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.
BRIEF INTRO TO DOPAMINE SIGNALLING
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.)
SIMILARITIES BETWEEN FOOD AND DRUG REWARDS
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.
DIFFERENCES BETWEEN FOOD REWARD AND ADDICTION-LIKE FOOD INTAKE
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