It's the genetics, stupid!

Some minor errors in the previous version are corrected.

By Jimmy Downs

Genetic variants linked to elevated obesity risk in children

A new study in Nature suggests that obese people likely have some genetic alternations in certain genes or certain key segments of DNA that either drive them to eat more than they need or use food in different ways.

The study found the loss of a key segment of DNA or missing CNV is linked to severe childhood obesity.

CNVs, multiple genes that are either duplicated or deleted from our DNA, are believed to play an important role in some complex diseases like autism and learning disabilities.

Dr Sadaf Farooqi from the University of Cambridge and Dr Matt Hurles from the Wellcome Trust Sanger Institute scanned genomes of 300 children with severe obesity and 7,000 control for types of mutation known as copy number variants (CNVs).

The researchers found that certain parts of the genome were missing in some children with severe obesity. Specifically, Dr. Farooqi was cited as saying that children with part of chromosome 16 deleted have severe obesity in their childhood or at a young age.

One particular gene on chromosome 16 known as SH2B1 is involved in regulating weight and handling blood sugar levels and people with this gene missing have a strong crave to eat and gain weight very easily, Dr. Farcooqi said.

Obesity genes don't neccessarily lead to obesity

A new study by researchers fromo Lund University in Sweden suggests that just because you carry some obesity genes do not mean you have to be obese and a modified diet and lifestyle may offset the predisposing influence from the genetic variants on the risk of becoming obese.

The researchers found that people with the genetic variant the fat mass and obesity-associated gene known as FTO gene did not have an increased body mass index if they followed an physically active life and or used a low fat diet.

Obesity by definition refers to a BMI over 30 in the United States, according to the Centers for Disease Control and Prevention.

In the study, Sonestedt E and colleagues exmained 4839 people in the population-based Malmö Diet and Cancer study with dietary data and information on the genetic variant FTO (rs9939609).  Anthropometric measures were made and leasure time physical activity was estimated.

They observed that there were interactive effects between fat intake and FTO genotype and between carbohydrate intake and FTO genetypes on BMI.

Of carriers of FTO genetypes, an increase in BMI was observed in TT carriers who reportedly used a high fat diet with a mean BMI of 25.3.  In AA carriers, a mean BMI of 26.3 was observed.

The researchers found the FTO variant was not correlated with a higher BMI among people with lower fat intakes whose mean BMI was 25.7 if they are TT carriers and 25.9 if they are AA carriers.

Among subjects having a low-carbohydrate intake, a mean BMI of 25.4 was observed for TT carriers and of 26.8 for AA carriers.

"The increase in BMI across genotypes was mainly restricted to individuals who reported low-leasure-time physical actiity," the researchers wrote.

Sonestedt and colleagues concluded that "Our results indicate that high-fat diets and low physical activity levels may accentuate the susceptibility to obesity by the FTO variant."

The results of the study were published in the Nov 2009 issue of American Journal of Clinical Nutrition.

Low physical acivity and high intake of fat and carbohydrate have been associated with increased risk of obesity or overweight.

Obesity has been increasingly cited as a major health issue in recent decades, acording to wikipedia.

An estimated 26.6 percent Americans suffered obesity.  If the trend continues, by 2015, 41 percent adults in the United States will be obese.

Source:

Am J Clin Nutr. 2009 Nov;90(5):1418-25.
Fat and carbohydrate intake modify the association between genetic variation in the FTO genotype and obesity.
Sonestedt E, Roos C, Gullberg B, Ericson U, Wirfält E, Orho-Melander M.
Department of Clinical Sciences in Malmö, Nutrition Epidemiology, Lund University, Malmö, Sweden. emily.sonestedt@med.lu.se