Until last year, Borris would never turn down a pork chop. He was partial to ice cream during the summer and loved a Sunday roast in the winter – including beef with Yorkshire pudding, pigs in blankets, mashed potatoes, and a selection of vegetables.
直到去年，鲍里斯（Borris）才拒绝吃猪排。他喜欢夏天吃冰激凌，冬天在星期日吃烤肉，包括牛肉和约克郡布丁、猪肉饼、土豆泥以及各种蔬菜。鲍里斯是一只5岁的骑士查理王猎犬（Cavalier King Charles Spaniel）。
Borris is a five-year-old Cavalier King Charles Spaniel. By the time his owner, Annemarie Formoy, entered him into the PDSA Pet Fit Club competition, which helps obese cats and dogs slim down, he was 28kg – almost double his recommended weight. It took two people to lift him into the car, he had arthritis in one leg and his breathing was laboured. Thanks to a tailored six-month diet and exercise regime he is now 7kg lighter and has just been crowned joint competition winner with Sadie the Labrador.
他的主人福尔莫伊（Annemarie Formoy）把他送到动物之家宠物减肥健身俱乐部（PDSA Pet Fit Club）参赛时，他已经28公斤重了，是正常体重的两倍。他一条腿有关节炎，而且呼吸困难，要两个人一起才能把他抬上车。经过6个月的节食治疗及锻炼，他轻了7公斤，和名为萨迪（Sadie）的拉布拉多犬获得了减肥赛的并列第一名。
Borris, at his heaviest, was not alone. The worldwide prevalence of pet obesity lies between 22% and 44%, and rates seem to be rising. The reasons why are fairly predictable. Owners of overweight dogs feed them more snacks and table scraps, are more likely to have their pets present as they prepare their own meals and are less likely to walk them daily. Owners of obese cats tend to use food as a reward and play with them less. If a dog owner is obese, the chances are their pet will be too (this doesn’t apply to cats).
But obesity also seems to be occurring even in some domestic and wild animals who aren’t being overfed or under-exercised. If these findings are true, something else must be driving obesity and uncovering those could help tackle our own epidemic with the condition.
More than 1.9 billion human adults are overweight. Of these, more than 650 million are obese – that’s about 13% of the world’s adult human population. The worldwide prevalence of obesity has nearly tripled since 1975. And childhood obesity has risen alarmingly too – an estimated 41 million children under the age of five are overweight or obese.
The first animal clue lies at the paw of the obesity-prone Labrador retriever. “Labradors are consistently the headline act when it comes to overweight dogs,” says Eleanor Raffan, a veterinarian and geneticist at the University of Cambridge. She and fellow researchers discovered that a genetic mutation present in around a quarter of Labradors, was associated with obesity. For each copy of the mutation – which occurred in a gene called POMC – a dog was about 2kg heavier. Most of the animals the researchers studied had one copy of the mutation, but fewer had two.
“These are dogs always in the kitchen when owners are preparing food, sticking around looking for a tidbit even if there’s not much chance of getting one, or scavenging yucky stuff on walks,” Raffan says. “But they’re not doing that because it’s fun. They’re doing it because they’re hungry.”
That’s because POMC mutations disrupt the brain’s leptin-melanocortin pathway, which regulates food intake and energy expenditure, ultimately influencing body weight. As a result, the behaviour of these Labradors becomes very food-motivated.
There’s a lesson here for humans, Raffan says. “The drive to eat is as every much of a physiological drive and dominating thought as the feeling of being thirsty.”
Genes play a role in human obesity (the average heritability lies between 40% and 75%), but obesity caused by a single gene is rare. POMC deficiency, associated with severe obesity in infancy, has been reported in fewer than 50 people worldwide, although there are likely thousands of undiagnosed cases. But mostly, human obesity reflects multiple genetic risk variants (each with small effects) interacting in a complex way with environmental factors.
The good news is that animals could help us disentangle those environmental factors, too. Factory farm animals are traditionally fattened with antibiotics that transform their gut so they need less food to gain weight. New regulations have pushed antibiotic use in UK food-producing animals to their lowest level since data were first published and the EU has banned antibiotics as growth promoters in feed.
If antibiotics fatten animals, could they be doing the same to humans?
The answer to that question lies in your gut. The microbiome describes the genomes of the vast colonies of micro-organisms – bacteria, fungi, protozoa, viruses, all 100 trillion of them – living in your digestive system. This community influences your weight: germ-free mice that receive gut microbes from an obese (human) twin gain more weight and body fat than mice that receive microbes from the lean twin. An imbalance in the microbiome possibly leads to not only obesity, but irritable bowel syndrome, coeliac disease, and type 2 diabetes.
So what causes this sort of imbalance? There is a genetic element. But in studies of animals, high-intensity sweeteners and food additives like the emulsifiers used in many processed foods have been linked to lower gut bacterial diversity. In humans, babies given antibiotics in the first six months of life led to an increased risk of being overweight in later childhood, according to one study. Six weeks of antibiotics for a heart infection was also linked to significant weight gain.
But before you throw away your life-saving antibiotics, remember these studies only show an association rather than clear cause and consequence. Certain antibiotics might even shift the balance of gut microbiota away from patterns associated with obesity. Knowing this, could we somehow modify our microbiome to tackle obesity? Work is underway to do just that, with probiotics and faecal transplantation under investigation.
Obesity isn’t just something that affects domestic animals, though. Wild animals fatten up, too, but it’s usually in relation to seasonal cycles and food availability: they’ve learned to eat when food is plentiful. But researchers have seen unexpected weight gain in yellow-bellied marmots (large grass squirrels) in Colorado’s Rocky Mountains between 1976 and 2008. Marmots are now waking up around a month earlier from their eight-month hibernation, likely because climate change has altered the time between first snow melt and first frost. These extra days mean more feeding and fattening time. In the short-term, an extra 0.3kg could improve survival chances during hibernation and reproductive success afterwards. (Sadly, marmots will ultimately pay a high price as climate change increases the frequency of summer droughts.)
Other environmental factors that affect obesity in animals – and perhaps humans – include sleep debt and light pollution. Mice exposed to constant light have higher body mass indices (BMIs) and glucose levels than those exposed to normal light/dark cycles.
Oestrogen-disrupting chemicals like bisphenol-A (BPA) – found in food cans, some hard plastics, and certain types of thermal paper used for receipts and tickets – are another potential culprit. Chemical manufacturers have challenged these links and the US Food and Drug Administration currently supports its safety, but the European Food Safety Authority is currently re-evaluating the toxicity of BPA and, in January 2011, the European Commission prohibited BPA for the manufacture of polycarbonate infant feeding bottles.
A note of caution is needed, though. Focusing on these non-food related factors can distract from the undeniable impact of supersized processed meals. The truth is we’re up against external influences that are hard to resist: ingredients designed to tap into our reward pathways, large portion sizes, and the commercial normalisation of routine sugar consumption, high fat snacks and sweetened drinks.
All this is coated by manipulative marketing and conflicted interests. Studies from obesity researchers with food industry ties were five times more likely to find no association between sugar-sweetened drinks and weight gain than studies whose authors reported no financial conflict of interest. One high profile researcher who argued against calorie listings by New York City restaurants had financial ties to Coca-Cola, PepsiCo, McDonald's, and Mars.
Animals are equally susceptible to the irresistible draw of processed food – city-dwelling tamarins in Medellín, Colombia, are fatter than their rural counterparts. Although more sedentary with easier access to fruiting trees, they also gorge on biscuits and marshmallows provided by locals. One Thailand macaque made international headlines recently when he became critically unwell through overfeeding by tourists.
If animals can teach us about the causes of obesity, they might also help us understand its treatment and prevention. And research in companion animals could hold greater relevance for humans since lab rats often do not share our genetic diversity, psychosocial stressors or environment. Raffan’s Labrador study highlighted the greater similarities between canine and human POMC, compared to the rat model we traditionally study. Crucially, though, animals deserve to be helped and healed in their own right – obese pets face osteoarthritis, cancer, cardiac and respiratory problems, reproductive disorders, urinary diseases, diabetes, and pancreatitis.
Overweight dogs also face reduced life expectancy – their lifespan is up to two and a half years shorter compared to dogs with a healthy body weight.
For animals, the solutions sound familiar: regular exercise and a balanced food regimen. Specialist diets improve satiety so that dogs feel fuller for longer. Raffan suggests that highly food-motivated dogs can benefit from less in the bowl and more (or all) from puzzle feeders that allow them to indulge their food obsession in a non-fattening way while keeping them mentally and physically active.
But her key message is that we shouldn’t view obesity as some sort of moral failing in either owners or their pets.
“We’re so used to condemning humans who are overweight as being just greedy and weak-willed,” she says. But, she points out, this is inaccurate: eating behaviour is susceptible to genetic drives – and dogs are an example of this. “Dogs don’t make value judgments. They eat because they’re hungry and this variability in dogs is hardwired.”
Experts writing in the journal Veterinary Record also caution against condemning owners without helping them or addressing underlying social problems. Although a pet’s forcible removal might be necessary if they are severely threatened, they acknowledge, “it cannot be a general solution to the widespread problem of canine and feline obesity”. They believe that many owners don’t intentionally overfeed their pets, as reflected by their tendency to underestimate their pets’ weight (it was a vet who told Formoy that her dog was in trouble. “Borris looked a bit big but you just try make excuses in your head,” Formoy says.) Similarly, few parents of overweight children recognise their child as overweight.
Socioeconomic status also influences obesity in both humans and animals, partly linked to neighbourhoods with less open green spaces and fewer fitness resources. Regardless of whether you’re talking about a pet or a person, obesity is a societal health issue, not a moral one – and needs wider policy changes to be addressed.
As for Borris, Formoy says that his competition win was bittersweet. Her father had been unwell when she signed Borris up. “He was my dad’s best mate and the competition encouraged my dad to go out on his mobility scooter with Borris by his side,” she says. Her father passed away in July. “I thought in my head, ‘Dad, me and Borris are still going to win this for you.’”
She and Borris have kept that promise. Today, Borris is busy chasing Charlie Cat around the house, his own arthritis and breathing difficulties relegated to the past. In his story of obesity conquered, Borris has a few lessons for us all.