As you might have noticed, Sci is really interested lately in the concept of food reward systems, in particular the issues associated with the effects of binge eating on reward systems in the brain, and the issue of “food addiction”.
And Sci is not the only one who is interested. Lots of other people in the scientific world (not to mention people outside the scientific world) are interested as well. And in the same issue of Nature Neuroscience that published the paper that Sci covered on dopamine and obesity in rats, David Epstein and Yavin Shaham wrote a commentary on the very same article. Yavin Shaham (the last author and thus the big kahuna) is a big guy in the dopamine and addiction world, and is an important researcher at the National Institute on Drug Abuse.
And these guys have some good points.
Points that Sci (figuring others probably don’t have easy access to Nature Neuroscience) wants to share with you.
Here we go.
Epstein and Shaham. “Cheesecake-eating rats and the question of food addiction” Nature Neuroscience, 2010
So. To give some background. These guys who published in Nature Neuroscience, Johnson and Kenney, gave some rats a “cafeteria diet”. When Sci saw those words, she assumed (like many people who study this sort of thing might assume) that they gave them the rat version of a high fat diet, which means lots of stuff like Crisco (yes, really) and sugar pellets and other things rats think are tasty. But it turns out (Thanks to commenter Beth for pointing it out), it really WAS a high fat diet, including things like cheesecake and sausage and bacon.
(Yeah, like that)
Commenter Beth wisely points out that this means their diet was high not just in sugar, but also in fat and salt, which could be confounds. Sci thinks the sugar and the fat are both good things to have in this particular study (in terms of natural reward mechanisms), but I don’t really know a lot on how the salt could be a confound for the effects they are looking for (though it could happen).
Anyway, the rats got the rat diet of their DREAMS for a while, and then were tested for things that you would normally use when looking at addictive responses. They required more self-stimulation in a brain-stimulation task, painful shocks failed to keep them away from the food, and there was even a physiological mechanism (well, a partial mechanism). The fat rats, like cocaine addicts and some binge eaters, showed lower levels of the dopamine D2 receptor. The authors even found that if you knocked down the D2 receptor, you could induce overeating in normal rats. Crazy stuff.
So with all of this evidence (and several other papers in similar areas supporting it), should we cry “food addiction”? Well…possibly. In some cases. Maybe.
And that’s what this commentary has to say. And I think they’re right. It’s really easy to look at this and say “we can become addicted to food!”. But that’s not the same as “everyone who is fat is addicted to food” or “the obesity epidemic is because we’re addicted to food”.
First of all, there ARE true binge eaters out there, people who overeat so severely that it is pathological. But there are not a lot of them. Cumulative lifetime risk is 3.9{9f43b4361d9a125bc126dd2a2d1949be02545ec69880430bc4fed2272fd72da3}. If you add in people who “sometimes” binge eat, or who don’t quite meet the DSM-IV criteria in other ways, the number rises to 11{9f43b4361d9a125bc126dd2a2d1949be02545ec69880430bc4fed2272fd72da3}. But that doesn’t account for the 34{9f43b4361d9a125bc126dd2a2d1949be02545ec69880430bc4fed2272fd72da3} of the US adult population that is overweight. It accounts for SOME of them, but not all.
Also, eating too much may not always be a result of “food addiction”. Scientists are finding that the environment and foods you are exposed to in the womb and when young can have effects on some genes, and can possibly account for some people’s weight problems. Shaham and Epstein makes all the points, and the main point of these is there are lots of factors involved in obesity, and food addiction may be only one of them, and may end up being very minor for all that we know now.
They also note that “addiction”, whether it’s to a drug or to food or to anything else, does not altogether obliterate the issue of choice, which is something that underlies most current behavioral treatments for addiction. If the consequences are bad enough, some people CAN stop. Sci isn’t entirely sure whether she agrees with him on this point (especially because success rates for behavioral treatment for addiction aren’t very high, and imply that for some people, no consequences are enough and the capacity for choice may be very desensitized).
But the point that Shaham wants to make of all this is that we shouldn’t take the idea of food addiction as an “excuse” for bad eating habits. “it’s there and we can’t help ourselves” is, for most of us, not necessarily true. Additionally, unhealthy eating and food addiction should not be tied strongly to obesity. They may cause obesity, but they are not the ONLY cause. The guys have a final line:
We would be mistrustful of any summary simpler than this: given enough access to cheesecake and bacon, rats display patterns of eating that resemble those that account to some unknown degree for human obesity and these patterns seem behaviorally similar to, and share some neuro-physiological substrates with, patterns of drug self-administration and withdrawal symptoms that resemble those seen in drug addiction.
I don’t think they’re wrong, I think this is an important distinction to make. We need to be careful about how we define food addiction based on only a few studies, and to what degree we can take these findings in terms of public health. Unfortunately, that big honkin’ paragraph up there makes a terrible headline. “FOOD ADDICTION” on the other hand, makes a great headline. And Sci admit she’s used it herself. But Shaham has a good point. Food addiction probably does exist. But is it the cause of everything? Probably not.
Epstein DH, & Shaham Y (2010). Cheesecake-eating rats and the question of food addiction. Nature neuroscience, 13 (5), 529-31 PMID: 20421898
