Is “junk” food addictive?

In the same week that (just in time for Easter!) we are (again) told that chocolate is “good for you”, come these depressing headlines:

Depressing not because of the news itself, but because of how that news inevitably is – has been, will be – abused by lazy reporting and lazy reading. True to the “addicts” that some of us apparently are, we look to the instant gratification of headlines and will happily regurgitate them at dinner tables, if not (even more depressingly) use them to explain away the need to take responsibility for what we put in our mouths. Francis Lam at Salon put it poignantly when he wrote that ‘seeing food in the dark light of addiction … filled me with a confused sadness‘, but I’d venture that many more people will be delighted at the news. Finally, we can point the finger at evil food (Good news, Mr. Creosote. It’s been the food’s fault all along!).

For those who missed the story, it involved three sets of rats. One group at rat food, one got evil fatty human food for an hour a day, and the third got unlimited access (nom nom nom) to evil fatty human food. Group 3 became obese, carried on eating despite electric shocks, and would rather starve themselves than eat from the “salad bar” when the evil food was removed. Their “addictive” behaviour was confirmed by lower levels of D2 dopamine receptors, which is similar to what happens to drug addicts, who need progressively more and more to achieve the same high. What remains unclear in the various digests of this story is the very important question of whether the rats who became addicted had some neurological imbalance BEFORE, or whether the food CAUSED it.

Sometimes the “democracy” of new media really is valuable, because in cases like these, we all actually have access to the original Nature Neuroscience report, which you can read for yourself here. I did read it, and as carefully as I could, though given my natural limitations in the jargon of rat experiments in Skinner boxes and phrases like ‘lentivirus-mediated knockdown of striatal D2Rs’, I can’t claim to understand it all. But I did understand this:

‘Notably, it is unclear whether deficits in rewards processing are constitutive and precede obesity, or whether excessive consumption of palatable food can drive reward dysfunction and thereby contribute to diet-induced obesity.’

In other words, to repeat myself, what remains unclear is the very important question of whether the rats who became addicted had some neurological imbalance BEFORE, or whether the food CAUSED it. This really is rather important, because if all the study showed was that rats who are perhaps already prone to addiction can become addicted to fatty food, then it really doesn’t tell us much at all, and it certainly tells us very little about food. Presumably, given the right conditions, these same rats could also become addicted to gambling, or to sex, or to the internet, or to counting sheep.

Unsurprisingly, there have been very few intelligent responses to the story, and they deserve to be pulled out of the cacophony. Here’s one, from The Atlantic:

‘There are a few things to note. One is that the authors do not know whether these brain dysfunctions (“the deficits in reward processing”) are a result of overeating, a result of the type of food itself, whether some unknown factor causes this type of response, or whether the brain is pre-wired (“constitutive “) to respond this way to any type of overconsumption. Also, the media has already up-regulated the story. When the press writes that something “may” be like something else, people tend to believe that the two are linked, and that a common mechanism is responsible for both things. We assume this because we assume that the media is telling us something new and relevant. This is unfortunate; we need be very careful in how we consume scientific studies, lest our brains become inured to the scientific method, which is provisional and careful and always open to revision.’

Another intelligent response, this one from Time, here.

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