Belfast Telegraph

Too skinny or too fat? Blame it on your genes says new research

By John von Radowitz

Being naturally overweight or skinny could be two sides of the same genetic coin, new research suggests.

Scientists have discovered that underweight people possess extra copies of certain genes.

Previously, the issue of missing identical genes was linked to obesity.

Last year the same research team found that people with the gene deletions were 43 times more likely to be clinically obese.

Chief scientist Professor Philippe Froguel, from the School of Public Health at Imperial College London, said: "It's.. the first example of a deletion and a duplication of one part of the genome (genetic code) having opposite effects.

"If we can work out why gene duplication in this region causes thinness, it might throw up new potential treatments for obesity and appetite disorders.

"We now plan to sequence these genes and find out what they do, so we can get an idea of which ones are involved in regulating appetite."

Genes are stretches of DNA that provide the coded instructions for making proteins.

They generally come in pairs and are housed in the chromosomes, the packaged bundles of DNA inherited from each parent.

However sometimes parts of either chromosome in a pair can be deleted or duplicated. When this happens, there can be too many copies of a certain gene or too few.

As a result, a gene might be abnormally active or not active enough.

The new research shows that a genetic propensity to be fat or thin can be caused by opposite chromosomal mistakes of this kind.

A study of DNA from more than 95,000 adults and children revealed that duplication of part of chromosome 16 was associated with being underweight.

The abnormality affected one in 2000 people, making men 23 times and women five times more likely to be extremely thin.

Like obesity, being grossly underweight can be harmful to health.

Half of all children in the study with the duplication were diagnosed with "failure to thrive", meaning their rate of weight gain was significantly lower than normal.

A quarter of those with the extra genes suffered from microcephaly, a condition marked by an abnormally small head and brain which is associated with neurological defects and reduced life expectancy.

The part of chromosome 16 highlighted in the study, published today in the journal Nature, contains 28 genes.

Duplications in the same region have also been linked to schizophrenia, while deletions are associated with autism.

Prof Froguel, who worked with Swiss colleagues from the University of Lausanne, said: "The dogma is that we have two copies of each gene, but this isn't really true.

"The genome is full of holes where genes are lost, and in other places we have extra copies of genes. In many cases, duplications and deletions have no effect, but occasionally they can lead to disease.

"So far, we have discovered a large number of genetic changes that lead to obesity. It seems that we have plenty of systems that increase appetite since eating is so important - you can suppress one and nothing happens. This is the first genetic cause of extreme thinness that has been identified.

"One reason this is important is that it shows that failure to thrive in childhood can be genetically driven. If a child is not eating, it's not necessarily the parents' fault."

Being underweight is defined as having a Body Mass Index (BMI), calculated by dividing weight in kilograms by height in metres squared, below 18.5. The "normal" range is 18.5 to 24.9, "overweight" 25 to 29.9, and "obese" 30 and above.

Irish Independent

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