By Kevin Klatt @nutrevolve
The concept of food addiction is of particular relevance to field of nutritional sciences. The conversation in popular media describes food addiction as though there is scientific consensus surrounding the topic. However, its lack of inclusion in the DSM-V leaves many evidence-based practitioners skeptical about using this kind of terminology. To understand this disconnect, I reached out to Jennifer Nasser, PhD, RD, to hear a researcher and clinician’s perspective on this controversial topic.
Dr. Nasser is an associate professor in the Nutrition Sciences Department at Drexel University’s College of Nursing and Health Professions. Her research focuses on the neurobiological aspects of food intake and preference. Her current research uses the non-invasive functional near-infrared spectroscope (fNIR) to measure brain activity under varying nutrient and metabolic conditions.
Q: Documentaries like FedUp, books such as Wheat Belly and seemingly countless articles circulating the internet throw around the term ‘food addiction’ as if it’s fact. What are your thoughts on the term ‘food addiction’?
A: The problem with the term “food addiction” is two-fold. One problem is that it is defined differently by different groups of people interested in the topic, i.e. the lay consumer uses addiction to describe “loss of control” over anything, but especially their favorite foods; the clinician uses the term to couple “loss of control” and feelings about “loss of control” with social and health consequences; and the behavior pharmacologists don’t use the term because of its clinical associations, rather they focus on the behavior and neurobiology associated with the five domains that characterize “drug addiction”:
Dependence = how difficult to quit
Withdrawal = presence and severity of symptoms in absence of substance
Reinforcement = ability to promote use over other substances i.e. “loss of control” over use
Tolerance = how much is needed to satisfy increasing cravings and level of stable need
Intoxication = mind altering stupefaction, excitement or euphoria that renders a person unable to act competently.
These domains are all based upon the principle that there is no “natural” satiety system for drug use and no beneficial need for “addictive” drugs. This brings us to the second and more important problem with the term “food addiction”, namely that there is a built in system meant to control food intake in the body and there is an obligatory need to consume food. Consequently, any determination of “food addiction” must be made while controlling for the contribution of the natural control system and need for food and nutrients.
Q: What is the neurobiological basis of this?
A: Many neurobiological systems are involved in controlling food intake. There are different orexigenic and anorexigenic peptides (with brain and gut sources) involved as well as neurotransmitters in the brain that contribute to the desire for food. Examples: orexigenic peptide- ghrelin, some endogenous opioids and endocannabinoids; anorexigenic peptides- leptin, glp-1, cck, amylin; neurotransmitters- dopamine, serotonin, norepinephrine, acetylcholine, endogenous opioids and endocannabinoids, gaba, glutamate.
Q: Is there a gold standard technique in this research? What lines of evidence will be required to prove/disprove that individuals may struggle with food addiction-related behavior?
A: The DSM-V committee that focused on addiction declined to add “food addiction” as a recognized mental illness stated that there is not definitive evidence for its addiction. One important piece of missing information is which nutrient(s) form the basis for the addiction. Is there just one “addictive” component to food? Is the addiction to the social associations surrounding food?
With respect to a gold standard technique: reinforcement by operant responding is used to determine the relative reinforcing value of drugs and to get them classified for addiction potential. Some people have published food reinforcement studies, myself included. However, if you compare across these studies you find that some are done when people are fasting and a few are done in the satiated, fed state. The results vary depending upon the feed status of the participants and there’s not agreement yet in the field as to the proper conditions for defining addiction potential of various foods.
Q: I’ve seen many argue that sugar lights up the same areas of the brain as addictive drugs, and, from this, conclude that it too is addictive. Coming from an evolutionary biology background, it makes sense to me that pleasurable nutrients would show this response in the brain. I’m not sure how the primate tree of life would’ve fared if they stumbled onto fruit and thought ‘meh’. How do you distinguish between a normal physiological pleasure response to nutrients and addictive behavior?
A: Good point. As I said above, one way is to compare responses in the fed and fasted state. (See Nasser et al. Obesity 2008 16:1816-1820).
Q: I first heard about loss of control (LOC) eating while reading some nutrigenetic research looking at specific FTO genotypes (rs9939609) and their relationship with this sort of eating behavior. Do you think that certain individuals are more prone to LOC eating?
A: Possibly, in addition to FTO, there’s some evidence that there are differences in the dopamine transporter gene and D2 receptor genes that confer more susceptibility towards LOC.
Q: The whole concept of LOC eating seems to narrow in on processed foods. Do you think this behavior is independent of processed food consumption? The focus on just sugar seems to be a bit unscientific. Dosage and context of the whole diet are always factors in nutrition – is there research to show they matter with LOC eating? I know there has been other research on the same FTO SNP associated with LOC episodes that used higher protein intake to alter appetite.
A: The focus on sugar is backed by scientific evidence with respect to sugar being the important reinforcing component even in sugar/fat mixtures (see Naleid et al 2008). With respect to neurotransmitter release, both sugar and fat have shown dose response in relation to dopamine release. (see papers by Hajnal and Bello). Both of these studies have used rats.
Part of the problem of defining the causative substance still comes down to having an agreement as to whether we’re talking about domains/characteristics of “addictive” like behavior or we’re saying that “activation” of similar brain regions by food and drugs of abuse constitute “food addiction.”
With respect to protein and appetite, I think that again we need to have agreement that experiments to investigate “food addiction” need to use fed, objective calorically satiated participants. Protein is a good satiating and satiety promoting macronutrient. If we agree on a standard physical condition for our participants, we could then look at the relative reinforcing power of various food components with respect to the five domains of “addiction” and get some standardized answers. From there we can then make a collective decision as to whether the reinforcing and/or other domain characteristics seen under standardized conditions rise to a level of concern that needs to be labeled as food addiction.
Q: The IOM recently convened a panel on food addiction. What were the takeaways from this?
A: The IOM is going to release proceedings from their meeting soon, so I think it’s best to wait for the official version of the consensus of the meeting.
Q: If people are interested in this topic, what journals or labs would you specifically recommend following?
A: Journals: Appetite, Physiology and Behavior, AJCN, Biological Psychiatry, Neuroimage, Science to name a few.
There are a lot of people actively working in this field and I don’t want to not mention anyone, so I would suggest doing a PubMed search, and also a RePORTER search on the NIH website to find those funded to work in food addiction, LOC eating and binge eating, as well as addiction in general.
Q: What are your caveats to other scientists and clinicians with interpreting this research?
A: I agree with the DSM-V committee that we need to define the component(s) of food that promote addictive behavior. Additionally I think it’s very important to define “addiction”-related factors as those that occur in the fed, satiated state. Until we satisfy our natural nutrient needs, the concept of addiction is irrelevant. It’s the food intake and accompanying calories that are consumed beyond metabolic need that create the negative health consequences.
