Overeating and Obesity: Should we really call it food addiction?

Mar 21 2012 Published by under Addiction, Behavioral Neuro

Nature Reviews Neuroscience came out with a perspectives article today on overeating and obesity, and the evidence behind the food addiction model that is gaining popularity. It's an issue that I myself have given a lot of thought to: is there REALLY such a thing as food addiction that's just like heroin addiction or cocaine addiction? And if there is...what IS it? What are the criteria?

Ziauddeen et al. "Obesity and the brain: how convincing is the addiction model?" Nature Reviews Neuroscience, 2012.


(I suppose I could insert the mainstream media obligatory demeaning headless photo of an overweight person here. But you know what? It's demeaning. Source

EDITED: I have now replaced the sloth picture. I thought sloths were just adorable, and it didn't even occur to me that some people might interpret a baby sloth as "slothful" or "laziness" in this context. I really didn't mean that. Just wanted adorable. This kitten will do instead. Sorry, I really didn't mean to be offensive!)

Whether to call it "food addiction" is something that I have been intellectually wrestling with for some time. I see a paper showing that D2 receptors are decreased in the striatum of obese individuals, like you would see in cocaine addicted individuals, and I start to think the food addiction model may be the way to go. But then I see another study showing the opposite. Or I think of the severe impairments in function present in drug addiction...and overeating just doesn't seem to go there. Or I consider the fact that obesity does not necessarily mean that someone is "food addicted", and conversely, binge eating does not necessarily mean that someone is obese.

So it's very nice to see an article like this, which does a review of where the convincing and less convincing evidence lies, talks about the limitations of the addiction model, and then proposes directions for research and new clinical practice definitions to better fit the current evidence. And it happens to agree with a lot of my ideas of what we might call "food addiction", and what differentiates it from overeating, and especially what differentiates it from obesity.

There are two views for a model of food addiction:

1. Certain foods with high fat/salt/sugar overly engage brain reward systems, and behave in a manner similar to drugs of abuse.

2. Food addiction is a behavior resembling drug addiction seen in a subgroup of people with obesity, as defined by the DSM-IV.

These two views are not mutually exclusive, but the type of evidence available differs. They both rely on environmental factors like the increased availability of highly palatable foods (during my walk to the meeting where I surreptitiously read this paper under the table, I walked past no less than 5 fast food places and 2 Starbucks, increased availability indeed). The first relies more on neurobiological ideas of how drugs of abuse behave, while the second focuses more on the behavioral definitions of addiction as used in the clinic. The authors of this paper consider both perspectives, the evidence as well as the limitations.

Diagnoses in the Clinic

Here are the DSM IV criteria for substance dependence:

Tolerance: increasing amounts of drug required for intoxication

Withdrawal symptoms when the drug is discontinued, including depression, shaking, sweats, seizures, etc.

Persistant desire for and unsuccessful attempts to cut back or cease use

Larger amounts of drug taken than intended

A disproportionate amount of time is spent obtaining the drug, using it, and recovering.

Important social, occupational, etc activities are given up or reduced because of the drug.

Substance use is continued in spite of knowing and experiencing adverse consequences of use.

First, it becomes readily apparent that we are dealing with a small portion of the obese population. The vast majority of overweight or obese people do not binge eat, or even eat that much more than normal weight counterparts. The increased availability of food, decreases in physical activity, and other environmental influences are more than enough to create excess weight without addiction-style eating. When we talk about people who are exhibiting food addiction-like behavior, we are generally talking about people specifically who binge eat. These people may not necessarily be overweight, and so using a BMI in diagnosis isn't going to help here.

But back to the DSM IV for substance abuse. You can make some of these conform pretty easily to chronic binge eating. Binging on larger and larger amounts of food corresponds to tolerance, distress during dieting could account for withdrawal, unsuccessful attempts to cut use clearly corresponds to dieting, and so on.

But at the same time, all of these comparisons have drawbacks. For example, eating larger and larger amounts of food as a measure of tolerance requires a comparison between satiety (when you're full) and the intoxication shown with a drug. While there is some neurobiological evidence for reward (though not intoxication) associated with initial food exposure, it decreases swiftly as the person eating approaches fullness. Not only that, binge eaters regularly eat past the point of satiety, eat when they are not hungry, and continue to eat to physical discomfort, which doesn't relate well to the highs associated with drug abuse. For many of the criteria (particularly the last 5), there's no real established measure for when, exactly, food intake becomes harmful. There is no evidence of food withdrawal (though there is certainly evidence of craving). So while many binge eaters could meet three or more of the criteria of the DSM-IV necessary for a diagnosis of substance dependence (the most common being increasing amounts of food, unsuccessful dieting attempting, and eating larger amounts than intended), it's not clear whether those criteria which apply to substance dependence really apply to food.

So while some of these criteria may apply fairly well for people with binge eating disorders, they do NOT apply to the majority of people who are overweight or obese.

Biological Correlations

I often see (and blog about) new neurobiological and genetic correlations with binge eating and obesity that are similar to changes seen in drug abuse. With regard to genetics, there are some studies showing that family histories of alcoholism are associated with increased obesity risk. A polymorphism in the mu-opioid receptor gene associated with increased reward sensitivity is also associated with drug addiction. The personality trait of impulsivity is associated with both increase obesity risk and increased substance abuse risk. But some similarities in genetic predispositions don't necessarily mean that the clinical presentations of drug abuse and binge eating will present the same way in the clinic. Not only that, it doesn't mean that drug abuse and binge eating occur via the same mechanisms.

Mechanisms

Of course there are the much vaunted PET and fMRI studies. In many of these studies, the researchers focus on the D2 receptor, a receptor for the neurotransmitter dopamine, a neurotransmitter associated heavily with reward and responses drugs of abuse.

D2 receptors, in response to drugs like cocaine, are very predictable. D2 receptor levels in the striatum of cocaine addicts are decreased. Always. It's been so repeated it's practically gospel. You see decreased D2 receptors in response to drugs of abuse in humans, monkeys, rats, mice. If drugs of abuse behave this way, and food was acting as a drug of abuse in obese patients, you might expect to see similar decreases in D2 receptors.

And sometimes, yes you do. But sometimes you don't. The results have been highly variable, depending on the groups used. Results are similar for things like activity in various brain regions as assessed by fMRI: that is, highly inconsistent. Many people see changes, but there's no real pattern to them. There may be a distinct neurobiological underpinning to binge eating or obesity, but it doesn't appear to really match that of drug abuse.

And finally, there's the issue of the highly complex biological and environmental interactions that contribute to the development of obesity. The authors argue that the complexity of factors contributing to obesity means that it may be hard to isolate the causes behind food addiction. I'm not sure about this point, myself, as the factors that contribute to obesity (genetics, environment, social factors, access, etc) all apply pretty equally to drug addiction. But I think the point about a lack of consistency in imaging studies is a strong one to make. There is great consistence in the drug abuse literature as to what changes you see in addicts, but the consistency has been much harder to find in obese individuals. I wonder what would happen if you limited the studies only to binge eaters, regardless of body weight.

Animal Models

Animal models currently show the strongest evidence for food addiction. You can you specific schedules and highly palatable foods to induce an addiction-like phenotype in rats, where they will escalate food intake and exhibit binge-like eating behaviors. High sugar diets in this paradigm can even produce a kind of withdrawal state, with increases in headshakes and forepaw tremor (though this hasn't been seen in humans). The D2 receptor levels in these animals fall in a manner similar to that seen in cocaine.

But there are limitations here, too. While the rats given highly palatable food may seek it out, press levers for it, and binge...they don't become obese. They tend to decrease intake of their normal food instead (which may be an important difference between rodents and humans). Not only that, the paradigms required to get rats to self-administer food like this are highly specific, much much more so than you would see in any human. So while I think that animal models could make great strides in understanding human obesity, we have to be careful in making claims.

Where do we go from here?

So, given all these caveats...is there a place for food addiction? The authors think so, and I am inclined to agree. However, it needs to be much more stringent than the current model of food addiction that many people want to embrace (the idea that sugar makes you addicted or that being overweight means you have a problem). Changes need to be made.

First off, it's important to separate food addiction from obesity. Binge eating does not necessarily mean you are overweight, and being overweight does not necessarily mean that you binge eat. Ranking by BMI is not going to work.

Secondly, it's important to differentiate food addiction from substance abuse criteria, as so many of the clinical criteria for substance abuse don't really translate to food addiction. The authors call for a set of measurable behaviors which can be clearly defined, and which demonstrate a change from normal food intake to compulsive eating. I would make the criteria here similar to those of binge eating disorder (or even merge the two).

Finally, things will have to change in how we study "food addiction" in humans. Getting a bunch of people with BMIs over 40 and popping them in a scanner isn't going to cut it. In order to get a picture of what food addiction really is, we need to use the measures that we could come up with that apply specifically to food addiction, and study only those who meet those measures. Again, just categorizing by BMI does not mean you get the correct subset of people.

All this doesn't mean we should throw the food addiction model out with the bathwater. The animal literature and binge eating in humans show indications that the food addiction model may be a good one. What this perspective suggests instead is that we need to take a more careful approach in adopting the model, to make sure that we are, in fact, modeling the right things. By modeling the right things and coming up with a useful definition of food addiction, we may be able to create a consistent picture of what changes are taking place.

Ziauddeen, H., Farooqi, I., & Fletcher, P. (2012). Obesity and the brain: how convincing is the addiction model? Nature Reviews Neuroscience DOI: 10.1038/nrn3212

40 responses so far

  • Something I read a while ago really resonated with me, and that is that substance addiction has same roots as food rewards (not the other way around) ... bad metaphor, but drug abuse is food abuse on steroids.

    So no, there is not intoxication, nor do you see the same kind of withdrawal problems. But largely because of the constant exposure to the problem substances, suffering from other criteria (can't cut back, giving up other activities, continuing despite adverse consequences) can be just as debilitating.

    As far as are all the obese/overweight addicts, no, but I think it's important to look at this as a continuum. Does everyone who drinks become an alcoholic? No. But is there a pathway from social drinking to problem drinking to alcoholism? Maybe not if you don't have the genetics for it. But then, I don't think makers of alcohol have the same teams of scientists studying how to manufacture foods to enhance their addictive properties (ref 60 Minutes on food flavoring: http://www.cbsnews.com/video/watch/?id=7389748n).

    Food addiction is a terrible label. People aren't addicted to "food" ... or at least what most people have been eating for generations. But modern foodstuffs chock full of salt, sugar, and fat that until recently couldn't be eaten 24x7? I think there can be a whole range of responses to these, including addiction.

    • Scicurious says:

      See, the thing is that the salt/sugar/fat/processed foods model? There are only a few studies showing that that model produces obesity and self-administration in rats. In humans, it's generally too complex to effectively study. It may be the case that these foods can be a problem, but I don't want to jump the gun and immediately refuse to eat all processed foods and panic over addiction. We ALL eat them, some of us are overweight, but vast majority of us are not binge eaters. The rates of binge eating are much lower than people think (many people classify themselves as binge eaters without really knowing what the phrase means).

      Regardless, I think it's important to really define what we're looking at when we talk about food addiction, rather than immediately diagnose the 2/3 of the population that's overweight as having a problem, without clarifying WHAT the problem is and what about the behavior makes it a problem.

      • Yeah, I would never diagnose the entire overweight population as being "addicted" per se. But I do think there's a continuum of behavior. And whether that's really a linear thing or whether there are just overlapping factors is where I think it gets interesting.

  • Great post, but when you say:
    "While the rats given highly palatable food may seek it out, press levers for it, and binge...they don't become obese. They tend to decrease intake of their normal food instead (which may be an important difference between rodents and humans)."
    I wonder if there isn't a large group of people where it works the same way: the people that can eat cake/chocolate and don't become obese because they will eat a little less of their normal food. And in rats there is only a small proportion of animals that really become addicted to cocaine if you make the criteria more stringent (http://www.ncbi.nlm.nih.gov/pubmed/20576893).

    I personally think that just like a sub-population of people/rats will become addicted to drugs of abuse, also a sub-population of people (and maybe also rats) will become addicted to food. It's just a lot harder to define that population when it comes to food.

  • AnyEdge says:

    I don't know anything about the neuroscience of addiction. But I do know about being addicted, and about abstinence from an addictive substance.

    I can only say that I truly and sincerely hope that overeating is not a true addiction. Because my experience is that there is only one treatment for addiction: permanent and total abstinence. And that won't work for food.

    My heart goes out, very sincerely, to people with overeating problems. I can't imagine a way to overcome it, given that abstinence is not an option.

    • Most people who call themselves food addicts do not find all food problematic. Abstinence of trigger foods (often sugar and refined wheat) is certainly an option.

      I don't know that that is required, as I suspect that there's a threshold under which it doesn't register, but many folks can and do abstain if necessary.

  • Maia Szalavitz says:

    Nice analysis!!! I want to point out one error though: there is *no* brain change that is found *always* in all addicts, or even in all cocaine addicts. If there were, NIDA would be shouting from the rooftops about this very clear evidence of addiction being a brain disease, diagnosable via these changes.

    The reality is that some addicts have significant DA changes and some don't and nothing absolutely predicts recovery or ongoing addiction, only probabilities. The best predictors of recovery remain social factors like support or having a good job— not brain chemistry.

    A few additional comments: of course food reward is going to share the same properties as addictive reward: the brain evolved to make food "addictive" and not to make us into drug addicts. Drugs affect the reward system that there's to make us eat and have sex— they wouldn't work if they didn't. We get it backwards, as someone pointed out above, when we claim food is addictive because it affects the drug areas. No, drugs are addictive because they affect the food areas!

    Also, while the DSM criteria include tolerance and withdrawal, they are neither necessary nor sufficient to define addiction (you have to meet a certain number of those criteria but can exclude tolerance and withdrawal and still qualify). Cocaine doesn't produce much tolerance (in fact, it produces sensitization to some effects where a smaller dose produces a larger effect. sadly, this is for bad effects not good ones). It doesn't produce classic "physical" withdrawal symptoms either: just things like irritability, sleepiness and craving. Because you don't get "physically" ill when you kick (though of course the mental symptoms have physical correlates in the brain), Scientific American notoriously reported in the early 80's that it wasn't addictive. Obviously, this is not true and so not having tolerance or withdrawal doesn't mean something isn't addictive.

    Addiction is seriously, seriously complicated ;-)

    • Scicurious says:

      Fair point about nothing being found absolutely, but the D2 receptor decrease is about the closest that anyone comes. We certainly accept it in the animal lit that if you give a chronic stimulant, you WILL find a D2 decrease in striatum. I tend to think in terms of the animal lit here.

      Also, I don't know that food reward WILL share all the same properties as drug reward. I think they will, and do, certainly share SOME, but food intake has far more complexity to it even than drug intake, with appetitive hormones from the GI system helping to control food craving and intake in ways that don't happen with addiction. So I think there will be significant differences in the way we deal with binge eating and the things that we find because of this.

      Yeah, seriously complicated. :)

      • Maia Szalavitz says:

        Right, but the animal lit doesn't always show "addiction"— often times they are using animals forcibly given the drugs, not just animals who lever pressed and are more comparable to people with addiction. The fact that only 10-15% of people who use these drugs become addicted to cocaine and heroin is important to keep in mind here: even the most "addictive" drugs aren't addictive to most people!

        And sure, food reward is more complicated, but natural pleasure has to share the same underlying mechanisms otherwise you have to posit that we have brain systems that just sit there waiting for us to take drugs.

        • Scicurious says:

          Yes, the addiction lit has very strongly established that self-administration is the gold standard. The neurobiological changes associated with noncontingent administration differ in important ways.

          Of course I think the pleasure bit of addiction has the same underlying mechanism, it's obvious that we weren't born waiting for cocaine, but I think food has, well, more to it. Gut hormones in particular which control behavior, which drugs don't interact with.

  • Pascale says:

    I would argue that we are all "addicted" to food; as we evolved, systems that favored taking in calories when we could by rewarding us with "pleasure" allowed members of our species to survive later famine. Those who didn't want to gorge on honey when the hive fell out of the tree (or other fortunate times) might not have the reserves to make it through the lean times.
    My question is not why some of us eat more than we should; it's why some of us can stay so lean in these modern times of easy food.

  • [...] Scicurious, a neuroscientist and an excellent blogger, has read the article, and has a nice run-down.... Some of the ideas being discussed here overlap with Stephan Guyenet’s research. Some [...]

  • The Real Cie says:

    First of all, I have to say I am pleasantly surprised by the polite and respectful comments I see here. Usually when the words "obesity" and "overweight" are mentioned, you get a lot of "blah blah blah, bad fatties, blah blah" crap that should have been dealt with back in junior high.
    Both obesity and addiction are multifactoral. Some people who are obese do have eating disorders, some don't. And even with a binge eating disorder it can't be treated in exactly the same way that alcoholim or drug addiction is. A person can avoid alcohol or drugs. Everyone has to eat. And while it's easy enough to say "well, just avoid the high calorie, high sugar foods," that can be akin to saying to an alcoholic "go into the liquor store and just buy soft drinks and non-alcoholic beer." A person may be able to do the "right thing" when everything is going well, but when life is going poorly, resistance may be futile.
    I have theories that certain food additives predispose people to gaining weight more easily. Monosodium glutamate, for instance, has been shown to cause those who consume it to continue to be hungry.
    There is no easy answer to any of the questions posed. But I am glad to see articles like this where people are taking a respectful approach, and where the commenters do the same. Thank you so much!

  • Beth says:

    I want to point out that the "mainstream media obligatory " photo being referenced here was added by the editorial staff at Boingboing, and not by the author of that accompanying article. It is a weird and upsetting graphic that was posted without getting cleared by Guyenet first, and I very highly doubt it would have been included if it had been up to him. The absence of that kind of inflammatory imagery on his own blog is evidence of that. The topic of obesity tends to provoke emotional reactions, and I agree, photos like that do not help anyone. Unfortunately, as you point out, the media is not very sympathetic when dealing with obesity.

    That being said, thanks to Scicurious for a well written article, and thoughtful commenters.

  • Leah says:

    Personal experience: I am overweight and struggle with binge eating. When I ruptured my Achilles and had surgery to repair the tendon I spent 2-3 weeks post-surgery on hydrocodone. During that time my desire to binge evaporated. My husband hypothesized that the hydrocodone worked on the same receptors as the bingeing. I'd love to know if there's any research that supports this hypothesis.

    For me, bingeing definitely feels like an addiction to foods that are high in fat, carbohydrates, and sugar - you'll never find me bingeing on spinach.

    As for withdrawal, when I stop bingeing, I definitely become irritable because I don't have bingeing to help me cope and keep my mood stable. In a recent diet attempt I ate a more normal diet but allowed myself to binge on pre-selected relatively low-calorie food, i.e. blueberries, so I could at least get my fix of hand-to-mouth comfort. This seemed to help but but as with most diets, I couldn't sustain it and went back to bingeing.

    Thank you for the great summary of the article. It's exciting to see this type of research move ahead.

    • Scicurious says:

      Leah, your experience with hudrocodone makes me think of the genetics studies showing that some people with addictive disorders have opioid receptor mutations which make them more sensitive to reward, something mentioned in the article.

    • jt says:

      I knocked out a smoking addiction with a night of other, not quite legal substances. It surprised the hell out of me, but I figured it must have temporarily fried the receptors that demand nicotine. FWIW

  • Hi scicurious,

    Found your post via Boing Boing. Just a quick comment. Highly palatable food can and does produce obesity in animal models, a point that Ziauddeen et al recognized in their paper. I make rodents obese in the lab all the time with highly palatable food. The most effective means of doing this is the "Cafeteria Diet", which is just human junk food like cookies, pork rinds, chocolate, etc. Similar studies have been performed in humans by Eric Ravussin's group and the results essentially confirmed.

    What they said in the paper is that intermittent sugar or fat access doesn't always produce obesity, which is true. But if you provide highly palatable/rewarding food in unlimited fashion, the animals do become obese, even if they retain access to normal food.

    You can attenuate the fat gain that is produced via these diets by doing interventions (pharmacological or genetic) that dampen the responses of reward or hedonic circuits, suggesting that those circuits contribute to fat gain. That doesn't mean the animals are addicted per se, but it does mean that reward/hedonic circuit functions are involved in the fat gain. Cheers,

    Stephan

    • Scicurious says:

      Hi Stephan,

      Thanks so much for stopping by! As it happens, though I haven't covered your research specifically, I did do a post a while back on the "cafeteria style" diet:

      http://scientopia.org/blogs/scicurious/2010/03/30/dopamine-and-obesity-the-food-addiction/
      http://scientopia.org/blogs/scicurious/2010/05/05/cheesecake-eating-rats-and-food-addiction-a-commentary/

      I'm glad you clarified that your rats become obese, that was a detail I had forgotten and which is very different from the studies using just fat or sugar. Have you done any studies looking at self-administration of food (particularly things like progressive ratio scheduling) for increases in food "reward" or binge eating? I see that other studies have shown changes in D2 receptors, but do you see differences in reward related behaviors as well?

      And do you have a hypothesis as to why the combination of junk food is more successful at inducing obesity in comparison to other models like sugar or fat alone? I'm afraid I come at this from the drug addiction literature and thus I'm not so familiar with aspects of this work.

      Thanks again for stopping by!
      Sci

      • Hi Scicurious,

        Just read your posts. Good stuff. I think we're basically on the same page. I don't study reward specifically in my lab-- I study body fat homeostasis mechanisms in the hypothalamus. But casual observations lead me to think that our rodents are highly motivated to obtain the obesogenic diet (Research Diets D12492 60% fat (plus sugar) pelleted diet). Once they've been exposed to it a few times, if I place a pellet in their cage, they'll devour it at any time of day, even if they were just asleep, whereas they would typically ignore chow. They'll even grab it out of my hand whereas they would never do that for chow. There are studies showing that rats will endure extreme cold and foot shocks to get a cafeteria diet, even when regular chow is freely available.

        So to answer your question, we haven't done anything like progressive ratio scheduling, but the rats do appear to be highly motivated to obtain the diet. I don't know if it's been done with our pelleted diet, but I'm pretty confident I know what the outcome would be. In our hands, Wistar rats will double their body fat levels in about a week if you give them these pellets ad lib.

        The reason why the cafeteria diet is so much more fattening than diets that are just high in sugar or fat is pretty simple IMO. The cafeteria diet is much more rewarding and palatable, because it's composed of foods that were literally professionally designed to maximize reward and palatability in humans. Imagine ice cream without the sugar. Now imagine ice cream with sugar, but without the fat. Now imagine it with sugar and fat, but no flavor. Now imagine regular ice cream with a bitter flavor added. Imagine warm soda without any carbonation. Not as appetizing. The point is that the total reward/palatability value of foods depends on the sum of a variety of factors. These factors tend to be "optimized" in processed food, because if they weren't, they'd be out-sold by the nearby product that is.

        The cafeteria diet is the most accurate rodent model of human obesity IMO, because it's the only model that causes persistent hyperphagia like one sees in obese humans. Rodents fed these high-fat pellets (in our hands) overeat for about 10 days, but then their food intake returns to normal. They continue gaining fat, but it's due to increased feed efficiency (lower expenditure) rather than higher calorie intake. Caf diet-fed rats continue stuffing their faces indefinitely. In humans, if you measure carefully via doubly labeled water, body mass is highly correlated with calorie intake. Almost without exception, when relevant confounders are controlled for (gender, age, activity level), obese people both eat more and expend more calories than lean people. Maintaining an obese state requires a high calorie intake because larger bodies use more energy. The obesity epidemic has correlated with an average increase of ~300-400 kcal/d in this country.

  • Steven says:

    Being a former drug addict and food addict of the compulsive binge type, I can assure you that food addiction is very real. I was not obese as my body was quite resistant to obesity as obesity is only a symptom of the cause and one of many.

    I cured my addictions through lots of research on the subject, appropriate use of herbs, talk therapy and a raw food diet.

    Personally I feel the current model of addiction ignores the varying degrees of addiction only concentrating on the extreme end of the scale.

    The majority of people on the planet suffer from mild to moderate addiction. Why else would someone consume something that is bad for ones health, the environment and others whether it is socially acceptable or not?

    Addiction is caused by an imbalance in the brain of natural feel good chemicals which also act as neuromodulators. Major addicts have gene variations that minor to moderate addicts do not have which they are born with. Minor to moderate addicts create the imbalance by taking substances that mimic their own neurochemistry directly or indirectly. Major addicts push their already depleted brain circuitry to the extreme edge hence their extreme behaviour.

    These imbalances are quite easy to correct if you know how and treatments that are used to fight depression and OCD also work on drug and food addicts. The symptoms of addiction on health my be a little trickier depending on the severity of the impact that your particular addiction has had on you.

    The best place to start is to eat a nutrient rich diet (vegan), take the appropriate herbs and to correct your intestinal/gut flora imbalance with probiotics and vitamin b12. Gut flora is also responsible for the manufacture of feel good chemicals in the brain particularly serotonin. Approximately 90% of the human body's total serotonin is located in the enterochromaffin cells in the gut.

  • aidel says:

    Perhaps thinking of binge eating as one in the spectrum of compulsive behaviors (which can sure look like addiction) would be more appropriate. Obesity is such a complex issue -- not only are you dealing with the brain aspect, but also hormones, gut flora, socio-economic conditions, and I'm sure I missed some.

    Over the course of losing 100lbs, I have discovered that the number of calories I need to maintain a healthy weight is only 1200 (I'm 5'2"). Unfortunately, I still feel hungry if I limit myself to 1200 kcal and as a result have gained back 20 of the 100 lbs. Although I exercise, I'll be the first to assure you that the calories in/calories out model is FAR to simplistic. And I'm grateful that you didn't go there with this post!

  • Jim Kornell says:

    Anecdotal data point. A runner friend, no visible signs of obesity, not a binger, was a self-diagnosed food addict. Behaviorally he was fine (and he was not worried in particular about food-related behavior), but he explained to me that he thought about food *all the time* -- when eating breakfast he was already planning and fretting over lunch and how far away it was, how he would make it there, etc.

    • aidel says:

      Again, I would say that this is an example of the obsessive component of obsessive/compulsive behavior. Not exactly the same as addiction.

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  • […] of an obesity epidemic. But as behavioral neuroscientist Bethany Brookshire (aka scicurious) notes in this overview of overeating and obesity, should we really call it a food addiciton? Can it really and truly be said that […]

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  • […] at all. While binge eating and binge drug use might be comparable in some ways, they also have many differences in terms of access and social consequences. In the end, that night with the ice cream pint may be […]

  • Many people find help in Food Addicts in Recovery Anonymous. Some of us have been diagnosed as morbidly obese while others are undereaters. Among us are those who were severely bulimic, who have harmed themselves with compulsive exercise, or whose quality of life was impaired by constant obsession with food or weight. We tend to be people who, in the long-term, have failed at every solution we tried, including therapy, support groups, diets, fasting, exercise, and in-patient treatment programs.



    FA has over 500 meetings throughout the United States in large and small cities such as Boston, San Francisco, Los Angeles, New York, Charlotte, Grand Rapids, Atlanta, Fort Lauderdale, Austin, and Washington, D.C. Internationally, FA currently has groups in England, Canada, Germany, New Zealand and Australia. If you would like more information about FA, please check out our website at www [dot] foodaddicts [dot] org. If there aren’t any meetings in your area, you can contact the office by emailing FA at foodaddicts [dot] org, where someone will help you.

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