Pippa, a 12-week-old Labrador retriever, was minding her business, lazily chewing a stick. But when her owner uttered a single word, “biscuit”, it was like Pippa was possessed. Ears pricked, she was at attention, eyes locked on her human, eager for a treat.
While the word for the treat differs from owner to owner, this reaction is relatable to all dog owners, especially lab moms and dads. This is no accident.
This insatiable appetite is a quirk of the Labrador breed, encoded in their genes. It’s one of the reasons why labs are particularly prone to obesity. And according to a new study at the University of Cambridge, Labradors and some humans share some of these genes that influence appetite and body weight.
“We found that dogs at high genetic risk of obesity were more interested in food,” said Natalie Wallis, joint first author from the University of Cambridge’s Department of Physiology, Development and Neuroscience. “Dogs at high genetic risk of obesity showed signs of having higher appetite, as has also been shown for people at high genetic risk of obesity.”
A Tale of Two Species and Appetites
The research team recruited owners of pet Labradors to measure their dogs’ body fat, assess their “greediness,” and provide saliva samples for DNA analysis. They found that dogs with a high genetic risk of obesity were more likely to pester their owners for food and scavenge for scraps.
The gene that was most associated with over-the-top appetite is DENND1B. In Labradors, this gene is strongly associated with obesity, and dogs carrying a particular variant of it have about 8% more body fat than those without it. When the researchers parsed databases of human genomes, they found the same gene lurking in the DNA of people prone to obesity.
DENND1B operates within the leptin-melanocortin pathway, a system in the brain that regulates hunger and energy use. Leptin is a hormone produced by fat cells, which signals the brain to reduce appetite and increase energy expenditure when the body has sufficient reserves. So DENND1B may have a major impact on how hungry you feel and how much energy you burn.
The study led by Dr. Eleanor Raffan also identified four other genes linked to canine obesity, though their effects were less pronounced than DENND1B.
In a previous study, Raffan singled out a mutation in the POMC gene in Labradors, which is also linked with regulating hunger and how they burn calories. Due to this genetic legacy, Labradors not only feel an increased urge to eat but also have a reduced rate of metabolism, meaning they burn fewer calories from the food they eat. This mutation was inherited from the St. John’s water dogs, an extinct breed that thrived on a high-calorie diet to survive the cold maritime conditions of Canada centuries ago.
What This Means for Human Obesity?
The parallels between canine and human obesity are striking. Just as 40-60% of pet dogs are overweight or obese, a similar proportion of humans face the same struggle. Both species have evolved over thousands of years in the wild between cycles of feast and famine. To cope, we’ve developed mechanisms to store fat as an energy reserve. But in a world of abundant food (and tasty treats), these once-adaptive traits can become a liability.
Yet, with strict diet and exercise regimes, even these high-risk dogs could maintain a healthy weight, the researchers found — though it required significantly more effort from their owners.
There’s an old line in the weight loss community: calories in, calories out. But that doesn’t fully capture the whole picture. Studies show that the type of food in your diet, irrespective of calories, matters a lot. Consuming whole foods still “packaged” in their original fibers and polyphenols — the cellular wrappers and colorful compounds in plants that confer many of their health benefits — leads to more calories lost through stool, when compared with processed foods that have been “predigested” by factories into simple carbs, refined fats and additives.
Burning Calories
A full accounting of calories also depends on how effectively your body burns them to power your movement, thoughts, immunity and other functions — a process largely orchestrated by your mitochondria. Healthy people typically have high-capacity mitochondria that easily process calories to fuel cellular functions. People with metabolic diseases have mitochondria that don’t work as well, contributing to bigger appetites, less muscle, and increased fat storage.
A healthy gut microbiome produces a full range of beneficial metabolites that support calorie-burning brown fat, muscle endurance and metabolic health. But not everyone has a microbiome capable of converting bioactives into their active metabolites.
And then, as these studies show, you have the question of genetics. By comparing genetic data from Pippa and 250 other Labradors with human genetic studies, the researchers discovered that DENND1B also plays a role in human obesity, although its effect in people is less pronounced.
“This work shows how similar dogs are to humans genetically,” said Dr. Eleanor Raffan, who led the study. “Studying the dogs showed us something really powerful: owners of slim dogs are not morally superior. The same is true of slim people. If you have a high genetic risk of obesity, then when there’s lots of food available, you’re prone to overeating and gaining weight unless you put a huge effort into not doing so.”
“We showed DENND1B is produced alongside melanocortin receptors in the brain and alters signaling by them,” the researchers added.
Hard Work Still Works
But genetics doesn’t mean you or your canine are destined to be overweight. The study found that owners who strictly controlled their dogs’ diet and exercise prevented even high-risk dogs from becoming obese — though it required more vigilance. Similarly, people with high genetic risk of obesity can stay lean, but it takes more work.
“This goes for dogs and humans alike — they have a genetic drive to overeat,” Raffan told The BBC. “But it all speaks to the same important bit of biology, which is that obesity is not about having low willpower.”
Drugs like Ozempic target pathways that influence appetite, and the DENND1B discovery could open doors to further understanding of how the brain regulates body weight.
The findings appeared in the journal Science.
