The Labrador that cannot feel full, and why the assistance dogs carry it most. · published 22 September 2026
A 14 base-pair deletion in the POMC gene damages part of the signal that tells a Labrador it is full — worth about 1.9 kg of body weight per copy — and it runs at 45 per cent in Labradors selected as assistance dogs versus about 12 per cent in pets, because breeding for trainability quietly selected for food motivation; those dogs stay lean anyway, which is the point: the gene sets the appetite, the household sets the weight.
These are the working notes, unedited. Everything the video
states as fact comes from here, and nothing else may be stated as fact.
The sections on limits and on what the finding does not show are
part of the brief, not an afterthought — see
the method.
The work: Eleanor Raffan and colleagues, “A Deletion in the Canine POMC Gene Is Associated with Weight and Appetite in Obesity-Prone Labrador Retriever Dogs”, Cell Metabolism, May 2016. They looked for a genetic reason Labradors are the breed most reliably described as food-obsessed.
What they found. A 14 base-pair deletion in POMC, the gene for pro-opiomelanocortin. The deletion disrupts the sequences coding for two peptides, beta-MSH and beta-endorphin, which are part of how the signal to stop eating gets made after a meal. A dog carrying it is not being badly behaved. It is working with a damaged off-switch.
The numbers, which are modest and should be stated as such. 310 Labradors were genotyped for the association, 383 more for how common it is, and 296 flat-coat retrievers as a comparison. Each copy of the deletion was worth about 1.9 kg of body weight and roughly a 10 per cent increase in food motivation on a standard owner questionnaire. That is a real effect and a small one — a third of a standard deviation. It is not a switch that makes a dog fat.
The part that turns the story around. In pet Labradors the deletion allele runs at about 12 per cent. In Labradors selected to become assistance dogs it runs at 45 per cent — 76 per cent of them carry at least one copy, against 22 per cent of pets. Nobody was breeding for obesity. They were selecting for trainability, and a dog that will work hard for food is easier to train. The trait that makes a Labrador good at guiding a person is the same trait that makes it fat in an ordinary home.
And the assistance dogs are not fat. They carry the appetite gene at nearly four times the rate and stay a healthy weight, because their food and exercise are controlled by someone following a routine. That is the whole finding in one comparison: the gene sets the appetite, the household sets the weight.
Limits
One breed and its close relative — the deletion was absent from 38 other breeds and found only in the flat-coat retriever, so this is not an explanation of dog obesity in general, let alone human obesity. The authors are explicit that owners control how much food and exercise a dog gets, and they did not claim to quantify how much of obesity the deletion explains. An association in a few hundred dogs is a starting point, not a mechanism proven end to end.
What this does not show
Not that a fat Labrador is nobody’s responsibility — the assistance dogs prove the opposite, since the same genotype stays lean under a controlled routine. Not that a lean Labrador lacks the gene. And not a licence to test your dog and give up: the practical lesson runs the other way, because knowing an animal is hungrier than it looks is a reason to measure the food, not a reason to stop.