Binge Eating: When Should We Call It An “Addiction”?

The recent New York City soda ban controversy has contributed to increased discussion about the “addictive” properties of sugar and its contribution to the obesity epidemic. While I do not deny that there is an overabundance of high-sugar/high-fat foods in the societal milieu, and that the rewarding properties of these foods encourages their overconsumption; I think it is a mischaracterization to refer to the typical overeating associated with the “obesity epidemic” as reflective of a widespread “sugar addiction” that millions have fallen prey to.

Stice, Figlewicz, Gosnell, Levine, and Pratt (2012) have recently released a review in Neuroscience and Biobehavioral Reviews entitled “The contribution of brain reward circuits to the obesity epidemic.” In the paper, the authors elegantly describe the overlap between food and drug rewards while also highlighting major differences.


Before discussing the parallels between food and drug rewards, we should first introduce some of the neurological correlates of reward processing in general. All stimuli of motivational significance elicit dopamine release in a subcortical region called the nucleus accumbens.

These stimuli can range from food, drugs, sex, and even social interaction.  This dopamine release is argued to act as a “teaching signal” that encourages further pursuit of the particular reward when it is encountered at a later time. Drugs markedly enhance this dopamine release, “hijacking” the reward system, and making drugs the most highly pursued reward. The “sugar addiction” crowd argues that sugar can confer similar effects on reward circuits.

When dopamine is released from one neuron, it travels a short distance between neurons (called the synaptic cleft) and binds to a dopamine receptor on the other neuron. The effect of dopamine is entirely dependent on the receptor that it binds to.

Moreover, different brain regions have different distributions of these various receptors, so the effects of dopamine release are not as simple as we often like to think they are.

(For more information on dopamine signalling, please check out Tetyana’s post here.)


Repeated consumption of both sugary foods and psychostimulant/opiate drugs is associated with (1) decreased dopamine D2 receptor binding in reward-related brain regions and (2) increased D1 receptor binding. Furthermore, obese mice, when compared to lean mice, show additional reductions in D2 receptor binding that correlate with escalating palatable food intake and weight gain. The relative activation of D1 versus D2 receptors is associated with encoding the reinforcing properties of ALL kinds of rewards (e.g., sex, food, drugs, social interaction).

Changes in D1 and D2 receptor densities is argued to be reflective of the brain’s attempt to maintain homeostatic balance of dopamine levels in response to the bombardment of rewards, like foods and drugs.


However, these changes do not necessarily justify claims of sugar addiction-induced obesity. The authors are quick to point out that it may not be caloric intake per se that contributes to the changes in D1 and D2 receptor densities. Rather, it may be that increased intake of tasty, rewarding foods induces changes in reward circuits that parallel the brain changes that occur with repeated drug use. But: this does not necessarily confer addiction, or even obesity.

Rats that receive limited access to palatable foods (and don’t gain weight) show the same pattern of increased D1 and reduced D2 receptor binding, Human studies indicate that individuals, regardless of their body mass, display enhanced activity in these same reward-related brain regions upon exposure to a tasty milkshake.

Thus, it is likely that intermittent access to sugary foods, regardless of overall caloric intake, induces neuroplastic changes in reward circuits that parallel changes observed with repeated drug use.

Perhaps some of the parallel findings in D1 to D2 receptor ratio changes between drug users and obese individuals are reflective of similar, binge-like consumptions of both food and drugs or an underlying propensity to attribute high value to all types of rewards. The more those rewarding substances are consumed, the more changes occur in the brain to counteract (and compensate for) the bombardment of the dopamine system by consumption of those rewards*.

Indeed, some obese individuals may truly display disordered eating patterns that have “addiction-like” components. But does repeatedly consuming calorie-rich foods really make all obese individuals sugar “addicts?” Myself and the authors of the Stice et al. review are skeptical.

While overconsumption of high fat foods may contribute to addiction-like binge eating, I doubt that most obese individuals are really spending substantially less time with family and friends, skipping out of work obligations, and spending a majority of their time thinking about where to get their next sugar-fix? Some may argue that such behaviors do not develop because sugary foods are so readily available, and thus do not require significant life sacrifices be made for their procurement. Therefore, it is argued that binge eating is still “addiction-like,” despite obvious effects on day-to-day behavior.

Instead, I argue that the only binge eating that can truly be called “addictive” is that surrounding binge food intake among those with eating disorders, where individuals often obsessively restrict their food intake and then later binge on high-calorie foods. Like drug addicts, these individuals spend an inordinate amount of time obsessing over food intake and hiding their behaviors from others. They skip out on social interactions to engage in their behaviors.

Furthermore, the way these individuals overconsume food is not reflective of “mindless overeating,” just because tasty food is available at their fingertips; it is ravenous, compulsory, and abnormal. Sometimes food is even tossed away as an attempt to avoid further binge intake, and then subsequently consumed straight out of the trashcan when the individual “gives in” to the behavior.

Additionally, some eating disordered individuals who binge eating are known to consume foods that most individuals would avoid or find repulsive, a behavior known as “food concocting.” Concoctions can range from Oreos and mashed potatoes to hot sauce, peanut butter, and pancake mix. Most of the concoctions consisted of high fat foods or refined sugars and it has been argued that this behavior reflects neuroplastic alterations that enhance the hedonic value of food rewards in order to encourage sugar and fat intake during times of starvation (Boggiano, Turan, Maldonado, Oswald, & Shuman, 2013).  Indeed, concocting is also observed in famine victims.  The precise neural mechanisms of this effect remain to be elucidated.

I am in the camp arguing that it is the intermittent exposure to highly palatable, often sugary foods, often coupled with some compensatory food restriction and significant distress that results in food intake that can in any way be called “addictive”—not simple overconsumption of high-calorie foods. Both caloric restriction and intermittent sugar intake alter dopamine transmission in response to rewards (Corwin, Avena, & Boggiano, 2011), and intermittent—but not continuous—access to high-fat substances induces the typical “sawtooth” pattern of binge-restrict behavior in animals; reflective of human ED behaviors where individuals restrict food intake in between periodic episodes of binge eating.

Thus, perhaps it is the combination of these two behaviors, bingeing on fatty foods and subsequently attempting to restrict caloric intake, that produces an exaggerated response to food rewards and encourage compulsory food intake akin to compulsory drug intake.

Stice et al. do not go into the details of eating disordered behavior in their review, but they point out that most overeating is likely not a reflection of addiction, even if similar neural circuits are involved. What was most salient to me was that they acknowledge the public discourse regarding the pervasiveness of “sugar addiction.” In response, they mention that such a characterization can have the effect of trivializing the significant daily struggles and life consequences that those with eating disorders live with.

*EDIT:  However, changes in D1 and D2 receptor densities may not necessarily = addiction.  These changes occur in animals that repeatedly self-administer drugs of abuse, but many of those animals don’t exhibit drug withdrawal symptoms.  They also are likely to have not undergone stringent tests of drug pursuit in the presence of punishment, nor have many of them been tested for “compulsive-like” drug-seeking behaviors.  Perhaps these changes are indicative of a potential progression to the addictive state, but they may not necessarily indicate it.  Likewise, these similar changes in obese individuals do not necessarily confer a “sugar addiction” or “addiction-like” food intake.

For more discussions surrounding drug self-administration, the progression to drug addiction, and parallels between this developmental process and binge food intake, please visit another guest blog I recently posted in the “Memoirs of An Addicted Brain” website.


Boggiano, M., Turan, B., Maldonado, C., Oswald, K., & Shuman, E. (2013). Secretive food concocting in binge eating: Test of a famine hypothesis International Journal of Eating Disorders, 46 (3), 212-225 DOI: 10.1002/eat.22077

Corwin, R., Avena, N., & Boggiano, M. (2011). Feeding and reward: Perspectives from three rat models of binge eating Physiology & Behavior, 104 (1), 87-97 DOI: 10.1016/j.physbeh.2011.04.041

Stice, E., Figlewicz, D., Gosnell, B., Levine, A., & Pratt, W. (2012). The contribution of brain reward circuits to the obesity epidemic Neuroscience & Biobehavioral Reviews DOI: 10.1016/j.neubiorev.2012.12.001


Liz received her PhD in Psychology at the University of Toronto. For her PhD, she used behavioral pharmacology techniques to study nicotine reinforcement. Liz is interested in the neurobiology of addictive/compulsive behaviours. She hopes to teach psychoeducation courses and empower individuals to take charge of their own recovery with enhanced knowledge of the inner workings of the brain.


  1. I have some questions.

    I don’t know all that much about obesity. Do you have what the prevalence of BED (or I guess BN, as well) is among obese individuals? I would assume it is not really that high (<5%)? Just a guess.

    The argument that food is addictive and that that's what accounts for at least a considerable portion of the "obesity epidemic" makes me skeptical. Yes, food is tasty, but we have a complex system to regulate food intake. It is hard to believe it would go hay-wire in all--or even most--individuals who are obese.

    My hunch is that sedentary lifestyles, increased consumption of high-calorie foods/higher food portions (which is *not* in itself bingeing), and perhaps stress and poor sleep schedules explain more of obesity than the "food is addictive" argument. But again, I really don't know all that much about this--not as much as I know about AN and BN.

    What do you think are the differences (from a neurobiological and psychological perspective) between those who binge eat without compensation (reasonable restricting after doesn't count to me, because it is natural you wouldn't eat normally after consuming a ton of calories) and those who do, particularly those who vomit?

    A lot of addictive drugs are receptor agonists or antagonists, but is food like that???? Increased intrasynaptic dopamine and/or similar changes in receptor density ratios seems like a rather crude analysis of similarities. Which is basically what you said.

    Are there any withdrawal effects in quitting binge eating "cold turkey"?

    When it comes to bulimia, I also wonder if the addictive-like component has to do with bingeing, purging, both, or whether it varies among individuals (and temporally within individuals, too).

    It seems that you are saying that addiction should be categorized on a behavioural level, as opposed to the neurobiological (or dopaminergic, really) phenotype? Is that a correct conclusion?

    • All excellent points!

      -among obese individuals, the figures I’ve seen are around the 5-8% for BED. Perhaps this disorder is nuanced and hard to diagnose

      -in terms of the neurological differences between those that binge and severely restrict, as in anorexia-bulimia, and those that don’t severely restrict, I would say there may be some differences prior to the onset of the disease (e.g., anorexic individuals displaying more OCD-like behaviors). However, I do think that there is some commonality between intermittent binge food intake, subsequent decreased food intake, and the stress that surrounds it that confers common sensitizations of dopamine circuits. I guess the issue is that it is hard to model such variability in a preclinical models (i.e., rats).

      –In relation to foods and reward, you are correct to point out that drugs usually act as high affinity agonists at a few receptor subtypes (alcohol is probably an exception…dirty, dirty drug). Kent Berridge at Michigan and Anthony Levine at Minnesota have pointed to a significant role for opiates in the pleasurable aspects of food consumption. The stimulation of mu-opioid receptors inhibits the GABAergic projections to dopamine neurons (i.e., disinhibition), thus resulting in enhanced limbic DA release. This is pretty similar to other drugs, but yes, rather crude. We still need more information regarding exactly how transient DA release differs between food and drugs and the complexity of the neural networks involved.

      That leads me to your last point, I do think that we need a more comprehensive understanding of food AND drug rewards in order to accurately delineate between addictive vs. non-addictive states. It is notable to me that most drug self-administration studies in preclinical animal models do not involve measures of withdrawal symptoms and do not analyze pursuit of the drug in despite negative consequences. I can say that most animals in self-administration studies are likely not “addicted” to the substance (i.e., don’t really display substantial signs of withdrawal, albeit some studies do). We are still at a very crude level of understanding when it comes to the neurobiology of addiction. Sure, alterd dopamine transmission within striatal circuits is involved, but what about the specifics of altered network connections? How do frontal and striatal circuits really communicate in addicts versus non-addicts? I suppose I do still think a psychological perspective is needed in order to delineate between those that are addicted and those who aren’t.

      I also think it would be an interesting question to explore differences in addictive like components between those that binge and those that binge and purge. Purging is supposed to be reinforcing as well, but I haven’t seen anything as of yet regarding a synergy between the two behaviors on addiction-like symptomology. I’ll be on the lookout.

      Also, I don’t know about “cold-turkey” withdrawal effects. I guess the issue is that we all HAVE to eat, so it’s incredibly hard to remove that source of “reinforcement” at once, like you can with a drug. It’s incredibly hard to stop, that’s for sure! And heck yeah you can crave doing it.

      • What you write has reminded me of another important point: habit =/ addiction. Some things are hard to stop because we are used to doing them in a specific environment (as you know, of course). The environment itself is triggering, but that doesn’t mean the behaviour is addictive per se.

        I think there’s also a recency effect. I know that I am much, much more likely to binge and purge if I had done it a day ago, versus if I hadn’t done it for months. Some things also become a habit: a thing you have to do before bed. But say you stop doing it (like you go into treatment) and you don’t necessarily experience withdrawal or even craving (you can experience craving, of course, but I don’t think it is a must).

        On the point about purging being reinforcing. I would say that for me, it definitely is. I like the purging part as much as (if not more) than the bingeing part. I’ve written about this before: there’s a misconception that purging is this terrible thing we put ourselves through to get rid of the guilty calories. It is true sometimes, and it is true for me too, sometimes. But it is not necessarily true.

        I think purging is very anxiolytic and I look forward to that feeling after a purge. I’ve binged without compensation (any compensation) but I think the purging adds another component that makes the behaviour much harder to stop because it not only brings positive components to the ritual but it also makes bingeing almost consequence-free.

        And yeah, I really want to know the differences between individuals who binge eat but don’t restrict and those that binge eat and restrict (and I don’t mean severe restricting, but even mental rules about what they can and can’t eat that we know predispose individuals to a kind of black/white thinking, especially when they “screw up” and eat the “wrong” food).

        I would NOT say that bingeing = food addiction when you are depriving yourself of food! It is a survival behaviour. And I find I’m *much* more likely to binge when I mentally risk as opposed to actually restrict calorically but without mental effort (undereating by accident, but without rules about what I can’t/can eat, or an attempt to actually restrict intake.)

        • I’m glad you point out that habit doesn’t = addiction. Funny, several of us refer to “habitual drug-seeking” behavior in the addiction community. Basically, this refers to the pursuit of drug reward despite (1) the drug being devalued or (2) a change in the type of behavior that is reinforced to obtain the reward. As you may guess, this involves those dorsal striatal circuits that are also involved in habits. Thus, I suppose addictions have a habitual component, but not all habits are part of an addiction.

          In regards to your point about bingeing = addiction, it is really fascinating that you have a completely different opinion from me. I totally think bingeing is rewarding, at least during the start of the episode. I suppose it has something to do with the altered palatability of high fat foods that make them more reinforcing after a period of restriction. In fact, the whole behavioral sequence of restricting and then letting go was the reward for me. Then it escalated to a point where it was no longer reinforcing, but I couldn’t stop. I think that’s where the “habitual” component came in.

          I do find it interesting that food restriction is a good way to alter sensitivity to drug reinforcement in preclinical self-administration studies. Perhaps they are just replacing the reinforcement their bodies actually need (food) with an artificial one?

          • Well, I do think bingeing is rewarding–especially after a period of restriction. But it is hard for me to separate that from purging. It is physically rewarding, because I’m letting myself eat foods I don’t usually, or in amounts I don’t usually. But when I’d binge without compensation, it wasn’t nearly as rewarding. It was accompanied by guilt, shame, and regret. Bingeing and purging, not so much. I’m annoyed at myself, bored, regret wasting money on food, but I don’t feel nearly as many negative feelings. Sometimes none at all. Sometimes it is just a thing I do to release stress when I’m anxious: and it works. I am able to focus much better after, most of the time. It depends on a lot of factors, though.

            I mean, when you are “marathon” bingeing/purging. I don’t think any of it is rewarding or fun. It is all dreadful and food tastes like cardboard, but some of us can’t seem to stop. (Probably because, at least in part, of the blood sugar crash after a purge.) So, it is similar to habitual drug-seeking behaviour, I think, at that point.

            But at this point, it is really hard for me to separate those two. I like the feeling after a good purge to the point that I’ve binged on foods that I normally eat, that aren’t high-fat/high-carb, *just* to purge.

            But, there’s a thrill in bingeing after a period of restriction. I think it feels liberating, in a way.

            I guess I’m still left wondering about the differences between those who compensate and those who don’t–as well as those who restrict and those who don’t.

            So, someone who binges intermittently, with periods of restriction, craves the binge. But if someone were to eat high-fat/high-calorie foods on a regular/continuous basis, wouldn’t you say they’d crave it, too?

          • I would think that if there is a component of planning, stress-agitation before the binge, and then a transient sense of relief during the binge (perhaps coupled with feelings of guilt/shame afterwards), that would probably be more addiction-like. I think those individuals would also crave it too. I should have emphasized the stress coupled with intermittent palatable food intake. As we pointed out, that probably only reflects a few small proportion of the population that regularly overconsumes palatable foods (by overconsume, I mean in a energy-positive way). Thus, I hypothesize there are probably more similarities between binge/purge or binge/restrict individuals and those that regularly binge in a disordered way rather than the majority of those that may overconsume foods because they are tasty and available and make us feel good.

  2. Hi Liz, I disagree that binge eaters do not have “seeking” behaviours.

    I am a binge eater myself. I may reflect an atypical subgroup but I do have sessions that are in private when I decide to stuff myself.

    I could chose to spend this time outside, watching tv, with my friends, etc etc but I dont. During times of stress and loss of control it gives me great satisfaction – pleasure, almost sexual gratification – to go and buy a loads of unhealthy snacks and eat them all. It is not just the “high” but there are other psychological aspects. The feeling of being full, or over full. The “rebelliousness” of it. The completion – finishing everything. Very odd… interesting article!

    • I would actually agree with you that, what you describe, is reflective of a more addiction-like behavior (see response to Tetyana). My argument is that the binge eating that is present in a MAJORITY of individuals that regularly overeat is probably not reflective of disordered eating or evidence for a widespread “sugar addiction” epidemic coming to a body near you. It may be hard to switch to healthier eating patterns for the large majority of the population, because who wouldn’t want to eat fast food over salads? That’s natural. I just think it is a mischaracterization to portray pervasive bad behaviors as something reflective of the struggles that drug addicts and individuals with ED have been through.

  3. Tetyana- You wrote :” I Like the feeling after a good purge.”and that you look forward to the feeling that purging gives you, that it calms you,etc. I wouldn’t have listened to anyone years ago.In fact,I didn’t listen to my doctor when he told me that my teeth would all rot,or when I admired teeth of recovered bulimics and an eating disorder therapist who was a recovering bulimic -they all had such gorgeous teeth! It turned out their teeth were all FAKE.Did I listen?No,of course not.Trust me, when you’re having your front teeth drilled down into little “Sticks” then having them crowned with fake teeth, that “Good Feeling” you felt after a purge.the one to which you look forward,will be one you look backward to with deep regret. I realize you have an eating disorder,as do I,obviously,but it sounds as if you are almost romanticizing purging to me.

    • Hi DJS, I am not and was not romanticizing purging. I was explaining how I felt and what I experienced at the time.

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