Dopamine and Obesity: The Food Addiction?

Sci picked this paper today partially because it was handed to her on a platter by the fantastic Dr. Pal, and partially because today she is SO HUNGRY. She’s had a TON of food already today, and is still entirely ravenous. Maybe it was looking at this paper too long.
(Cereal break)
Anyway.
As I’m sure most of y’all out there are aware, obesity is a problem in the US. No one is sure whether it’s due to increased portion size, increased availability, decreased physical activity, changes in gut bacteria, issues with our behavioral approaches to food, or all of the above. But scientists have been working for a while not only to look at the effects of overeating and obesity, but also to look at what CAUSES these things in the brain and body. And today we present a paper on an interesting piece of this puzzle, one that Sci has had a good deal of interest in: the idea of overeating as an addiction-like phenomenon.
ResearchBlogging.org Johnson and Kenney. “Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats.” Nature Neuroscience, 2010.
special-k.jpg
(If we’re going to talking about food and addiction, behold Sci’s drug of choice)


A lot of us get a lot of good feelings out of eating. Eating creates feelings of pleasure and reward, which is obviously a pretty evolutionarily successful strategy. Not only that, foods that are of higher “value” to the body, like fats(butter), proteins (steak!), and foods high in calories (CHOCOLATE), taste better than those that don’t mean much (like celery).
Obviously, if something is going to give you feelings of pleasure and reward in the brain, it will probably use the system of pleasure and reward that you have conveniently set up for the purpose. The neurotransmitter dopamine (about which Sci does love to blog), is associated with feelings of reward, and is one of the neurotransmitters that gets highjacked by certain addictive drugs like cocaine. And so scientists have hypothesized for some time that, just as the dopamine system is dysregulated in drug addiction, perhaps it is also dysregulated in problems with other natural rewards, like food intake problems.
This isn’t a far fetched thought. The symptoms of severe binge eating disorders are similar to some of the symptoms of drug addiction. People who are severe binge eaters* will continue to overeat even though they KNOW it’s bad for them and even though society is not kind to those who are overweight. This is similar to drug addicts, who continue to take drug even though they get in trouble and even though they KNOW it’s a terrible thing to do. In addition, severe binge eaters will often try very hard to reduce their food intake, trying lots of diets, and consistently fail, which is very similar to many drug addicts, who try desperately to stop taking the drug, quitting or attempting to quit many times, and continuing to relapse.
With all these similarities, it might be a good idea to look at how chronic binge eating disrupts the dopamine system, a system closely associated with the rewarding feelings caused by drugs and food, and see whether chronic binge eating can cause changes that are like the changes caused by chronic exposure to drugs.
And for this, you need the fat rat.
fat rat1.jpg
(Sci would like to note that it makes her feel famous to google an image and find it…on her own site. So famous! I’m the #2 image search for “fat rat”!)
So they took some rats, and divided them into three groups. The first group (we will call them ‘chow’) got access only to normal boring old rat chow. The second group got limited access for 1 hour per day to a high fat diet, which is super tasty to rats (we’ll call them the ‘snackers’). The third group got their high fat diet cafeteria style, most of the day, every day (we will call them ‘fat’ because that’s what they got). They then asked a whole bunch of questions using these three groups of rats.
Question 1: Do “fat” rats have reward responses that are different from other rats?
Well first, let’s take a look at ’em.
food addiction 1.png
Above you can see the three groups of rats. You can see that the chow rats and the snacking rats (labeled “restricted” for restricted access) gained a lot less weight over time than the rats who got all the high fat food they could eat. By then end, the “fat” group weighed twice as much as the chow group!!! They also took in a much larger number of calories than the chow and snack groups, and most of their calories were in the form of that tasty, high fat food.
The authors then decided to look at how these rats responded to reward. For this they used something called “brain stimulation reward” or BSR. Scientists have known for a long time that if you put an electrode in an area of the brain called the lateral hypothalamus and run an electric current through it, you get an intense rewarding effect in rats. It’s so intense that rats will willingly press a lever for it, and will even ignore food, sex, and other nice things to press the lever.
But in this case, they found that the “fat” rats pressed MORE for BSR than the control rats did. The “fat’ rats had a changed response to reward. This change continued even AFTER the rats were taken off their high fat food.
Question 2: Ok, fat rats have changed reward responses, how does this connect with dopamine?
To answer this question, the scientists looked at the dopamine D2 receptor. This is one of the two types of dopamine receptors in the brain. More importantly, several people (including the current director of NIDA, Nora Volkow) have shown that people (and animals) who are addicted to cocaine have low numbers of D2 receptors, and that people and animals WITH low D2 receptors “like” drugs more and are more likely to abuse them. So, if binge eating were like drug abuse, we might expect D2 receptors to go in the same direction.
And sure enough, this is what they saw:
food addiction 2.png
Sci loves this figure in particular because you can see a lovely correlation. Ah, a picture indeed worth a thousand words. Or at least a healthy paragraph. As you can see, as weight goes up (the light, grey, and black dots), the levels of D2 receptor expression (in the gel at the bottom of the picture) go DOWN. So the far rats had changes in reward, and had LOWER D2 receptor levels!
And you might think that’s enough, and that is indeed a pretty little paper. But then these guys got GOOD.
Question 3: We know that the fat rats had lower D2 and changed reward responses. If WE lower the D2, will their reward changes and food intake go along with it?
Now, you might ask, HOW do you change the receptors in a rats head?! Well, we scientists are just that cool. There is a technique called viral-mediated gene expression. Basically (very very basically), you take a harmless virus (this one was a lentivirus), which is not much more than a protein packet with some DNA inside, that is capable of getting into animal cells. You take the DNA in the virus, and you split it up, and insert your gene of choice. In this case, they took a gene that would knock DOWN, or reduce, the amount of D2 receptors. Then you slip that DNA back in your virus (usually with an extra gene to make it glow all nice), and then inject that virus into the brain area you want. And you get this:
food addiction 3.png
That pretty green glow is where they injected the virus, and where the virus infected the cells. In this case, you’re looking at the rat striatum, which is an area in the dopamine system where reduced D2 receptors are linked with increased propensity for drug abuse. In this case, the virus they injected made the cells glow green, and ALSO knocked down the D2 receptors in that area (and ONLY that area, which is part of what makes it awesome). So now, these rats (new rats, not the fat and chow rats), had artificially low levels of D2 receptors in the striatum.
Then the authors did the same thing that they did with the first group, they had them do BSR. And the rats that had knocked down D2 receptors showed dysregulated BSR, just like the fat rats from before! Interestingly, these rats didn’t eat more, but they also had not previously been exposed to the high fat diet, and it’s possible that they just couldn’t handle as much food at a time.

Question 4: Do these fat rats continue to overeat even in the presence of punishment?

This is an important question to ask to make this work really relevant to the way that humans binge eat. To do this, you give a rat access to the high fat food, but you add in a painful foot shock (not one that causes damage, just short and painful). You pair the foot shock with a light. The rat will learn that the light means shock and will (presumably) stop eating. Sure enough, when the light came on, the chow rats and snack rats stopped eating. The fat rats, however, DIDN’T. Their food intake wasn’t sensitive to punishment anymore, something which may indicate that they will continue to overeat even though it’s bad for them. This ALSO worked when they tried it with the rats that had artificially knocked down D2 receptors, they also just kept on eating, showing that the decreased D2 receptors may have something to do with the way the rats were responding for food.
However, they couldn’t get the fat rats to binge eat, when they gave them a short term access. So the model isn’t perfect.
So what does all this mean?
All these data put together means that binge eating of highly tasty foods in rats causes changes in D2 receptors and reward systems which are similar to the changes seen following drugs of abuse. This could mean that binge eating in this model is similar to drug abuse in other models, and that changes in D2 receptors could be part of the similarities.
Sci likes this study for several reasons. First, it’s really complete. They started with getting the rats fat, looking at differences, and then seeing if they could induce the differences, and come up with a similar behavior. It’s a good study that way. It’s also good because they were able to play with receptor levels without using rats that were already a binge eating model, and without working with receptor knockout animals, which could have lots of other differences. This helps make the study design very clean.
And this study could be important. It makes a link between overeating and changes in D2 receptors (something that has been seen in humans), and suggests that this link is similar to changes seen with drug addiction, showing that chronic overeating and drug addiction could have some similar mechanisms. This could be very important in how scientists move forward in trying to treat chronic overeating in humans, and in how we approach the problem, as one of addiction rather than an unwillingness to get to the gym.
But it also highlights how difficult treating chronic overeating can be. Even if overeating IS just like drug abuse (and it’s probably different in several ways), it’s not something that is easily cured (and we haven’t cured drug addiction yet, which tells you how far we have to go!). After all, in the end, the goal for drug addicts is to QUIT, to cease drug taking entirely, or as much as possible. But you can’t ever QUIT eating. Instead, it’s something that needs to be moderated and controlled, which makes it almost harder to treat. But understanding some of the mechanisms behind it is one of the first steps to solving the problem.
Johnson, P., & Kenny, P. (2010). Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats Nature Neuroscience DOI: 10.1038/nn.2519
(*Keep in mind, when I’m talking about binge eating disorders, I am not talking about Sci’s extra bowl of Special K or your pint of ice cream that I know you picked up at the grocery store today and ate in front of the TV. No, Sci is talking about severe binge eating, people who simply cannot stop themselves, and who end up extremely overweight as a result, with corresponding quality of life issues, who are very often extremely unhappy. So don’t go taking the results of this study as proof that you’re a food addict. Some of you may be, but most of you probably aren’t.)

27 Responses

  1. this is interesting, but it seems importantly different from the human model: the fat rats would appear to have been caused to be that way by experimental design. A normal human adult in the US is basically in the position of the “fat” group: 24/7 access to high-calorie, high-fat, or otherwise desirable food. (Granted, it may be more or less ready to hand at any point or from person to person, but it’s available if you want it.) Yet only some become chronic overeaters; most don’t. Is there research in whether undifferentiated (beforehand) rats exhibit different responses to the availability of high-fat food? Did they try upping D2 receptors in “fat” rats or in knockdown rats and see if either group became less susceptible to overeating? That’s where the money would be in human-focused scienceπŸ˜‰.

  2. just a further thought– if we take the rats as somehow “normal” , and if the ones in that study really do show such a universal response to food availability, then your opener of “obesity is a problem in the US” seems somehow off, like saying “illiteracy is a problem in the US” because there are still some people who exhibit it. We seem to be doing much, much better than rats would in our shoes!

  3. It’s interesting to see that they look at the response from Binge eating, but what about what causes it in the first place? what causes the craving’s.
    I personally have had eating problems and have been up and down in my weight all my life, my major problem being craving’s and binge eating. at one point in my life I was having some depression and was prescribed Effexor. to my surprise once taking it my cravings and binge eating stopped.
    More recently I was diagnosed with ADHD and the ADHD medicine had close to the same effect (Just not as strong).
    Now if they could narrow down what active ingredient in these drugs is doing what is causing this and what part of the brain that it is affecting then maybe we could actually cure much of the obesity that exists today.
    Maybe much of our Obesity is simply a Chemical Imbalance?

  4. RodM: Actually, we already know how those drugs work to curb appetite, they are stimulants which act on the dopamine system, and one of their side effects is decreased appetite. But because they are stimulants, they have other effects as well, and it’s probably not a good idea to be giving them to everyone who wants to lose weight, though in extreme cases it might help. Also, some stimulant drugs (the most famous one is Phenfen) DO help you lose weight, but some of them have some nasty cardiac side effects which means you can’t take them in higher doses.
    And while some of obesity today may be a chemical imbalance, probably a lot of it is other factors, including food availability, reduced physical activity, and other things. Just fixing the chemical imbalance may just cover up the other things that are causing the problem.

  5. Makes me wonder if restoration of the D2 neurotransmitter levels would alter the reward/punishment response, so that the rats who became “binge” eaters started paying attention to the electric shocks. Obviously wouldn’t be a cure, but would give the rats a leg up on attempts to stop eating so much.

  6. Scicurious:
    I agree.
    Though we know that these drugs do help do we know exactly Why? do we know what “Chemical Imbalance” is being affected and what component of the drug is causing the reduced appetite and cravings?
    I know that this side effect does not occur for every body that takes these drugs. which might indicate that there is indeed a chemical imbalance. Is there a chemical in the Brain that many binge and overeater’s have less of the others? IF we look at this (Maybe we have?) then maybe we could one day find a treatment that would correct that imbalance with out the side effects of the drugs that are available? (after what Effexor did to my sex drive I would never recommend anyone to use it for weight loss!πŸ™‚ )

  7. These aren’t binge eaters! Binge eaters are the snackers, these are gorger fatty rattys.
    What’s interesting to me is that having yummyfatty food for one hour a day DIDN’T interfere with punishment. You can binge, gain weight, but still not be an addict if you just don’t get enough ben and jerry’s. Us cereal junkies may be ok. Phew.
    Also, why go through all the trouble of having an amazingly well honed lentivirus in a SPECIFIC part of rat BRAIN (I understand this is not ho-hum on the technical level!) and then NOT come up with something in the dopamine pathway to target for the fatty rattys to make them NOT fatty. Or maybe they tried that and it didn’t work?πŸ˜‰
    (also, sci, nagging detail… they didn’t put in a gene [aside from the GFP], did they? They put in an artificial miRNA, right?)
    And finally, sci, what’s the y axis on the one graph of D2 receptors? 800 what?
    And are “H” and “L” for a high and low group, and what’s the difference between them?

  8. becca, good questions.πŸ™‚ Perhaps they didn’t get to an upregulation of D2 to see if they could come up with a reversal (say putting it in the fat rats), that might be a future direction.
    And yes, not a gene, but I wasn’t about to explain the concept of miRNA in a paper about DA.πŸ™‚
    The 800 refers to body weight, 800 grams is the fattest rat. The H and L were for heavy and light groups respectively, they did a median split on the weights of each group and looked at D2 levels that way.
    RodM: We do know a good bit about why increases in DA caused by stimulants cause decreases in feeding behavior (we call it an anorectic effect). But the DA system is ALSO what is dysregulated in problems like drug addiction, and so just changing up the levels of DA in the brain is not a cureall by any means. Certainly the side effect doesn’t occur in everybody, but there are lots of variations in drug effect in individuals. I think that perhaps we will someday come up with a drug that does the things you suggest, but I also think that day is probably a long way off.

  9. http://www.scientificamerican.com/article.cfm?id=can-newborn-neurons-prevent-addiction
    have you seen this study? am trying to connect the dots here…
    if lack of newborn neurons can result in addiction to drugs, why not food?

  10. Sci – your scientific credentials are lacking showing it.
    Your interpretation of this scientific research is way out of line and no scientist, in particular a biological psychologist would accept your conclusions.
    Most important to the discussion of your errors is the issue of dopamine in the human. You treat it as if it was like water in the body and could be measured as such. It is not measurable. Secondly, to extrapolate excessive eating disorders with cocaine abuse or “addiction” is also completely out of alignment with scientific fact.
    Cocaine consumes the bioamines of the brain, a special reserve of amino acid like compounds, necessary for brain function. Depletion of the bioamines leads to depression in cocaine users. It has little to do with dopamine uptake or production from the perkinge cells in the fissure of Rolando.
    There is not a condition of cocaine addiction as there is heroin addiction, a true addiction. Cocaine addiction is related to the hypothalmus of the human brain, regulating pleasure.
    Thirdly, the rats in the experiment live in what my biological psychology professor at the University of California called “enlightened prison.” Cocaine addicts and food “addicts” live in a self regulating world of their own volition. Food consumption is connected to many areas of the body and brain, and registers “satiation.”

  11. Sci – your scientific credentials are lacking showing it.
    Your interpretation of this scientific research is way out of line and no scientist, in particular a biological psychologist would accept your conclusions.
    Most important to the discussion of your errors is the issue of dopamine in the human. You treat it as if it was like water in the body and could be measured as such. It is not measurable. Secondly, to extrapolate excessive eating disorders with cocaine abuse or “addiction” is also completely out of alignment with scientific fact.
    Cocaine consumes the bioamines of the brain, a special reserve of amino acid like compounds, necessary for brain function. Depletion of the bioamines leads to depression in cocaine users. It has little to do with dopamine uptake or production from the perkinge cells in the fissure of Rolando.
    There is not a condition of cocaine addiction as there is heroin addiction, a true addiction. Cocaine addiction is related to the hypothalmus of the human brain, regulating pleasure.
    Thirdly, the rats in the experiment live in what my biological psychology professor at the University of California called “enlightened prison.” Cocaine addicts and food “addicts” live in a self regulating world of their own volition. Food consumption is connected to many areas of the body and brain, and registers “satiation.”

  12. Christine: I’ll gladly take criticism where it’s due. But.
    “Most important to the discussion of your errors is the issue of dopamine in the human. You treat it as if it was like water in the body and could be measured as such. It is not measurable.”
    Um. Yes. It is measurable. I know many people who measure it all the time in various ways, and I can give you a large pile of citations on any method of your choice, including, but not limited to: electrophysiology for dopamine cell firing, microdialysis for extracellular and tissue dopamine levels in the living and post-mortem brain, PET imaging for dopamine receptor levels, and voltammetry for analysis of dopamine release and uptake in tissue and in freely moving animals. I would love to see a citation as to where you get the idea that dopamine is not measurable.
    “Cocaine consumes the bioamines of the brain, a special reserve of amino acid like compounds, necessary for brain function.”
    And here, Christine, is where I see your “scientific credentials are lacking showing it” as you put it. This is simply not true, and Sci has ample evidence. Cocaine blocks the dopamine, norepinephrine, and serotonin transporters in the brain, increasing the levels of these monoamines in the extracellular space, not ‘consuming’ them. These are not amino acids and they are not ‘reserved’ in any way. Even Wikipedia will tell you this. If you have ample evidence to prove your point, I’d love to see it. You’d turn the entire field of dopamine research on its head.
    “There is not a condition of cocaine addiction as there is heroin addiction, a true addiction. Cocaine addiction is related to the hypothalmus of the human brain, regulating pleasure.”
    1) Yes, there is cocaine addiction. See the DSM-IV. If that does not satisfy you, I can recommend a large number of reputable scientific articles on the subject.
    2) The hypothalamus does not regulate pleasure, in the human brain or in any other species as far as I know. It may have influence, but it is not the main area where cocaine exerts its effects.
    “Food consumption is connected to many areas of the body and brain, and registers “satiation.”
    Yes, but it is ALSO connected with areas of the brain associated with pleasure and reward, and those are the areas that Sci is concerned with here.
    In other words, Christine, you have asked no questions and have shown up with a pile of ‘facts’ that have no evidence to support them. Citations, or at least a reasonable attempt at logic, are needed before you attempt to criticize.

  13. Do they ever study other things that can make these D2 thingies behave differently? I think that’s a big part of human obesity and lack thereof. I like food fine — I’m Italian, so I have to. πŸ™‚ But I’m also thin.
    However, I like playing piano, making things, and messing around with my viola, too. Maybe the reason I don’t get food-addicted in an environment of high-fat, high-calorie foods is that I can get my brain-zing reward from other things. Rats can’t do that; they aren’t much on intellectual stimulation.
    I know that’s obvious, but I think that translating it to humans is a lot harder than people think, mostly because we can find equally visceral rewards in abstract mental things that don’t actually exist (like music for me), or in creating things that actually use up materials and energy. What is the equivalent for a rat? And what happens when that “eat a lot and get a chemical reward” system has a zillion other systems with which it interacts? Rats don’t have many other things to do other than eat and make more rats. Humans have a zillion competing urges, some of which are purely intellectual, and all of which can create equally satisfying rewards in the brain.
    Put this all together, and I’m not sure that rats will ever be a decent model for human behavior … Not until you find one that will put off eating or making more rats for a pointless pleasure that it discovered or invented on its own.

  14. Do they ever study other things that can make these D2 thingies behave differently? I think that’s a big part of human obesity and lack thereof. I like food fine — I’m Italian, so I have to. πŸ™‚ But I’m also thin.
    However, I like playing piano, making things, and messing around with my viola, too. Maybe the reason I don’t get food-addicted in an environment of high-fat, high-calorie foods is that I can get my brain-zing reward from other things. Rats can’t do that; they aren’t much on intellectual stimulation.
    I know that’s obvious, but I think that translating it to humans is a lot harder than people think, mostly because we can find equally visceral rewards in abstract mental things that don’t actually exist (like music for me), or in creating things that actually use up materials and energy. What is the equivalent for a rat? And what happens when that “eat a lot and get a chemical reward” system has a zillion other systems with which it interacts? Rats don’t have many other things to do other than eat and make more rats. Humans have a zillion competing urges, some of which are purely intellectual, and all of which can create equally satisfying rewards in the brain.
    Put this all together, and I’m not sure that rats will ever be a decent model for human behavior … Not until you find one that will put off eating or making more rats for a pointless pleasure that it discovered or invented on its own.

  15. Janis: It’s true, rats can’t play the viola (though it would be SO CUTE if they did), but you give a rat a wheel and the little dude will GO TO TOWN.
    But yes, you are right, translating to humans is never perfect, and drug self-administration in rats is not the perfect answer. It’s just a model. And models will always have problems. A rat is never going to be able to sell its grandmother for its next hit. But if you want to study the effects of chronic drug or food intake in the brain (which we do), or determine whether new drugs have rewarding or reinforcing properties (which we do), or try to find drug therapies to treat drug intake problems (which we do), a rat model can really tell you a lot. It can’t tell you everything, but it is certainly better than cells in a dish or nothing at all. The real trick, though, is to not over-interpret the data that the rat models give us, and to keep in mind that models can really only tell us so much.

  16. Wow, I wonder when they are going to get all of these D2 related drugs out on the market for treatment of addiction!

  17. You refer many times to the rats’ “high fat diet.” My understanding of the study (though I haven’t read the full paper) is that their diet was a junk food diet including Ho Hos, sausage, pound cake, bacon and cheesecake. Thus the diet was clearly also high in sugar and salt.
    I don’t disagree that the diet was high in fat; just think that saying “high fat diet” (like CNN did in their report) implies that fat is the culprit, when it may be one of the others or a combination of two or more.

  18. Hi Sci, I thoroughly enjoy your blog and the way in which you make research accessible. However, two minor remarks.
    * In figure A, you write that by the end the fat group weighed twice as much as the chow group. However, as far as I can see, the fat group gained twice as much as the chow group.
    * In the figure below figure A, it would have been helpful if you would not have omitted that the values on the y-axis are body weight. I know, it could be inferred from your text, but still…

  19. Hi Sci, I thoroughly enjoy your blog and the way in which you make research accessible. However, two minor remarks.
    * In figure A, you write that by the end the fat group weighed twice as much as the chow group. However, as far as I can see, the fat group gained twice as much as the chow group.
    * In the figure below figure A, it would have been helpful if you would not have omitted that the values on the y-axis are body weight. I know, it could be inferred from your text, but still…

  20. What is the research on the effects of starvation on the brain’s D2 receptors? Anorexia often changes over to binge eating over time, but it seems as though starvation shouldn’t do the same thing to dopamine receptors that binge eating does. I can understand how one eating disordered presentation can switch to the other over time on a human behavioral level, but I would be really curious to see what chemical changes are underlying this behavior change.

  21. I found it interesting to see that restricted access to rewarding food (“snackers”) substantially mitigated the behavioral and physical effects of the high-fat food.
    I wonder if that sheds any light on common social restrictions on “bad” behaviors (e.g. many people consider it socially unacceptable to drink early in the day, early in the week, etc).
    It also suggests there might be relatively palatable behavioral modifications that could be effective: giving up cake altogether is a hard sell, but restricting its availability to a limited time per day is feasible.

  22. I found it interesting to see that restricted access to rewarding food (“snackers”) substantially mitigated the behavioral and physical effects of the high-fat food.
    I wonder if that sheds any light on common social restrictions on “bad” behaviors (e.g. many people consider it socially unacceptable to drink early in the day, early in the week, etc).
    It also suggests there might be relatively palatable behavioral modifications that could be effective: giving up cake altogether is a hard sell, but restricting its availability to a limited time per day is feasible.

  23. Would Sci like to tell me where my TV is? I was unaware I owned one. :p
    Seriously, nice article.

  24. Would Sci like to tell me where my TV is? I was unaware I owned one. :p
    Seriously, nice article.

  25. Beth: Not sure where you’re getting the ho-hos. As far as I can tell, the high fat diet was actually Crisco, which is the rat’s high fat binge food of choice (really).
    Yvonne: Figure A, yeah. Oops. Thanks.

  26. Sci, regarding Beth’s comments – it says in the methods: “The cafeteria diet consisted of bacon, sausage, cheesecake, pound cake, frosting and chocolate, which were individually weighed before being made available to the rats”.
    I was reading the methods trying to determine the age of the rats when they were first given access to the junk food diet… I couldn’t find it exactly, but it sounds like given the time it took to acquire the rats, do the surgery, recover from surgery, and train them, they weren’t particularly young.
    The reason I was wondering – I was thinking about the rats with the decreased D2 receptors not over-eating. And thinking about how, in my own experience, people who grew up in households with healthy diets and relatively little access to junk don’t seem interested in junk when they are older… not just that they are used to not eating it, etc. – but when they do eat it they don’t seem to enjoy it in the same way and don’t seem to crave it at all, etc. I guess I’m just wondering what role age of introduction plays in this – that somehow your system could be “set up” to get a “jolt” from eating junk – but if you have relatively little experience with junk until a certain age, you don’t get this same jolt (and it would be much harder to develop that kind of system at a later age?). I wonder if people have done experiments like this – basically having the same 3 groups as this study, but with different ages – do the young rats exposed to the high-access junk diet develop a food addiction more quickly and gain more weight than older rats?

  27. Sci, regarding Beth’s comments – it says in the methods: “The cafeteria diet consisted of bacon, sausage, cheesecake, pound cake, frosting and chocolate, which were individually weighed before being made available to the rats”.
    I was reading the methods trying to determine the age of the rats when they were first given access to the junk food diet… I couldn’t find it exactly, but it sounds like given the time it took to acquire the rats, do the surgery, recover from surgery, and train them, they weren’t particularly young.
    The reason I was wondering – I was thinking about the rats with the decreased D2 receptors not over-eating. And thinking about how, in my own experience, people who grew up in households with healthy diets and relatively little access to junk don’t seem interested in junk when they are older… not just that they are used to not eating it, etc. – but when they do eat it they don’t seem to enjoy it in the same way and don’t seem to crave it at all, etc. I guess I’m just wondering what role age of introduction plays in this – that somehow your system could be “set up” to get a “jolt” from eating junk – but if you have relatively little experience with junk until a certain age, you don’t get this same jolt (and it would be much harder to develop that kind of system at a later age?). I wonder if people have done experiments like this – basically having the same 3 groups as this study, but with different ages – do the young rats exposed to the high-access junk diet develop a food addiction more quickly and gain more weight than older rats?

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