europeans carried two copies of the variant.

Obesity is one of the most challenging problems for public health in the UK," he said.

"The discovery of a gene that influences the development of obesity in the general population provides a new tool for understanding how some people appear to gain weight more easily than others."

http://news.bbc.co.uk/1/hi/health/6547891.stm
See! I told you it was my genes! :D
 

witchflame

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#18
They'll be the genes and viruses that cause said persons to move their arm, open there gaping maw and fill it full of frigging crap 24/7 then. I've met plenty of 'em and they just cannot see that their constant shovelling is whats causing their condition not their 'genes', 'viruses' or (and this is my personal favourite) 'glands!'. PIES PIES PIES!!! ;) :lol: :twisted:
 

rynner2

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#19
It confirms my prejudices about certain types of people to see that they can ignore scientific evidence against their prejudices about certain types of people... 8)
 

Rrose_Selavy

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#20
Genetic disposition rarely means fatalistic inevitability - in other words. just because some people might have a natural tendency to be obese -or doesn't mean they have to be., though it may make it relatively more difficult than others to keep to healthy weight.

-
 

crunchy5

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#21
It's reckoned by someone speaking on rad 5 that 16% of the UK pop have the gene in question, but iirc 70% of the UK pop are over weight, hmm.
 

witchflame

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#22
rynner said:
It confirms my prejudices about certain types of people to see that they can ignore scientific evidence against their prejudices about certain types of people... 8)
well rynner, now I'm confused :lol:
It was meant to be tongue in cheek. But I'm sure you have come across the aformentioned 'type' in your lifetime also. :mrgreen:
 

Kondoru

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#23
But it must have a benificial effect if its so common?

Perhaps its because static people are more suited to modern life than those who are on the go.
 

rynner2

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#24
Kondoru said:
But it must have a benificial effect if its so common?
In times when food was scarce, ie, for most of mammal evolutionary history, a metabolism that could thrive on limited amounts of food would obviously do better than less efficient types who needed much more food.

But in modern times, over much of the world, food is abundant, so now the first type are getting more food than they need and are getting obese, while the second type are finally getting the amount of food they need to survive and thrive.

If 'abundant food' remains with us for the next few millenia, selection may work against the obese types, and the relevent genes will tend to be weeded out - until the next period of famine hits!
 

elvissa

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#25
In some ways, the news seems fairly obvious, because a tendency to gain weight can be seen to run (or slouch) in families. So it must be genetic.

The other thing I feel I have to say though is that when people say "obese", do they mean according to the BMI scale? Which is actually quite cobblers-esque? Because apparently a footballer like Sol Campbell could be considered "obese" on the BMI scale, as it doesn't take into account that weight might be caused by muscle, instead of fat.

I however do not have that excuse. A sedentary job and a fondness for chocolate doesn't equal a size zero.
 

rynner2

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#26
rynner said:
It confirms my prejudices about certain types of people to see that they can ignore scientific evidence against their prejudices about certain types of people... 8)
This article expresses what I meant quite well:
Jemima Lewis: Fat people need understanding, not derision

It is a strange fact that the more porkers there are, the less forgiving society becomes towards them
Published: 14 April 2007

I have a friend, apparently sane in most respects, who says he doesn't like fat people "because they are unhappy". I've always thought this was rather like saying you don't like black people because they are oppressed. Perhaps fat people would be more chipper if they weren't constantly being judged and found wanting by self-righteous bigots.

In any case, I hope my friend is feeling pretty ashamed of himself now. A team of British scientists has just announced that it has discovered why some people are predisposed to porkiness: it's not lack of willpower, or inner sadness, but a gene called FTO which affects one in six of the British population.

People who carry two of these genes are half a stone heavier than the average, and 70 per cent more likely to be obese. Those who have inherited just one FTO gene will also struggle to stay at a comely weight: they are 30 per cent more likely to become obese, and 25 per cent more at risk of diabetes.

The scientists - evidently fearing a mass stampede to the sweetie counter - were quick to point out that biology isn't necessarily destiny: we can still control our weight by eating sensibly and taking exercise. Nevertheless, their finding is a useful corrective to the prevailing trend of anti-fattist contempt.

It is a strange fact that the more porkers there are in Britain, the less forgiving society becomes towards them. The skinny rich look with regal disgust down upon the - now literally - lumpen masses. Those of us with the money, culinary know-how and determination to keep our FTO genes at bay derive a self-congratulatory thrill from television programmes such as BodyShock or Fat Club, whose protagonists look like human landslides.

There is an increasing impatience and disgust towards those who "let themselves go". Corpulence no longer suggests, as it once did, the good life - but rather a life of TV dinners, slack-jawed parenting and pies shoved between the school railings.

Last year the food critic Giles Coren (another noisily anti-fattist friend of mine; are they trying to tell me something?) made a programme called Tax the Fat, in which he argued that the obese were costing the Government £4bn in healthcare, transport and benefits, and should be penalised accordingly. "Being fat is a choice," he declared. "A choice to consume dwindling resources, to use more energy, to take up more space."

We now know it isn't as simple as that. Not that we should have needed scientists to tell us. You only have to look around you, at your colleagues or friends, to see that people are built differently.

The skinniest girl at my office is Ali, a 30-something beauty with eyes like a Manga heroine and a body like Lily Cole. Ali begins each day with a bowl of cereal and a chopped banana, followed by a Twix. For elevenses, she might stave off the hunger pangs with an almond croissant or a chocolate muffin. At lunch she inhales a salad or sandwich, before noisily unwrapping another king-size chocolate bar.

Come tea time, the smell of toasting hot cross buns fills the office, prompting groans of longing from her less metabolically blessed colleagues. Before long it's time for cake - and being a generous sort Ali buys a big one, with plenty of butter icing, and leaves it sitting on the kitchen counter, where it beckons to the weak-willed passer-by like a courtesan reclining on a chaise longue.

To know Ali is to know that life is unfair. But of course, that's something that all FTO carriers learn along the way. If fat people are indeed unhappy - and everyone is, in one way or another - it is because they know they will never be able to tuck in the way Ali can: with pure, guilt-free abandon. And knowing they can't just makes them long to even more.

This is why, as a separate scientific report showed last week, diets don't work. They only make the dieter even more obsessed with what he or she can't have. "To promise not to do a thing," observed Mark Twain, "is the surest way in the world to make a body want to go and do that very thing."

It is no coincidence that the seriously obese - especially women - often report that they have been dieting on and off since childhood, at the instigation of a body-conscious mother. Once food has been turned into something naughty, it is even harder to resist. It is easy for the naturally slim to talk about willpower: they have never truly had theirs tested.

Eventually, the scientists who discovered FTO may invent a drug that cancels its effects, making the naturally fat deflate like pricked balloons. Humanity will move one step closer to the homogenised ideal of physical beauty. In the meantime, could we please have a little more understanding for those of us whose genes tend towards the rotund? It's not easy battling your biological destiny - especially on an empty stomach.

http://comment.independent.co.uk/commen ... 447667.ece
 

rynner2

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#27
Five-ton ambulances answer 999 calls by supersized patients
Hospitals compelled to use Fire Brigade to carry obese patients put reinforced vehicles on the road
By Sophie Goodchild and David Ricketts
Published: 22 April 2007

Britain's obesity epidemic is forcing the NHS to introduce specially adapted ambulances for overweight patients.

Nearly a quarter of hospitals have brought in vehicles which have strengthened stretchers, hoists and suspension, new figures show. More than a third of those surveyed said they were planning to introduce the ambulances, so they could cope with call-outs from the obese.

The NHS spends an estimated £7bn every year on obesity- or bariatric-related disorders. People are classified as obese when their body mass index (BMI) goes over 30. Nearly a quarter of British adults are now overweight, which has created huge problems for ambulance crews.

In Suffolk, for example, St John Ambulance brought in vehicles with wider ramps and a strengthened floor after a call-out to a patient weighing nearly 65 stone. It took more than 30 people, as well as members of the Fire Brigade, to get him to hospital.

Keith Hotchkiss, St John's transport co-ordinator, said the bariatric ambulances, which cost up to £90,000 each, were vital because they relieved the burden on other emergency vehicles responding to 999 calls.

"My job is to question the caller on things such as location, weight and height, and that gives us an idea of the number of people we need to send out," he said.

Normal ambulances can only carry patients who weigh up to 20 stone, compared with up to five tons in bariatric vehicles. This meant that obese people often had to be carried in the back of vans until the introduction of bariatric ambulances.

South Western Ambulance Trust already has six vehicles and plans to introduce 23 more. "In the past, the Fire Brigade have to help us lift obese patients," said Lynne Paramor.

How Britain's obesity problem tips the scales

BIGGER COFFINS: Funeral directors are being obliged to order larger-sized coffins from the United States to take expanding Britons on their final journey.

LARGER FURNACES: Cematoriums are installing new furnaces to cater for coffins up to 44in wide.

FAIRGROUND RIDES: Designers are installing larger seats and altering the normal way of strapping passengers in by their shoulders. Instead, they are fastened in around the waist. G Force, in Tamworth, has a larger seat at the rear of each six-seater train.

NEW AMBULANCE TROLLEYS: Wider and reinforced to cope with extra weight. They also feature clamps that fix to the ambulance floor.

http://news.independent.co.uk/uk/health ... 472146.ece
 

rynner2

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#28
Scientists working on formula milk that prevents child obesity

· Use of hormone could be only 10 years away
· Research raises medical, legal and ethical questions

Polly Curtis, health correspondent
Monday April 23, 2007
The Guardian

British scientists are working on a baby formula which would chemically restructure the metabolic system of children to ensure they never became obese.
Studies in mice have found that large doses of the appetite-controlling hormone leptin during infancy permanently prevent excess weight gain and reduce the chances of type 2 diabetes.

Now researchers at the University of Buckingham say a leptin-enriched baby milk which does exactly the same is less than 10 years away, raising a plethora of medical, legal and ethical questions.

Other specialists in the field condemned the search for a medical answer to obesity, saying it is a modern social ill and that people need to address their lifestyles, not look for an artificial quick fix.
More suggested the translation to baby food would be impossible as people would not put their children forward for trials of the formula when they did not know the risks involved.

The research is reported in the journal Chemistry and Industry today.

Leptin turns off appetite throughout life, but the scientists last year proved that high doses in mice through pregnancy and early life permanently reduced weight. They now believe it plays a role in hard-wiring the brain's appetite response in infancy.

Mike Cawthorne, who led the researchers, said: "The supplemented milks are simply adding back something that was originally present: breast milk contains leptin and formula feeds don't
.

"Yes, it raises ethical questions. Obesity is a social problem, but it's also a health problem which costs us millions of pounds a year and is getting worse. It's not just a social problem.

"New ideas always face scepticism, but I think this is very, very likely within several years' time."

Previous experiments in treating obese people with leptin have failed as people continued to overeat. And though some research has linked bottle-fed babies to childhood obesity, none has concluded that breast-fed babies resist obesity throughout life.

Nick Finer, clinical director at the Wellcome Clinical Research Facility at Addenbrookes Hospital, Cambridge, said: "The concept that adding something to a food that could permanently alter brain development is exciting but at the same time so scary that it would mean a wholly new approach about how such treatments can be tested and approved for use. Would the first trials be in newly born children?

"The importance of leptin (and other hormones) at determining the development of brain circuits that control energy balance is an area of current research interest. The leap to a functional food being effective or safe is enormous."

Stephen O'Rahilly, head of the Diabetes, Obesity & Insulin Action department at Cambridge University, described it as "science fiction". Francesco Cappuccio, professor of cardiovascular medicine and epidemiology at Warwick University said: "Leptin is very easily destroyed by stomach acids so I'm not sure how they think they will get it ingested through baby milk."

Prof Cawthorne, whose work is being funded by a government research council and a private individual who has no connections with industry, said babies could ingest leptin because their digestive systems were less developed.

Whether or not infant formula with leptin should be classified as a food or medicine was a question that would have to be resolved, he said.

"It is still a grey area," he added. "One could argue that as you're replacing something that should be there, it's not pharmaceutical."

A spokesman for the Food Standards Agency said: "If you make a functional food using ingredients that are already on the market, then you wouldn't have to go through a safety assessment. But if it includes new ingredients then you would, and it depends on the sort of ingredients."

http://www.guardian.co.uk/medicine/stor ... 11,00.html
 

Hot_Cross_Nun

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#29
Re. Rynner's post above, "Scientists working on formula milk that prevents child obesity."

Why go to all that bother, expense and uncertainty when we can cut out the middleman?

Mike Cawthorne, who led the researchers, said: "The supplemented milks are simply adding back something that was originally present: breast milk contains leptin and formula feeds don't.
I believe far more resources should go towards encouraging mothers to feed their babies with the one and only substance that's absolutely tailor-made for them - mother's milk.

Of course, there's no profit to be made from that, is there?
 

Dingo667

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#30
Thing is with fatties that regardless of reason [be it genetic or whatever] the fact is that only food can make you fat. If all fatties went to live somewhere where food is sparse, the outcome will be [not might be] that they'll loose weight.
Yes willpower is needed, but it is also needed for other things in life [not smoking, overcoming phobias etc]. It is hard but it is doable.
Before anyone says something, my family from daddy's side is genetically obese. I have the tendency to be slightly more than thin. However I do realise this and as much as I love food, I know when to stop.
The reason I do this is that I am incredibly vain [almost to the point of narcissism 8) ]. Seeing my belly grow over my trousers like a pie is usually enough for me to put the reigns on when it comes to eating. I won't go on diets, I just don't eat out and stay away from sweets and fatty stuff for a while until I look amenable again.
Yes it is a little bit of work which could easily be forgotten if I was lazy or uncaring towards myself.

Some say its depression that makes people eat. They hate their looks and then they comfort-eat. Bloody hell, I have had my bouts of depression but that actually stopped me from eating. If I was depressed due to my weight, I would never touch any food again until I lost all the crap.

I don't hate fatties [even though it might come across as that but let me explain]. I think that anyone is entiltled to do what they wish with their bodies, what I can't stand is a) pretending that you can't change it [i.e the old virus, genetics excuse] and b) moaning if others find you unattractive.
I personally love slightly chubby men for example but as soon as they get obese I don't anymore.
Some chubby or even slightly obese ladies can be very pretty [when they have accepted their weight and stop moaning about it]. But I don't do this bull*hit about the american chat show mottos when there is a clearly very fat unsightly person sitting there and people tell her/him: You are soooooo beautiful!
No they are not!
To say so is very cruel. I recon that if enough people would tell the truth, it could give a little inspiration to loosing weight.

Take away the food and the person will be slim. There is NO exception to anyone on earth. If you are obese you have eaten too much. End off.
If you like food and you are fat, I take my hat off to you for honesty and let you be. You shovel cakes into your gob with dainty fingers and cry that you are a victim I will call you a fatty.
 
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