Obesity is written in our DNA and predicts, like a genetic prophecy, the body type we will have. A few decades ago it was easier to rebel against that fate — to fight our genetic programming and keep extra pounds at bay. But in an obesogenic world, surrounded by ubiquitous cheap and addictive food products, it is increasingly difficult. A series of recent scientific articles has strengthened this idea, which is gaining traction in the age of Ozempic and is helping to challenge the notion that obesity is a matter of personal choice or willpower.
New research published in PLOS Medicine found that genetics largely explains the relationship between parents’ and children’s body mass index (BMI), while suggesting that other biological mechanisms play a much smaller role. To reach that conclusion, researchers analyzed data from tens of thousands of Norwegian families. The study estimated that genetics accounted for about 79% of the association between mothers’ and children’s BMI and 94% of the association between fathers’ and children’s BMI by age eight.
The figures are striking, but they do not mean we should fall into genetic determinism, says Tom Bond, a researcher at the University of Bristol and lead author of the study. “Obesity is determined by a combination of genes and the environment,” he says. “If children are raised in a healthy environment, they can avoid becoming overweight, even if they inherited genes that increase their risk of obesity.”
Bond’s observation gets to the heart of the issue. Understanding how genes and environment interact may be key to explaining — and ultimately tackling — the current obesity epidemic.
In this regard, Bond’s study fits neatly with another paper, also published last week in PLOS Medicine. That research examined BMI and obesity-related genetic variants across four generations of Britons born in 1946, 1958, 1970 and 2001. The findings suggested that while the genetic makeup of the population has remained largely unchanged, today’s obesogenic environment has strengthened the link between genetic predisposition and obesity.
“Obesity has risen far too quickly to attribute it to genes, but the current environment may make genetic predisposition weigh more,” says José M. Ordovás, senior investigator at the Jean Mayer USDA Human Nutrition Research Center on Aging. In comments to the scientific portal SMC, Ordovás welcomed the study, arguing that “rather than changing our view of obesity, it reinforces it.”
Dr. Dolores Corella Piquer, a pioneer in nutritional genetics research, is less effusive. “This study is based on statistical models and does not perform concrete genetic analyses,” she explains. “These studies have the problem of being highly dependent on the statistical algorithms they use, and on the population they analyze. They provide very general theoretical estimates.”
Even so, they offer clues about what may be driving current trends. Obesity rates have tripled over the past four decades, and understanding why is crucial if the epidemic is to be tackled effectively.
“The environment determines overall obesity rates in the population, while genetics is a key factor in determining which individuals within that population develop obesity,” Bond says.
The same genetic inheritance is passed from parents to children and carried across generations. Yet its impact on people’s lives is not fixed, because the environment has changed dramatically. A genetic tendency to gain weight may have had few consequences 50 or 60 years ago, when fast food was still a rarity in countries such as Spain. Today, however, with supermarket shelves packed with highly processed foods specifically designed to be appealing and difficult to resist, pushing back against one’s genetic predisposition has become far more challenging.
There is no single genetic variant that determines a person’s susceptibility to obesity. More than 3,000 have been identified. These small mutations are scattered throughout our genetic code and collectively influence, to a significant degree, our relationship with food. Genetics is estimated to account for between 40% and 70% of the risk of obesity. That does not mean people are prisoners of their DNA, but it does mean biology plays an important role. For those struggling to maintain a healthy weight, understanding that reality can be crucial.
Genetic mutations may even limit the effectiveness of powerful weight-loss drugs. A study published in Nature analyzed the genomes of 27,000 people undergoing treatment and identified two variants in the genes targeted by second-generation obesity drugs: the GLP-1 and GIP receptors. The findings could help explain why some patients lose dramatic amounts of weight while others see little benefit. Third-generation anti-obesity drugs target a third hormone, potentially broadening their effectiveness.
For that reason, some experts speak of “obesities” in the plural. This biological variation is not visible from the outside. Obesity is a highly visible condition, one surrounded by aesthetic judgments and social stigma. Yet many of its underlying differences become apparent only when a person’s genome is analyzed.
A study published in Nature Medicine found that genetic differences help explain why some people with obesity remain relatively healthy, while others develop serious conditions such as diabetes and cardiovascular disease.
Genetics does not absolve the environment of responsibility, nor does it make obesity a preordained fate. What it does challenge is a deeply rooted assumption: that everyone starts from the same place. Understanding that biological inequality may be the first step toward addressing an epidemic that stems not from a single cause, but from the interaction of many.
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