- I find that when I start eating certain foods, I end up eating much more than planned.
- I find myself continuing to consume certain foods even though I am no longer hungry.
- I want to cut down or stop eating certain kinds of food.
- I have found that I have elevated desire for or urges to consume certain foods when I cut down or stop eating them.
If this sounds like you, you may be experiencing food addiction. These are a couple items from the Yale Food Addiction Scale1 (or the YFAS), a scale used to identify and measure addictive patterns of eating. Food addiction might be one reason “you can’t eat just one” Lay’s potato chip, and importantly, may be contributing to the Western World’s obesity epidemic.
Food addiction is a recently developing idea, and it’s still being debated in the scientific world (see here for a scientific journal review on the subject). However, many people outside of academia readily accept the symptoms as totally relatable. A study done by Malika and colleagues2 found that “not only do…women believe in the concept of food addiction, they embraced it.” When describing her own experience, one woman said, “I was addicted to food. I didn’t eat out of emotions, I didn’t eat for any other reason other than, I just had to have it.” Does this sound familiar? Take a second to think about the symptoms yourself. The following is a substance dependence checklist (bolded) from the fourth edition of the Diagnostic Statistical Manual, or the DSM-IV-TR, which psychologists in the United States use to assess and diagnose mental illnesses. This list was adapted from drug and alcohol addiction symptoms in order to measure food addiction symptomology and diagnose food addiction. I’ve annotated the list (italics) so you can see how these symptoms are assessed by the YFAS.
(1) Substance taken in larger amounts and for longer periods than intended; you may eat more than you mean to eat, or you may not stop when you want to stop.
(2) Persistent desire or repeated unsuccessful attempt to quit; you may find yourself yo-yo dieting, or being unable to cut certain foods out of your diet.
(3) Much time/activity to obtain, use, recover; you may go out of your way to find certain foods, or you may feel ill or guilty after eating and need to recover for some time.
(4) Important social, occupational, or recreational activities given up or reduced; you may avoid situations because you know that certain foods will or will not be there.
(5) Use continues despite knowledge of adverse consequences (e.g., failure to fulfill role obligation, use when physically hazardous); you may have a medical condition and eat certain foods even though they will aggravate your condition.
(6) Tolerance (marked increase in amount; marked decrease in effect); you may need to eat a greater amount of a food after a while in order to feel the same pleasure.
(7) Characteristic withdrawal symptoms; substance is taken to relieve withdrawal; you may get headaches or feel irritable when you cut out certain foods.
So how do you stack up? Of course, it’s a little more nuanced than just being addicted to all foods, as you may have guessed, and it’s not an all or nothing kind of thing, either. In the rest of this post, I’ll talk about the details of food addiction, where the idea came from, and what might be happening in the brains of those addicted to food!
Food Addiction Basics
One very important detail to understand is that not all foods are addictive. Think about a time that you strongly craved a certain food, or you went out of your way to satisfy a craving for that certain food, or you couldn’t stop eating that certain food even though you told yourself, “Just one more, and then I’ll stop…” Likely, these certain foods that you’re thinking about aren’t kale or broccoli, but rather chocolate or pizza. It is essential to make this distinction when talking about food addiction because of the inherent properties of certain foods. Everyone knows that fried chicken wings and soda doesn’t make up the healthiest diet, but it’s important to understand what makes these foods different than the others. The answer to that, from an addiction perspective, is all that added fat and sugar. This is what food addiction researchers call processing. These highly processed foods are the most associated with addictive-like eating behavior, and are most likely to alter your brain’s circuitry!
To understand why highly processed foods are implicated in addictive-like eating, let’s look at another substance that has been established as addictive. The coca leaf is a harmless leaf used for thousands of years by the indigenous people of South America as a chewable energy boost. However, once the leaves are dried and stripped, the energy-giving alkaline substance becomes isolated. This processed substance, cocaine, is highly rewarding, and without the protection provided by the other non-addictive materials in the leaves, it’s absorbed extremely quickly into the bloodstream, rather than being buffered by the plant fibers. This can lead to a more addictive-like response. (To write this, I had to Google search “how to make cocaine,” so I’m really hoping that the FBI doesn’t come knocking on my door anytime soon).
Like cocaine, highly processed foods are transmutations of their naturally occurring cousins. In natural or raw foods, there are natural sugars, such as those in fruits and vegetables, and oils, such as those in nuts and seeds. However, through boiling, mixing, pressing, adding, chopping, frying, you-name-it, the rewarding properties of foods become isolated and augmented. White sugar, for example, starts as sugar cane and must go through an extensive process of crushing, filtering, and boiling before it becomes the white crystals we all know and love.
One quantity of interest for food addiction researchers is called glycemic load. This is a measure of how quickly and how much a food affects blood sugar levels. Highly processed foods, like candy bars, have an extremely high glycemic load, meaning they cause blood sugar levels to spike and drop very quickly, like the way cocaine affects the body. Natural foods may have high sugar content (an apple has more than 20g of natural sugar), but the glycemic load is fairly low, because even though the blood sugar level rises quite high, it takes a while for it to rise and fall, similar to how raw coca leaf is processed.
Brain Stuff on Food Addiction
So what does “food addiction” look like in the brain?
First, let’s take a look at the neural framework of addiction in general, and why we think that this is a viable framework with which to talk about food addiction. (I have to show a little school pride and say that this theory originated at my alma mater, the University of Michigan). Kent Berridge and Terry Robinson proposed the idea of “incentive-sensitization4” (see abstract). Here are the basics of their model:
(1) Addictive substances can change neural systems.
(2) Usually, the changed systems are those associated with motivation and reward.
(3) These changes cause the brain to be “sensitized” to the substance and substance-related cues.
(4) The change in brain systems doesn’t affect “liking,” only “wanting.”
In food addiction terms, this means that the neural network responsible for motivation and reward are altered by highly processed foods, and this network becomes particularly sensitive to these foods and cues related to these foods, like a McDonald’s advertisement for crispy golden fries. (Yum, I might have to take a snack break soon). Importantly in this framework, wanting is not the same as liking. Let’s take the fries as an example, if I eat McDonald’s fries every day, I’ll probably get sick of them after a while. I won’t like them anymore. But if my reward network has been altered, now every time I drive by McDonald’s or see a McDonald’s advertisement I’ll be cued to want McDonald’s fries so badly that I’ll stop and get some, even though I’m so sick of McDonald’s fries.
So what does this motivation and reward network look like? Formally it’s called the mesocorticolimbic dopamine system, and it underlies all natural drives and desires, like food and sex. It’s made up of dopaminergic neurons, which are neurons that produce the neurotransmitter dopamine, which is known for its role in motivation and reward processes. These neurons start in the ventral tegmental area (VTA), and project to the nucleus accumbens (NAc or NAcc), the prefrontal cortex (PFC), and other areas in the forebrain.
Drug consumption hijacks this system and sends way more dopamine than the brain normally would from the VTA to the other areas in the system. According to incentive sensitization, the more this process occurs, the easier it is for dopamine to be released in response to drug consumption or cues4.
But what does this have to do with food? Well, eating highly processed foods and seeing food cues seems to hijack this same reward and motivation system. Let’s look at a 2011 study6, during which participants were scanned while looking at milkshake cues and drinking milkshakes.
When drinking chocolate milkshakes, as participants endorsed more addiction criteria from the YFAS, brain areas in the reward circuit “lit up” more, or showed more activity, indicating a greater reward response. In other words, more addicted individuals’ reward systems were different, and more sensitive, than less addicted individuals’. Participants with higher YFAS scores also showed more activation after anticipating the milkshake; when they were expecting a milkshake and then tasted the milkshake, the individuals with higher YFAS scores showed greater reward response than participants with low YFAS scores.
These results show us that addictive-like eating could be from increased anticipation of rewarding food, also known as wanting. These individuals may be more sensitized to food cues, as predicted by the incentive-sensitization model. This means that when someone who is addicted to a certain food sees a cue associated with that food, the reward process may start preemptively, getting ready for the reward to come. This drives motivation and increases the reward response to that food.
So What Does This Mean?
One current focus of food addiction is clinical, in order to inform therapeutic techniques for individuals who feel that food addiction is severely disrupting their daily lives. One of the next steps in food addiction research is to understand the extent to which this may affect “healthy” individuals, or those who do not have diagnosed food addiction. For example, investigating the possible role of food addiction in why diets fail so often.
Because of the implication this research holds for marketing and public health, this research could be hugely impactful on the regulations of advertisements and marketing of certain foods, especially in the United States, where regulations of food marketing are scarce. See how this research could affect public policy in the U.S.
What do you think? Does food addiction seem like a good model with which we can explain compulsive overeating and the inability to cut down on certain foods? Should public policies be changed because of this research? Comment with your thoughts!
1Gearhardt, A. N., Corbin, W. R., & Brownell, K. D. (2009). Preliminary validation of the Yale Food Addiction Scale. Appetite, 52, 430-436. doi:10.1016/j.appet.2008.12.003
2Malika, N. M., Hayman Jr., L. W., Miller, A. L., Lee, H. J., & Lumeng, J. C. (2015). Low-income women’s conceptualizations of food craving and food addiction. Eating Behaviors, 18, 25-29. doi:10.1016/j.eatbeh.2015.03.005
3Schulte, E. M., Avena, N. M., Gearhardt, A. N. (2015). Which Foods May Be Addictive? The Roles of Processing, Fat Content, and Glycemic Load. PLoS ONE, 10(2): e0117959. doi:10.1371/journal.pone.0117959
4Robinson, T. E., & Berridge, K. C. (2000). The psychology and neurobiology of addiction: an incentive–sensitization view. Addiction, 95(S2), S117-S91.
5Cass, D. (2011). Age Dependent Effects of Repeated Cocaine Exposure and Withdrawal on Cortical Activity. Eukaryon, 7, n.p.
6Gearhardt, A. N., Yokum, S., Orr, P. T., Stice, E., Corbin, W. R., & Brownell, K. D. (2011). Neural Correlates of Food Addiction. Archives of General Psychiatry, 68(8), 808-816. doi:10.1001/archgenpsychiatry.2011.32