Genes influence every aspect of human physiology, development, and adaptation. Obesity is no exception. Yet relatively little is known regarding the specific genes that contribute to obesity and the scale of so-called “genetic environment interactions” – the complex interplay between our genetic makeup and our life experiences.
Does genetics play a role in obesity?
Obesity results from the energy imbalance that occurs when a person consumes more calories than their body burns. It’s a serious public health problem because it is associated with some of the leading causes of death in the U.S. and worldwide, including diabetes, heart disease, stroke, and some types of cancer.
In recent decades, obesity has reached epidemic proportions in populations whose environments promote physical inactivity and increased consumption of high-calorie foods. However, not all people living in such environments will become obese, nor will all obese people have the same body fat distribution or suffer the same health problems. These differences can be seen in groups of people with the same racial or ethnic background and even within families. Genetic changes in human populations occur too slowly to be responsible for the obesity epidemic. Nevertheless, the variation in how people respond to the same environment suggests that genes do play a role in the development of obesity.
How Could Genes Influence Obesity?
Genes give the body instructions for responding to changes in its environment. Studies of resemblances and differences among family members, twins, and adoptees offer indirect scientific evidence that a sizable portion of the variation in weight among adults is due to genetic factors. Other studies have compared obese and non-obese people for variation in genes that could influence behaviors (such as a drive to overeat, or a tendency to be sedentary) or metabolism (such as a diminished capacity to use dietary fats as fuel, or an increased tendency to store body fat). These studies have identified variants in several genes that may contribute to obesity by increasing hunger and food intake.
This drove research to find a genetic test that might be able to identify newborns at risk of becoming severely obese by middle age. Researchers say they have come up with one, and that it might allow interventions in childhood to avoid that fate. The test examines more than 2 million spots in a person’s genetic code, seeking variants that individually nudge a person’s obesity risk up by a tiny amount. They then drew on previously published data about those variants to create a risk score.
A high score didn’t guarantee obesity, nor a low score rule it out. But middle-aged people with scores in the top 10 percent were 25 times as likely to be severely obese as those in the bottom 10 percent, scientists reported in a paper released this month by the journal Cell.
Those two groups were separated by an average weight difference of about 29 pounds (13 kilograms). Analysis showed the genetic propensity to obesity began having an effect on weight around age 3. Up to about age 8, “you might be able to make a difference in the kids who are born susceptible to obesity,” said one author of the study, Dr. Sekar Kathiresan of Massachusetts General Hospital in Boston and the Broad Institute of MIT and Harvard. “But it will take further research to see whether intervening would work.”
As evidenced by 17% of the study participants with the highest scores still maintaining a normal weight, Dr. Kathiresan stressed even if one inherits a propensity for obesity, “you still have control over your fate. You’re not fated to be obese.” Analyses showed that people who remain lean despite an inherited propensity for obesity ate better and were more physically active than others with a high score who got fat. “It seems clear” he stated ” that those individuals who’ve inherited susceptibility have to work that much harder to keep the weight off.”
Rarely, a clear pattern of inherited obesity within a family is caused by a specific variant of a single gene (monogenic obesity). Most obesity probably results from complex interactions among multiple genes and environmental factors that remain poorly understood (multifactorial obesity).
Any explanation of the obesity epidemic has to consider both genetics and the environment. One explanation that is often cited is the mismatch between today’s environment and “energy-thrifty genes” that multiplied in the distant past, when food sources were unpredictable. In other words, according to the “thrifty genotype” hypothesis, the same genes that helped our ancestors survive occasional famines are now being challenged by environments in which food is plentiful year round. Other hypotheses have been proposed including a role for the gut microbiome impacting weight (see post).
Genetic changes are unlikely to explain the rapid spread of obesity around the globe. That’s because the “gene pool frequency of different genes across a population-remains fairly stable for many generations. It takes a long time for new mutations or polymorphisms to spread. So if our genes have stayed largely the same, what has changed over the past 40 years of rising obesity rates? Our environment: the physical, social, political, and economic surroundings that influence how much we eat and how active we are. Environmental changes that make it easier for people to overeat, and harder for people to get enough physical activity, have played a key role in triggering the recent surge of overweight and obesity.
Most people probably have some genetic predisposition to obesity, depending on their family history and ethnicity. Moving from genetic predisposition to obesity itself generally requires some change in diet, lifestyle, or other environmental factors. Some of those changes include the following:
• The availability of food at all hours of the day and in places that once did not sell food, such as gas stations, pharmacies, and office supply stores;
• A dramatic decrease in physical activity during work, domestic activities, and leisure time, especially among children;
• Increased time spent watching television, using computers, and performing other sedentary activities;
• The influx of highly processed foods, fast food, and sugar-sweetened beverages, along with the ubiquitous marketing campaigns that promote them.
The Bottom Line: Healthy Environments and Lifestyles Can Counteract Gene-Related Risks
Understanding the genetic contributions to obesity will generate a better understanding of the causal pathways that may lead to obesity. This information might someday yield promising strategies for prevention and treatment. No one is diminishing the impact our genes may have on us but it’s important to remember that overall, the contribution of genes to obesity risk is small, while the contribution of our toxic food and activity environment is huge. Genes may set up circumstances for who can become obese, it’s our environment that determines how many actually will become obese. Many people who carry these “obesity genes” are not overweight. We are not locked into a future, healthy lifestyles and healthy choices can and do counteract these genetic effects.
Sources:
-hsph.harvard.edu/obesity-prevention-source/obesity-causes/genes-and-obesity/
1ncbi.nlm.nih.gov/pmc/articles/PMC2955913/
-cdc.gov/genomics/resources/diseases/obesity/index.htm
-cell.com/cell/fulltext/S0092-8674(19)30345-9
-cell.com/cell/fulltext/S0092-8674(19)30290-9
-nytimes.com/2019/04/18/health/genetics-weight-obesity.html
-apnews.com/60317e7a5ab54f1684c21eace9b953f9