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Originally posted by ofhumandescent
The articles and books I have read on obesity strongly link genes and DNA to obesity.
Originally posted by Skyfloating
Originally posted by ofhumandescent
The articles and books I have read on obesity strongly link genes and DNA to obesity.
Such books are mainly propaganda from the socialist/leftist sector of society that thinks people are not responsible for their fate and require welfare. 9 out of 10 obese people are obese due to overeating and lack of exercise. if it were any different you would find just as many obese people in Europe. But you dont.edit on 19-5-2011 by Skyfloating because: (no reason given)
And who really cares. Your spirit isn't overweight, too thin, too tall, too short, pidgeon toed, doens't have a speech impediment, doesn't need glasses, but if you're filled with Unconditional Love and see through the traps of the world, including any form of prejudice, your soul is so beautiful.
Originally posted by Unity_99
People's weights are known, by the valid studies, to vary according to: inheritance
Originally posted by Unity_99
And who really cares. Your spirit isn't overweight,
Originally posted by Skyfloating
Where are all the obese Europeans?
Also - whats next? Extra tax on smokers? Drinkers? People with a sweet tooth? Where does it end?
Originally posted by blupblup
[
Really?
Britain is almost overtaking the US in terms of obesity.... Sad but true.
Originally posted by Unity_99
People need to #1. Stop judging others over anything. They have no right to even look at another person, think a bad thought, unless they have something good, positive and loving to say. PERIOD.
There is right and wrong answer.
It's one of the hardest things to do in the world in my opinion, I'd find it much easier to quit smoking.
Indeed that is one example, another example is those with psychological issues. E.g. unknowingly eating to fill a void or because that's the only happiness/stimulation one may have in their life.
Being fat has nothing to do with tax, its a ridiculous suggestion as I'm sure you will agree.
Obesity gene acts on DNA
5 November 2007
British scientists have made a second breakthrough in under a year in understanding why some people are more liable to gain weight than others.
The Oxford University team, led by Professor Chris Schofield, has been studying FTO, a gene that earlier this year was linked to obesity. In a report of their research, published online this week in Science, the scientists show that the protein corresponding to the FTO is an enzyme, or biological catalyst, that modifies DNA.
Previously, researchers discovered that one variant of the FTO gene causes an average increase in weight of 3kg. However, they were unable to determine what the gene does and why the variant leads to weight gain.
In the new study the team found that, remarkably, the FTO protein resembles enzymes that produce the penicillin antibiotics in bacteria and others that enable humans to sense and respond to changes in oxygen levels – for instance at high altitude. FTO is most closely related to the AlkB family of enzymes that in bacteria repair DNA damaged by chemicals.
The team of Oxford, Cambridge and London scientists went on to show that purified FTO can carry out this repair role and that the FTO protein is targeted to the cell nucleus as expected for a protein that modifies DNA.
Oxford researcher Professor Chris Ponting, one of the key scientists involved, commented: ‘this is an astonishing finding. We never expected this first ‘obesity gene’ to have such a direct effect on DNA’. The Cambridge group led by Professor Steve O’Rahilly discovered that the FTO gene is turned on in regions of the brain concerned with appetite regulation and that FTO levels decrease following fasting.
Professor Frances Ashcroft, a member of the Oxford team, said: ‘obesity is a rapidly growing problem worldwide that significantly enhances the risk of diabetes, cardiac disease, high blood pressure and cancer.’
This breakthrough provides new leads for investigations into how chemical changes to our DNA cause an increase in fat mass and will ultimately help in the development of new drugs to treat obesity.
For more information contact Professor Chris Schofield on +44 (01865) 275625 or email [email protected] or contact Professor Frances Ashcroft on +44 (01865) 285810 or email [email protected]
Alternatively contact the University of Oxford Press Office on +44 (01865) 283877 or email [email protected]
Notes to Editors
*A report of the research entitled ‘The Obesity-Associated FTO Gene Encodes a 2-Oxoglutarate-Dependent Nucleic Acid Demethylase’ will be published online in Science Express on 8 November 2007.
*The team was led by Professor Chris Schofield of Oxford University’s Department of Chemistry with Professor Chris Ponting and Professor Frances Ashcroft from Oxford’s Department of Physiology, Anatomy and Genetics and, at the University of Cambridge, by Professor Steve O’Rahilly.
*In the UK it is estimated that 20% of men and 25% of women are obese, and that as many as 30,000 people die prematurely from obesity-related conditions every year. At the current rate of increase, three-quarters of the UK population could be overweight by 2025. Obesity-related conditions are expensive to treat and cost the NHS at least £500m a year.
Source; Oxford University
Chemical patterns on DNA mark out obesity genes
17:45 16 September 2010 by Andy Coghlan
For similar stories, visit the Genetics Topic Guide
Your genes play a big part in determining your body shape, but that role may not have been set in stone when your parents' egg and sperm got together. It now looks like chemical changes that happen to genes over a person's lifetime may influence how fat they become, without altering their inherited DNA sequences.
This is the first time that prolonged chemical changes to genes during life have been implicated in obesity and body weight.
The findings add to the mounting evidence that it's not only genes that dictate important bodily traits – environmental cues and conditions may also affect such traits by altering gene activity. These "epigenetic" changes influence whether genes are on or off, but do not change the DNA sequence.
The latest findings relate to epigenetic changes which involve methylation, the process by which the addition of chemicals called methyl groups to DNA can turn genes on or off, or moderate a gene's activity by changing the way it is read.
Icelandic obesity
A team led by Andrew Feinberg of Johns Hopkins University School of Medicine in Baltimore, Maryland, and Daniele Fallin of the Johns Hopkins Bloomberg School of Public Health, also in Baltimore, mapped methylation in the DNA of 74 adults with a range of body types, looking for patterns that seemed likely to have been prolonged and set early in life, or even in the womb.
To do this, they first screened the volunteers' DNA in 1991, and picked out 227 regions with methylation patterns that varied between the individual members of the group by an unusually large amount. They then screened the same people in 2002 to distinguish which methylation patterns had not changed over the 11 years, reasoning that the variation in these patterns must have occurred early in life, then become fixed, having a persistent effect on traits such as body weight or intelligence.
Of the 227 methylated sites, 119 were found to be the same in 2002 as they had been 11 years earlier. Feinberg and Fallin then matched these groups to the body type of the individual. They found 13 methylated genes that were more likely to be present in the participants who were overweight or obese.
These chemical changes could have arisen in response to environmental conditions, such as the childhood diet of the individual or even of their mother during pregnancy.
"We don't know yet the degree to which genes and environment add up to give these stable methylation changes, but we believe both are important," says Feinberg.
Usual suspects
The 13 methylated genes include those that make metalloproteinase enzymes, which have already been implicated in obesity through studies on mice. Another, called PRKG1, plays a role when insects and nematodes forage for food.
The researchers caution that it is not yet possible to say whether the methylation changes are a result of environment influence, perhaps in the diet, or whether they are ultimately genetic because they are orchestrated by other genes.
But if specific methylated genes linked with obesity can be identified, they may provide new ways to screen people for risk of becoming overweight or obese. "The results do suggest the importance of including epigenetic analysis with genetic analysis in personalised medicine research to predict risk," says Feinberg.
"Relationships between epigenetic markers such as methylation patterns and particular disease or body states are hard to establish with confidence," says Bryan Turner, a geneticist at the University of Birmingham, UK.
Journal reference: Science Translational Medicine, DOI: 10.1126/scitranslmed.3001262