You’d think it was a moon landing! Everybody is all excited about a genetic basis for childhood obesity, and the headlines proliferate.
It all started with an international group of collaborators known as the Early Growth Genetics Consortium, or EGG. They gathered the most extensive collection ever, of DNA from children with common obesity (as distinguished from the kind caused by a handful of rare diseases that were already identified).
In the past, investigations of twins who were raised apart served to throw suspicion on genetic makeup, in at least some instances of obesity. Studies of obese adults have pointed to genetic involvement, but by the time a person grows up, so many other forces have acted on her or him, it’s hard to untangle the cause and effect.
Because there are so many other factors to account for, statistics of this kind are meaningless unless the amount of data is simply enormous. So it took the cooperation of groups in many parts of North America, Europe, and Australia to amass the information needed here.
The EGG project is a meta study, combining the results of 14 different studies. Overall, the information was derived from the medical histories of 5,530 obese children and 8,300 control subjects. The common European ancestry is one of the important things to remember when assessing the ultimate usefulness of the study.
The author explains:
The study team identified two novel loci, one near the OLFM4 gene on chromosome 13, the other within the HOXB5 gene on chromosome 17. They also found a degree of evidence for two other gene variants. None of the genes were previously implicated in obesity.
Here is the fun part: Although the connection is far from being understood, one thing seems obvious to the researchers. Three of the newly scrutinized genes have a real close affinity with what goes on in our old friend, the intestinal tract, which Childhood Obesity News has been exploring lately.
ScienceDaily quotes one of the scientists who worked on this monumental project, Struan F.A. Grant, Ph.D, who is associate director of the Center for Applied Genomics, located in Philadelphia:
This is the largest-ever genome-wide study of common childhood obesity, in contrast to previous studies that have focused on more extreme forms of obesity primarily connected with rare disease syndromes. As a consequence, we have definitively identified and characterized a genetic predisposition to common childhood obesity… This work opens up new avenues to explore the genetics of common childhood obesity. Much work remains to be done, but these findings may ultimately be useful in helping to design future preventive interventions and treatments for children, based on their individual genomes.
For WebMD, Brenda Goodman fills in a little more, emphasizing that just because a genetic component may have been discovered, it doesn’t mean a child born with it is fated to be obese. She also elicits a response from a scientist who was not involved in the EGG study, Dr. William S. Garver, who teaches molecular biology and biochemistry, and who has also studied the relationship between genetics and obesity. Goodman quotes Garver as saying:
Common obesity is a very complex disease — not only genetic or environmental (high-fat diet, inactive lifestyle) — but an interaction between these two factors. It is likely that most common obesity genes interact with an environmental factor or other ‘modifying genes’ to promote weight gain.
Another reporter, Nanci Hellmich of USA TODAY, also asked a source unconnected with the big newsmaking study. Her informant was Ruth Loos, who directs the Genetics of Obesity and Related Metabolic Traits Program, located at New York’s Mount Sinai School of Medicine. Loos says the study:
… [S]hows that the genetic susceptibility to obesity begins at an early age. However, this does not mean that those who are genetically susceptible are destined to become obese adults, because a healthy lifestyle remains an important factor that can reduce one’s genetic susceptibility… If some of these genes turn out to be drug-able targets, then maybe this could lead to new medication. But that is indeed years away, it will require much more detailed physiological research.
Michael Smith, for MedPage Today, also consulted an outside source, not involved with the EGG study. From Albert Einsten College of Medicine, Keith-Thomas Ayoob commented:
We may know more about childhood obesity, but until there’s a magic bullet, the treatment will be the same. Kids still need to have better diets and they really need to be more active.
If these genes have been inside humans all along, then why is the present-day childhood obesity such a seemingly well-defined phenomenon, with an obvious beginning in time? If they haven’t been there all along, where did they come from? Or rather, what caused them to change into hostile genes that want to make us fat?
A lot of questions remain to be answered, and the best thing to do at this point is maintain an attitude of cautious optimism, while not expecting the NoFat pill to hit the market next week. And remember how Dr. Grant phrased it:
This work opens up new avenues to explore… [T]hese findings may ultimately be useful…
All excellent, but hardly the equivalent of a moon landing.
Your responses and feedback are welcome!
Source: “Genes Identified in Common Childhood Obesity,” ScienceDaily, 04/08/12
Source: “Genes Pinpointed for Common Childhood Obesity,” WebMD, 04/08/12
Source: “Gene variants increase risk of childhood obesity, study finds,” USA TODAY, 04/09/12
Source: “Obese Kids: Genes and Junk Food Share Blame,” MedPage Today, 04/08/12
Image of “Cernan Moon” is used under Fair Use: Reporting.