Is addiction to blame for our high-fat diets?

 

The ‘rats on cheesecake’ study has generated discussion around the contentious issue of linking food addiction and obesity, writes CLAIRE O'CONNELL

IS IT possible to be addicted to junk food? Studies on rats are showing that if they have plenty of access to foods high in fat and sugar – the kind of fare that in excess can quickly lead to obesity – the reward pathways that light up in their brains show the hallmarks of addiction.

It’s a contentious area, but Irish researcher Dr Paul Kenny has been making strides in understanding the molecular changes in the brain – in animal models at least – associated with seeking the reward of junk food even when the consequences are known not to be good.

Originally from Finglas, educated at Trinity College Dublin and now an associate professor at the Scripps Research Institute in Florida, Kenny has been looking at neurobiology of addiction.

“It’s well established that dopamine transmission plays a key role in drug addiction and reward-related behaviours,” he says.

“My interest in this was to try to look at the molecular biology of the process.”

Kenny turned his attention to behaviours that are linked with obesity, and decided to see the effects eating junk food could have on dopamine in the rat brain.

“It was the idea that junk food is comfort food, and can it be addictive,” he says.

“We wanted to see can an animal develop dependence on this type of food and demonstrate addictive-like behaviours.”

The experiment used three sets of rats. One had bland standard lab-rat chow, while another had chow with a restricted session of palatable food – such as bacon, sausage, cheesecake and chocolate – once a day. The final group had chow plus free, 24-hour access to the “cafeteria” food whenever they wanted it.

So what happened? “It was remarkable to see,” recalls Kenny, who last week picked up the Jacob P Waletzky award from the Society for Neuroscience in the US.

“The animals that had just the chow took about 100kcals per day, so they had a really nice steady weight gain, they looked really healthy.

“And the animals that had one-hour access to the junk food binged, but they only consumed the same number of calories, they didn’t over-consume.”

But while the one-hour rats were keen to jump on the cafeteria fare and guzzle it when it became available, their 24-hour full-access counterparts got into lazy snacking mode, describes Kenny: “They got really sedentary. And they would graze continuously, it was really noticeable.”

There was another difference between the one-hour wolfers and the 24-hour junk food fans – the reward pathways that lit up in their brains.

“In the limited access group – the binge eaters – there was no real change in the activity of their brain reward system,” says Kenny.

But the 24-hour junk foodies looked bad. “They had the same type of crash in reward activity that you would see in an animal that is overusing cocaine or heroin, they showed this real hallmark of a disruption in their brain reward activity.”

One theory is that when the molecular reward system gets overstimulated – in this case by the lure and capture of cheesecake and the like – the brain responds by toning down certain activities, explains Kenny.

“You stop eating the food or doing the drug, all you are left with is this deficient sub-functional brain reward system,” he says.

“So you have gone from a state where you indulge in a food because it is nice, to now you need the food because otherwise without it you are going to feel really bad.”

One of the key suspects in the reward pathway is the D2 receptor, which Kenny’s group thought may become deficient in the full-time junk food rats. So they experimentally “knocked down” the D2 receptor to see if it would accelerate the process of crashing the brain reward system.

And it did: when the D2-receptor deficient animals were offered free-for-all junk food, they snapped into an addiction-like response, he recalls. “Almost immediately [the rats] had a crash in their brain reward systems, it happened almost overnight, and they were compulsive almost immediately as well.”

So in essence, their lab data show that when you combine a knocked down D2 receptor with an environment that promotes obesity, you have lit the fuse for a big bomb – in rats at least. Kenny also notes that other work has linked low D2 receptor activity with a higher risk of obesity in humans.

When the “rats on cheesecake” study was published in Nature Neuroscience earlier this year, it generated discussion around the contentious issue of linking food addiction and obesity.

One comment piece carried by the same journal warned that “ . . . parallels between drug and food ‘addiction’ should be drawn with caution”.

Kenny agrees the topic is a controversial one and the rat model lacks some of the brain structures and social drives that crop up in humans and may influence behaviour.

“The whole concept of an addiction to food really rubs some people up the wrong way, and I can totally understand that,” he says. “But we are trying to take some of the stuff we know from addiction and see if those systems are involved in obesity as well.”