Gone But Not Forgotten
Aug 18, 2002
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.


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
Hmm - one is reminded of what Dennis Leary had to say about obesity being casued by a virus... ;)
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.
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.
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.
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
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.
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. :?
"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! :?
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
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.
"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!

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.
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
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".
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.
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!
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
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
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
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?
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.
..or Australia:
Primary school kids in XXXXXL-size uniforms
May 6, 2007

CLOTHING manufacturers are catering for increasingly obese children by making school uniforms as big as size 30.

Primary Schoolwear in Sydney stocks boys' shirts in size 30, which fits a 122-centimetre chest and a 47-centimetre neck. Girls' clothes go up to size 26.

The company, which makes clothing for public and private schools around Australia, has had more demand than ever for larger-sized clothing, forcing it to expand its scale to XXXXXL.

Clothing of that size measures 110 centimetres around the waist, 46 centimetres more than the smallest size, XXXS, which is made to fit the average 10-year-old.

Jenni Mackillop from the company's NSW branch said parents often asked for specially made clothing to fit larger children. "We do see our fair share of little chubbies," Ms Mackillop said.

Preproduction manager Jo Kellock said the company had noticed a growth of up to five centimetres in waist measurements in the past two years alone.

National studies had shown that children had grown about two centimetres in height, on average.

Ms Kellock said designs had to be "straightened out" at the waist, where previously they were nipped in, to cater for the increasingly common "pear shape" among schoolchildren.

National studies have confirmed the popular belief that children are also growing taller.

At the other end of the spectrum, manufacturers have had to make tinier sizes for Asian migrant children who are often far smaller than their Western school chums.

Nutritionist Rosemary Stanton said that while studies had shown NSW children were playing more sport, they were still getting fatter.

"They may burn up 300 calories and then eat 400 calories," Dr Stanton said. "Children are thinking they are abnormal if they do not have junk food every day. There isn't any mystery. We know kids are eating more."

Children were walking to school less often because it was not considered safe. Junk food had become the norm because of the sheer amount of snack foods that were readily available, Dr Stanton said.

"The kids are the victims here," she said. "We've got to take child obesity seriously, but overwhelmingly it is society's problem."

Children who were very overweight faced psychological and social problems and were at greater risk of type 2 diabetes, sleep apnoea, asthma and heart disease later in life.

Dr Stanton urged Australian supermarkets to use a labelling system to advise people how often a certain type of food should be eaten.

http://www.smh.com.au/news/national/pri ... 68709.html
This has shattered all my illusions about Oz! :(
They're just as crap as the rest of us!
This has a whiff of a TV comedy sketch about it, but seems to be quite serious:
'Walk and work' treadmill helps shed pounds
By Roger Highfield, Science Editor
Last Updated: 2:17am BST 15/05/2007

Walking while you work might help fat people shed as much as 66 pounds - or nearly five stone - in one year, according to a study published today.

Vertical workstations, where office workers use their computers while walking on a treadmill, could shrink waistlines, according to research published in the British Journal of Sports Medicine.

A team led by Prof James Levine, a British scientist at the Mayo Clinic in Minnesota, compared the energy used at the "walk and work" desk with that used by 15 obese people seated at a conventional desk.

None of the participants did any regular exercise.

Energy expenditure was measured while working and walking for 35 minutes every hour, compared with that burned while working at a desk.

The average energy burned while seated at a desk was 72 calories per hour.

This more than doubled to 191 calories an hour while at the vertical workstation and walking at a rate of one mile an hour.

The authors calculate that if obese employees used the workstation for a couple of hours a day, they could boost their energy expenditure by 100 calories an hour. That could mean losing between 40 and 70 pounds over the course of a year.

Prof Levine said that study participants found the equipment easy to use and were able to work normally.

In fact, he said they wanted to continue using it after the study had finished. "Subject after subject said to me 'I want one'," he told The Daily Telegraph.

The "walk and work" desk is designed to allow people to work at a computer while walking on a treadmill at a speed of their own choosing.

It consists of an H-shaped frame that is supported by four locking rubber wheels, so that it can be moved easily.

The frame holds a Plexiglass panel on to which two adjustable arms are bolted - one to hold the computer screen and the other for the keyboard and mouse.

According to Prof Levine, who uses the vertical workstation, it is lack of activity, rather than fast food, that marks the major change in modern life,

He argues that an increasing reliance on cars, remote controls and escalators are among a raft of modern "innovations" that have contributed to the obesity epidemic, pointing out that by 2010 more than half of the workforce from developed countries will be working at computers.

The pilot study suggests that the vertical workstation could help to reverse the rising tide of obesity. It offers a way to provide a small but sustained boost in energy expenditure without changing work habits.

Health care costs caused by the obesity epidemic are estimated to be £100 billion a year in the US alone so the ''walk-while-you-work'' desk might prove to be cost effective, says Prof Levine, who has called for bigger trials to be carried out.
Kondoru said:
its actualy the best idea ever
...or maybe not!
The nine-to-five treadmill
By Denise Winterman
BBC News Magazine

Walking while you work can help shift those extra pounds, say scientists. But can you really work and exercise at the same time? The Magazine finds out.

As I type this sentence on my laptop I am at the gym, on a cycling machine and pedalling at 95 RPM. Feel the burn - I am.

Shame my hands can't keep up, it took me almost five minutes to key in the above without a single mistake.

In that time I have managed to misspell nearly every other word, mistakenly turn the typeface into italics and come dangerously close to a serious hamstring injury after an incident involving my foot, a pedal and a momentary lapse in concentration.

Scientists from the Mayo Clinic in America are right, you can lose weight if you exercise while you work. But you'll put it all back on when you are at home, eating biscuits while watching daytime television because you've been sacked for poor performance. :D

In controlled scientific conditions it might seem simple to combine the two, but in the local gym, with your laptop, there are a few obstacles to overcome before you can set about toning your muscles in tandem with your brain.

Health and safety is the first. Scientists may be certain about the benefits of walking and working, but my gym manager isn't. I am greeted with a computer-says-no look when I ask to use the treadmill and my laptop at the same time.

"Would be more than my job's worth if you hurt yourself or damaged that computer," the duty manager tells me.

It's the same response when I ask about the step machine, rowing machine - which would have been tough - and the elliptical trainer. But with the cycling machine, with its useful handlebars on which I can balance my laptop, we reach an accommodation.

Next, what to wear? Am I at work or at the gym? It's all so confusing but I opt for comfort rather than presentation.

Finally, there are the physical limitations to consider. While my mind is agile, my body is not. Co-ordination and balance are not among my strengths.

The average two-year-old child could out-perform me in the old rub-your-tummy-and-pat-your-head-at-the-same-time task. Just mention ice-skating and I slip over. It doesn't bode well.

Once pedalling I find the cycling relatively easy, but not the typing part of the task. In a 45-minute session I manage to write just four paragraphs. That's one paragraph every 11.25 minutes. Were this a time and motion study, I'd be racking up a lot of both... to little effect.

Effort level

So, my very unscientific findings when it comes to the work part of the task are as follows:

• It's not easy to balance the laptop on the handle bars
• It's not comfortable
• It's near impossible to type
• Concentration levels inevitably dip when you are constantly worrying about dropping and damaging an expensive piece of company property

But surely my body is benefiting? Just about. While I may be cycling at 95 RPM, the machine is telling me my effort level is only at two - it goes all the way up to 12. I feel like I'm working my body hard but apparently not.

When I try to cycle faster I can't concentrate on my work. I can't really afford to let my output slip any further or it will be Jeremy Kyle keeping me company every weekday and not my work colleagues.

Ultimately, the focus of the study is weight and losing it. I manage to burn off a total 176 calories - over the same period at my desk I would have shed a mere 54.

But as I walk back to the office I quickly grab a latte from the coffee bar, which, I find out - having drunk it - has roughly 200 calories, according to the website Calorie-Count.

So it's either off to the gym to cycle for roughly 6.1 minutes to burn off those 24 calories or sit at my desk working for just over 28. No prizes for guessing which one I opt for.

Graham Norton has just been having fun with this idea on TV
- quite hilarious!
Fat? Blame the bugs in your guts
Last Updated: 12:01am BST 29/05/2007

Could the explosion in the use of antibiotics have changed our digestive processes and triggered the obesity epidemic? Roger Highfield reports

We are not quite what we eat. We are what the vast numbers of microscopic inhabitants of our bellies digest, a finding that has huge implications for the worldwide obesity epidemic.

The rise of cheap, high-fat food and the fall in physical activity are known to be crucial influences on body weight.

But, in recent years, another possibility has emerged. The three to four pounds of bacteria swilling around our bellies play a central role in our digestion.

Given how a generation of these passengers lives, dies and is excreted within days, could the demographics of our gut bugs be changing to make us fat?

The hunt for obesity genes has traditionally focused on the relatively small number of human genes, which can only change slowly over the generations, and not on the vast numbers within quick-living bacteria that, in effect, predigest our food.

The human digestive system is home to about 100 trillion bacteria - around 10 times the number of cells in the major organs (there are another 25 trillion red blood cells, plus a few trillion brain cells).

The ecology of the human gut is at least as complex as that in soils or seas and acts as a metabolic organ.

You would be nothing without these microbial minions milling around inside your large intestine, performing crucial functions that your fancy, complicated human cells haven't a clue how to do.

Your talented residents can make vitamins, such as the B vitamins that we cannot synthesise, and consume plant carbohydrates with exotic names like arabinogalactans, polygalacturonates, and cellobiose, which you could not otherwise digest because you lack the necessary enzymes.

Some of the bacteria attack chemicals made by plants that could cause cancer or other illnesses if not neutralised.

Others scavenge hydrogen gas, a by-product of breaking down complex plant carbs (known as polysaccharides) in our diet, and convert it into methane, ensuring that polysaccharide digestion remains an efficient process. They help protect us against pathogens, too. In short, these gutsy little helpers keep us alive.

Our gastrointestinal tracts contain two dominant groups of mainly good bacteria, the Bacteroidetes and the Firmicutes, which help us to break down otherwise indigestible foods. The Firmicutes include Lactobacillus, Mycoplasma, Bacillus and Clostridium. The Bacteroidetes include Bacteroides.

What is fascinating is that Prof Jeffrey Gordon's team at Washington University School of Medicine has shown that our friendly gut bacteria may be doing us too much good.

He has shown that the intestines of obese people are swimming with a slightly different medley of microbes compared with slim people - obese people have more Firmicutes and fewer Bacteroidetes than the lean ones.

These differences were not due to an explosion in numbers of one species in the Firmicutes or a diminution of a single or a few species of Bacteroidetes: virtually all members of each group were altered.

The proportion of Bacteroidetes increases as weight is lost when someone eats a low-calorie diet, revealing how Bacteroidetes could help shed the pounds and how, perhaps, the Firmicutes should perhaps be renamed the Flabicutes.

Gut-wrenching experiments by Gordon's team confirmed the link between bugs and waistlines.

When the gut microbial community from obese mice was transplanted into sterile germ-free mice their body fat increased more than when microbial communities were transplanted from lean donors.

When mice lack any microbes in their guts, they are protected from the waistline-expanding effects of a fatty diet.

Equally remarkable, Gordon and his students have found evidence that a host gene, Fiaf (fasting-induced adipocyte factor) is manipulated by the microbes to help us to store fat.

It is, remarks Prof Gordon, as if the bacteria are helping their host (that two-legged bioreactor known as a human being) by ensuring energy reserves are laid down in case lean times lie ahead.

"We never dine alone: our microbes are able to sit at the dining room table together with us, consume for their own purposes the nutrients that are available, notably those we cannot digest on our own, and share the bounty with us," said Prof Gordon.

"This raises the question of whether differences in the mix of bacteria in our guts predispose some of us to obesity: the number of calories harvested from a serving of cereal may not be the same for everyone - some people may extract slightly more than others and over time this will add up."

Prof Jeremy Nicholson of Imperial College London has come to similar conclusions. He and his collaborators in France and China reported last week in Molecular Systems Biology how "good" bugs, such as lactobaccili, alter the way that fats are emulsified in the upper gut, making them less available to the body.

To probe the role of bacteria in fat digestion, he has worked with the Nestle Group in Lausanne to "humanise" mice by replacing their gut bacteria with human bugs.

This revealed the bacteria affect bile acids, which have a profound influence on the way the body absorbs and uses fat.

"Bile acids are responsible for the emulsification of fats (dissolving them, in effect), so if you change that you change the way fats are taken up by the body," he said.

Bile acids can also act like hormones to influence fat deposition. Gut bugs can thus alter the hormonal make-up of the host body, which can alter the environment of the bugs. This feedback makes the overall effect of our passenger microbes scarily complex.

Prof Nicholson believes that obesity could be linked to antibiotic use and misuse.

"We speculate that this might be a consequence of the widespread use of antibiotics that reselect the gut microflora (that we have evolved with over aeons) to cultivate a much less friendly set of bugs in our general population - eating too much and sitting around all day does nothing to help this, of course, and this is still undoubtedly the major contribution to obesity. But mapping the change in population obesity in the US over the last 20 years looks rather like the spread of an infectious disease."

Would it be possible to change the microbial balance to help a person slim?

For a start, they would have to see if other body weight-regulating mechanisms might step in to compensate for any changes.

The human gut also contains hundreds, and perhaps thousands, of microbial species, and the functions they perform affect each other and their hosts, so altering their ecology in a controlled way may be tricky.

Although there are products that claim to manipulate bacteria, such as prebiotics that help certain microbes and probiotics (such as yoghurts) that contain live bacteria, we understand too little to do this reliably.

But whatever we do, because of the stomach-churning effects of diet and antibiotics, Prof Nicholson says we can never go back to the way we were a few generations ago.