Articlesummary with A learning model of binge eating: Cue reactivity and cue exposure by Jansen - 1998
Introduction
During exposure, the cue is presented and the associated fear and/or avoidance behavior is prevented. The hypothesis of this article is that craving and excessive eating (binge eating), just like fear and avoidance behavior, are triggered by a cue and can therefore be treated well with exposure. An eating binge is excessive eating in a short period of time in which the person cannot control this. There are strong feelings of craving before the binge and people feel guilty after the binge.
Cue reactivity
Binge eating can be seen as a drug addiction. Relapse is very common here. If one returns to a situation in which he or she used drugs after rehab, he or she is confronted with the memories of this and the craving gets bigger. Cue reactivity is the response one has to a cue. This behavior is usually classically conditioned. Cues, such as taste, intake rituals and the environment, that were almost always present during the use of drugs will ultimately predict the effects of the drugs. This is the same with binge food. Cues that are not always present during a binge have less influence on getting a binge.
Three models have been developed that have elaborated the relationship between drug addiction and classical conditioning. These models have one common assumption, namely that cue reactivity predicts relapse. Cues, the conditioned stimuli, provoke a reaction (cue-reactivity). This response is the conditioned response. The conditioned withdrawal model from Wikler states that the conditioned response (CR) is the same as the unconditioned state of withdrawal. The conditioned compensation response model from Siegel states that the CR is the opposite of the unconditioned effects of the drug. The conditioned appetite motivation model from Stewart says that the CR is the same as the unconditioned effects of the drug.
These three classic conditioning models about relapse state that if one associates cues from the environment (CS) with drug use (US) for a longer period of time, these cues influence drug use. They cause physical reactions in the addict, such as craving, which causes them to relapse more quickly into drug use.
Binge eating and cue reactivity
You can compare binge eating with a drug addiction. Here, food intake is the unconditioned stimulus (US), the metabolic response to food the unconditioned response (UR). Food cues, such as smell and taste, can become a conditioned stimulus (CS). These cues can evoke cue reactivity; these are the conditioned reactions (CR). It is assumed that the learned cue reactivity increases the chance of binge eating. A strong US gives a lot of cue reactivity (CR), which leads to strong conditioning.
Predictions
The assumptions of the classical conditioning model are:
- Food intake (US) in combination with strong cues from the environment (CS) lead to cue reactivity; a huge urge to want to eat.
- Just the thought of CS will lead to cue reactivity.
- The provocation of cue reactivity in normal eaters leads to an enormous urge to eat.
- Treatments that cannot lower cuereactivity have greater relapses than treatments that can lower cue-reactivity.
Cognitive behavioral therapy with in vivo exposure is the best treatment for bulimia nervosa. CBT breaks through classically conditioned reactions, because an objective of the treatment is to develop a normal diet. This reduces the relationship between cues and binge eating, because the type of food is now also eaten without the cues. Eventually the cue reactivity will decrease and with it the need to eat.
Cue exposure with behavioral prevention: Practical aspects
The learning model of binge eating states that cues from the environment elicit reactivity, as long as the cues are reliable predictors for binge eating. So as long as the CS is systematically strengthened by the US. The model predicts that cue-reactivity will be extinguished when the CS-US relationship is broken. This relationship is broken if one is exposed to the cues, but avoids the binge eating that normally follows. This form of treatment corresponds to the treatment for phobias and OCD. During the exposure the cues are presented, while eating is avoided (response prevention). The purpose of the exposure is to generate a strong eating requirement. A disadvantage is that the therapist is a safety signal during these sessions; a cue not to eat. The patient must ultimately also be able to do without the therapist.
The exposures work better in vivo than in vitro. Exposure works better with flooding when it comes to binge eating. It causes greater craving, so ignoring this craving has a greater effect than if the craving were to be less large. Exposures of 50-90 minutes work best. The exposure sessions must often occur and in rapid succession. Five times a week works better than fewer times a week.
Cue exposure with behavioral prevention: Empirical evidence
Drummond & Glautier (1994) found that subjects who underwent exposure had better control of their binge eating than subjects who received no exposure. They had less relapse and ate less. No differences were found in failure between the two treatment methods. However, Monti et al. (1993) found these differences. They found higher drop-out rates in the group treated with exposure and coping training compared to the control group that received standard treatment. Cue exposure leads to significant decreases in craving, while the physiological responses to cues did not disappear. Cue exposure works primarily for reducing the need to eat during treatment.
So there are two ways to break the relationship between CS-US. Firstly, let people induce craving and not eat it. Secondly, people eat what they eat during a binge in places where they would not normally eat it. The conditioning model predicts that cue does not reduce reactivity and craving when avoiding the cues. Only exposure of the cues in combination with prevention of binge eating will reduce craving.
Conclusion
The learning model states that cues that precede binge eating (smell, taste, etc.) become conditioned stimuli that elicit cue reactivity/conditioned reactions.
If people suffer from binge eating, they will also have a depression more quickly. It is not smart to combine cue exposure with antidepressants. Although antidepressants reduce craving, and therefore probably reduce cue reactivity, this also ensures that the association between cues and binge eating is maintained. As soon as antidepressants are stopped, the cue reactivity becomes higher again and there will be an increase in binge eating.
Patients with anorexia should not do cue exposure. Their binge food is the only food they eat. Patients with bulimia should also not do cue exposure. As a result, you learn to reject food and this can go on to anorexia.
The best treatment is a combination of cue exposure with interventions that aim to develop normal eating habits and eliminate dysfunctional thoughts. Binge food must be treated with cue exposure. Dysfunctional thoughts should be treated with CBT.
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