Identical twins share identical DNA. So, if one twin is obese and the other is thin, the difference can only be accounted for in trips to the gym and food intake, right? Wrong.
A new study shows that some twins with dramatically different BMIs (one obese, one a healthy weight) have different "epigenetic switches." While the common understanding of genetics is that a person either "has the gene" for a particular condition or doesn't, the truth is more complex. A person who has one of the genes correlated with obesity may still have that gene "turned off" like a light switch. And that light switch can be on in one twin, and off in the other.
Researchers at the Max Planck Institute of Immunobiology and Epigenetics in Freiburg, Germany, made the finding, after discovering that mice with only one of two copies of a particular gene, Trim28, were either very lean, or very fat - there was little in between. This got lead researcher Emma Whitelaw and her team excited, because it suggested that they had found a purely epigenetic cause of obesity in some mice (and perhaps some people). Epigenetics is the study of genes in concert with their environment. While genetics studies genes in isolation (which is a good thing, for its aims), epigenetics examines how the environment affects those genes, convincing genes to express certain characteristics.
"Once the switch is triggered, it is a lifelong, epigenetically-driven decision that ends in a stable [result], either a lean or obese phenotype [mouse model]" says researcher Andrew Pospisilik, in a press release. "Such clearly separated phenotypes have a genetic cause.... The effect is akin to a light switch - on or off, lean or obese. Typically, we usually consider epigenetic control of disease to act much more like a dimmer, shifting phenotypes like body weight up or down gradually."
The next step was to examine the gene in humans. The researchers worked with childhood obesity specialists to study fatty tissue in lean and obese children, and found that the same epigenetic switch, Trim28, was at work in about half the sample, making some children obese and some children unusually thin. As a third check, the researchers examined previous published research on twins with "discordant" BMIs (again, one obese, one thin) and found evidence of the exact same switch being at play.
One theory for why this unexpected switch evolved is that life is hedging its bets. If one person is born with the switch turned "on," the other "off," then if one is unable to survive in the current environment, perhaps the other one will.
As for future treatments, hopes are high for those whose Trim28 gene is turned to "obese."
"Our next major goal is to see whether we can modify this process, whether we can turn the disease switch on or off by supplementing diet, minimizing stress, or giving epigenetically relevant pro-drugs," says Andrew Pospisilik, lead author of the study. "The hope is that we can permanently flip the system back to lean in one shot."
The study was published Jan. 28 in the journal Cell.
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