Do Our Genes Destine Us To Be Fat?
Jan 03, 2018 02:15PM
What’s New in Genome Project Research
“Like his father’s father and his father before him,” is a time-worn and traditional phrase used to convey the arbitrary nature of some familial life practices, behaviors, and outcomes.
How many times have you heard someone say, “I can’t help it; my mother was heavy, so I guess I will be, too?” While this may be an easy way to write-off or substantiate a less desirable aspect of one’s life, when it comes to being overweight or obese, it isn’t necessarily so, says researchers.
With obesity on the rise since the 1970s and impacting our healthcare system to the tune of $147 million a year, (the last year obesity impact numbers were verified and released was 2008) the need for research at the genetic level has only intensified.
Researchers from the Human Genome Project note that the increase in cases of obesity itself denotes that the problem is not wholly genetic in nature, as genes do not change, which points to an environmental component at play, as well.
Project studies of the full sets of DNA from thousands of individuals have suggested that obesity is not the mere work of one specific gene, but rather a combination of genes. This combination is not particularly influential, however, in producing a high number of obesity cases.
What’s Really Going OnA groundbreaking moment in the history of obesity/gene research was made in 2007, when the first obesity-linked variant was discovered, known as the FTO variant.
“FTO” stands for the “fat mass and obesity associated” gene found on chromosome 16 of a DNA sequence. Carriers with this FTO variant have a 20 to 30 percent higher chance of developing obesity than those who do not carry the variant.
Despite this discovery, researchers stress that these carriers are not doomed to a life affected by obesity. Their thinking is based on two more recent and significant studies that provided the proof that environmental influences play key roles in obesity development.
One set of studies focused on genetically pre-disposed individuals and the consumption of certain foods. Subjects who enjoyed sugared beverages on a regular basis were more likely to experience increases in their BMI (Body Mass Index) as opposed to those who did not drink them regularly. Similarly, subjects who chose to consume high-fat fried foods four to five times per week were more likely to become obese than their counterparts who chose not to partake in such a diet. Remember, both groups of individuals studied were FTO variant carriers.
The CDC (Center for Disease Control and Prevention) states that 36.5% of U.S. adults are obese.
The other studies conducted at the T.H. Chan School of Public Health involved some 200,000 individuals with the variant and their levels of physical activity. Those who were physically active decreased their risk of developing obesity by 7.3 percent versus those who did not exercise over the same period of time.
Clearly, these important environmental variables prove that you can alter your destiny concerning obesity even if you do carry the variant gene.
The One ExceptionIt is fair to note, however, that there is one caveat or circumstance where obesity and genetics cross paths and the outcome can be predetermined; this is in the case of “monogenic obesity.” As the prefix denotes, the condition, which is extremely rare, occurs when there is a mutation that produces a very high risk in a single gene. This risk, researchers say, is very hard, and sometimes impossible, to counter.
Where More Research Is NeededThere are several areas where research continues in earnest or is just getting off the ground.
Currently, the National Human Genome Research Institute is looking at what one might be tempted to call “reverse obesity.” If you have ever known someone who seems to defy the odds when it comes to weight gain, or the lack thereof, it can be very puzzling. They may never seem to eat the right foods yet, they do not battle the bulge. Researchers at the NHGRI are puzzled as well, and are studying if there are such things as gene variants that actually protect against obesity.
Another study is looking at a gene that is related to the production of a substance called adiponectin that is secreted by adipose tissue in the areas, like our bellies, that store fat. This hormone is produced at much lower levels in obese people and researchers want to know why.
Most recently, the first study of its kind is also said to be underway at NHGRI to look at the genomic links between those with continental African and African-American ancestry and obesity.
What they know right now is that approximately one percent of West Africans, African Americans, and others of African ancestry carry a genomic variant that increases their risk of obesity. Studies show that those who carry the variant, weigh an average of six pounds more than those who do not. Researchers hope these findings will provide further insight into why obesity seems to cluster in families.
While this research also seeks to address obesity’s designation as a global concern, it also points out that its prevalence among U.S. ethnic groups is by no means evenly distributed. African Americans have been found to have the highest age-adjusted rates of obesity, according to Charles N. Rotimi, Ph.D., chief of NHGRI’s Metabolic, Cardiovascular, and Inflammatory Disease Genomics Branch and director of the Center for Research on Genomics and Global Health (CRGGH) at NIH.
Overall, while researchers say that gene study is amazingly complicated and can’t explain everything there is to know about the pre-disposition for obesity, our genes do seem to play their most prolific role in certain groups of people who are exposed to certain environments. The search for answers and the research into those roles and environments is on-going.