Obesity News
Researchers piece together gene, obesity and fat distribution puzzle
EU-funded scientists have identified 18 new gene sites that impact overall obesity and 13 new sites associated with distribution of fat. The researchers from Europe, as well as Australia, Canada and the US, used a near 250,000-strong sample to investigate genetic links with human traits. The findings of the two studies, published in the journal Nature Genetics, shed light on why some people are more susceptible to obesity while others are not.
Part of the Genetic Investigation of Anthropometric Traits (GIANT) consortium, which comprises 400 experts from 280 research institutions worldwide, the scientists carried out a large-scale meta-analysis of genome-wide association studies (GWAS) providing insights on waist-hip ratio (WHR) and body mass index (BMI).
‘Different people have different susceptibilities to obesity,’ explains Dr Joel Hirschhorn from Children’s Hospital Boston and the Broad Institute in the US, one of the senior authors of the obesity paper who was involved in both studies. ‘Some don’t rigorously watch what they eat or how much they exercise and still resist gaining weight, while others constantly struggle to keep their weight from skyrocketing. Some of this variability is genetic, and our goal was to increase understanding of why different people have different inherited susceptibility to obesity.’
These studies succeeded in pinpointing genes that were never before suspected of influencing obesity. The results will help improve the categorisation and treatment of obesity in the future, according to Dr Hirschhorn.
The overall obesity study investigated the genetic determinants of BMI, which is determined by measuring a person’s weight in kilograms over height in metres squared. Data from 124,000 people from 46 studies uncovered 32 sites (of which 18 are new). The team found two novel variants, one of which is in the gene encoding for a receptor protein that responds to signals from the gut to influence insulin levels and metabolism, and another that is located near a gene known to encode proteins affecting appetite.
‘One of the most exciting parts of this work is that most of the BMI-associated variants identified are in or near genes that have never before been connected to obesity,’ comments Dr Elizabeth K. Speliotes from Massachusetts General Hospital and the Broad Institute, lead author of the BMI study and involved in both studies as well. ‘Through this work we are discovering that the underlying biological underpinnings of obesity are many, varied and largely uncharacterised.’
Their findings show that people with more than 38 BMI-increasing variants were about 15 to 20 pounds heavier than those who carried less than 22 such variants.
The second study investigated associations between gene sites and fat distribution. Evaluating the genetic determinants of WHR of 77,000 people in 32 studies, and checking against data of more than 113,500 individuals in 29 studies, the researchers found 14 gene regions associated with WHR, adding 13 new sites. It should be noted that seven of the identified genetic variations have stronger effects in females than in males, hinting that they trigger some of the differences in fat distribution between women and men.
‘By finding genes that have an important role in influencing fat distribution and the ways in which that differs between men and women, we hope to home in on the crucial underlying biological processes,’ says Dr Cecilia Lindgren of the Wellcome Trust Centre for Human Genetics at Oxford University in the UK, a senior researcher on the WHR study, who was involved in both papers.
The results in this study indicate that specific biological mechanisms play a role in regulating where the body stores fat. Genes that regulate cholesterol, triglyceride levels, and insulin and insulin resistance are associated with the regions impacting fat distribution.
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EU funding for the studies came from projects under Fifth and Sixth Framework Programmes (FP5 and FP6), specifically: EURO-BLCS (Biological, clinical and genetic markers of future risk of cardiovascular disease’), which was supported under the Quality of life and management of living resources budget line of FP5; as well as EUROSPAN (European special populations research network: quantifying and harnessing genetic variation for gene discovery’), MOLPAGE (‘Molecular phenotyping to accelerate genomic epidemiology’), PROCARDIS (‘A genome-wide mapping and functional genomics approach to elucidating precocious coronary artery disease’), and EURODIS (‘Functional genomics of pancreatic beta cells and of tissues involved in control of the endocrine pancreas for prevention and treatment of type 2 diabetes’), which between them received over EUR 25 million from the EU under the ‘Life sciences, genomics and biotechnology for health’ Thematic area of FP6. The studies were also backed by an EU Marie Curie Intra-European Fellowship grant.
European scientists that took part in the studies were from Austria, Croatia, Denmark, Estonia, Finland, Germany, Iceland, Italy, the Netherlands, Norway, Sweden, Switzerland and the UK.
Childhood obesity ad likens junk food to heroin
A controversial new ad which compares feeding children junk food to injecting them with heroin has restarted debate about the best way to tackle childhood obesity.
The Sydney-based agency which produced the ad says existing health advertising is not working to curb the problem.
It says it wanted to shock parents into action. But health experts say it has gone too far.
In the advertisement, a mother walks into a room carrying a brown paper bag. She sits down at a table next to her little boy who is colouring in.
She takes out some heroin and a syringe and ties a tourniquet around her son’s arm. The words on the screen say: “You wouldn’t inject your children with junk – so why are you feeding it to them?”
The producer of the Break the Habit ad and managing director of the Sydney-based agency The Precinct, Henry Motteram, says not resolving the signs of childhood obesity is “tantamount to child abuse”.
“We wanted the conversation to start. We wanted that conversation to be as big as possible and involving as many people as possible, hence why we decided to go down a shock tactic [path],” he said.
“Both obesity and drugs in general have a similar impact on people’s lives, both physically and psychologically in the long run.
“By no means are we saying that eating a hamburger is the same as taking a hit of drugs. The visual metaphor is about the long-term impact of this.”
The ad was posted on YouTube and attracted more than 500 comments. There was a diverse range of opinions from: “Thank you. Addiction is addiction, no matter what item or drug you put in there. Stop abusing your children!”
But others disagreed:
“Heroin will destroy your life and easily kill you. An occasional hamburger will not do either. They have nothing in common and this video is pure garbage,” said one commenter.
“That was bullshit. Somebody ought to slap the person who came up with that,” said another.
“If they want to do something about fat kids then the parents need to take the kids to a park or do something that involves running. Or maybe they should just get off their lazy arse and do something fun with their kids.”
‘Over the top’
Director of the Public Health Advocacy Institute, Professor Mike Daube, says childhood obesity is a massive problem in Australia, where 25 per cent of kids are now considered obese.
But he says the ad is over the top.
“This ad puts all the emphasis on kids. Then it puts all the blame on parents instead of people writing junk food [ads]. And then just for good measure it shows you how to inject heroin,” he said.
“So I’m not a fan of the ad. I admire anybody who has concerns about the obesity problem which is very real, but I don’t think this ad is the way to deal with it.”
It is a view shared by nutritionist Dr Rosemary Stanton.
“Heroin is dangerous, even in a small dose. And junk food isn’t dangerous in a small dose,” she said.
“But I do think that we need to make parents aware that it’s not safe to give their kids so much junk food [to eat]. And they currently aren’t aware of that.”
Dr Stanton says the first step to tackling childhood obesity is to get rid of junk food advertising.
“Sure it’s the parents who actually buy the junk food, but they buy it because the kids pester them to buy it,” she said.
“The kids pester them to buy it because they’ve seen the ads.
“So I think any society that is serious about doing anything about obesity in children and obesity in adults for that matter should look at stopping these highly persuasive, clever adults from encouraging kids to pester the parents.”
This afternoon, the Break the Habit advertisement was pulled from YouTube.
The agency says the parents of the young boy in the ad were concerned about all the media attention.
Study Says HFCS Does Not Cause Obesity
October 12, 2010
For years, high fructose corn syrup has been erroneously implicated as a prime suspect in the obesity epidemic. Inexact scientific reports and inaccurate media accounts have increased confusion about the sugar made from corn. New research proves otherwise.
A new study, presented on Saturday October 9, at the Obesity Society’s 28th Annual Scientific Meeting, further reinforces the facts about high fructose corn syrup. Results from the double-blind study revealed that fructose containing sweeteners (sugar, high fructose corn syrup) do not uniquely contribute to obesity when consumed as part of a healthy weight maintenance diet. The study also found that high fructose corn syrup no more contributes to caloric intake than table sugar (sucrose).
In the study, overweight or obese adults were placed on a 10-week eucaloric diet (an eucaloric diet provides your body with just the right number of calories necessary to maintain current body weight) which incorporated either high fructose corn syrup or sucrose-sweetened, low-fat milk. Participants’ consumption of low-fat milk accounted for between 10 to 20 percent of the daily allotted calories, representing typical levels of sweetener consumption. Study participants did not experience a change in body weight, percent of body fat, fat-mass, or percent of abdominal body fat. Additionally, there were no statistical differences between people given high fructose corn syrup and those given sucrose.
These results are meaningful for the food and beverage industry because they provide further scientific evidence that products containing high fructose corn syrup do not promote weight gain more than products containing sugar.