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NIDA researchers explain food addiction by showing how overeating can lead to changes in the dopamine pathways of the brain, and showing how these changes alter our ability to regulate impulses to eat
From the perspective of an MRI scanner, food addiction and drug addiction look similar.
Numerous brain imaging experiments have shown that drug addiction and food addiction lead to very similar changes to the functioning of the brain’s dopaminesystems. Based on this, researchers at the National Institute on Drug Abuse (NIDA) have developed a neurological model to explain how brain changes can lead to very unhealthy eating (food addiction).
Beyond eating from hunger, people eat to feel pleasure – and when we look at things at the neural level, we can see that eating highly palatable foods leads to activation of the brain’s reward circuitry, similar to the activation that is seen with the use of drugs and alcohol, along mesolimbic dopamine pathways.
Drug users who repeatedly stimulate these dopamine reward systems cause changes to the functioning and structure of the brain and these changes lead to behaviors and experiences which characterize addiction, such as compulsive drug taking, an exacerbated emotional response to drug cues (triggers and cravings) and a lessened ability to inhibit behaviors (an inability to resist urges to use). Addiction is considered a brain disease because of these neural changes which lead to compulsive negative behaviors.
In the NIDA food addiction model, vulnerable* people who repeatedly consume large amounts of highly palatable sugar or fat laden foods also over-stimulate dopamine reward systems and cause structural and functional changes to the brain which lead to a heightened response to food cues, compulsive eating and an inability to regulate intake.
*As some people experience food as more rewarding than others, are less able to resist temptation to eat appealing foods even in the face of potential weight gain and develop greater conditioned responses to food cues – some people are known to be more vulnerable to develop food addictions than others.
The Dopamine Model of Food Addiction
According to their model, people with food addiction and drug addiction have altered functioning across 4 basic types of brain processes and this altered functioning can be explained by changes to the structure and workings of various areas of the brain. The 4 brain processes altered by both food and drug addiction are:
Changes to reward and salience function
Changes to motivation and drive functions
Changes to learning and conditioning functions
Changes to inhibitory control and emotional regulation functions
Reward and Salience Functions
The brain’s reward and salience functions control how we pay attention and respond to positive and negative reinforcers in our environment.
People with food addictions show changes in the workings of this circuit to the effect that they are less able to successfully choose behaviors that will lead to long term positive outcomes and to avoid behaviors that will lead to long term negative consequences.
Food addiction altered reward and salience functions lead people to focus highly on the potentially rewarding aspects of eating and to rank the rewarding feelings of eating above most other potentially rewarding activities, (exercise, sex, etc.). This is very similar to how a person with an alcohol addiction learns to rank the rewarding feelings of alcohol above most other rewarding feelings. Since all people seek rewarding activities, it is not surprising that people who consider eating to be the most rewarding activity are prone to over-eating.
People with food addiction are also less able to focus on the negative aspects of their behaviors. Although an obese person might know of the health consequences of overeating, at the moment of eating the salience of these negative consequences is greatly overpowered by the salience of the potentially rewarding feelings associated with eating some highly palatable food.
So changes to the reward/salience circuit of the brain lead a person with food addiction to rank the pleasures of eating highly palatable foods above other pleasures and to lose the ability to effectively weigh the potential negative consequences of overeating against the likely positive rewarding consequences of eating something tasty.
Brain imaging studies have shown that people with food addiction show differences in the ventral pallidum, medial OFC and hypothalamus which likely account for the changes to the workings of the reward/saliency circuit.
Changes to Memory and Conditioning Functions
The repeated over-consumption of large quantities of highly palatable foods leads to changes in the way the memory and conditioning circuit in the brain functions.
Once food addiction changes the memory and conditioning circuit, exposure to food triggers an emotional memory and the expectation of a pleasurable reward. Exposure to stimuli associated with eating, such as the sight of a fast food restaurant, or sitting down to watch TV can also trigger emotional conditioning and a strong desire for a pleasurable reward.
These persistent emotional memories help to explain the cravings a food addict experiences for ‘pleasurable’ high density foods. Because food cravings are triggered by so many associative stimuli they can emerge with frequency and they can lead to binge eating even among people who are trying to change their eating behaviors.
Brain imaging studies show changes to the hippocampus, amygdala and dorsal striatum which explain the alteration of the functioning of memory and conditioning circuits.
Changes to Inhibitory Control and Emotional Regulation Circuits
People addicted to food show dopamine related changes in the dorsalateral prefrontal cortex, the orbitalfrontal cortex and the cingulated gyrus, all areas which are involved in emotional regulation and our ability to exercise impulse control.
Changes to Motivation and Drive Functions
Food addiction caused changes to the orbitalfrontal cortex, the dorsal striatum and the supplementary motor cortices cause an amplification in the drive to obtain food.
Studies show that when obese people are presented with a meal there is greater activation in prefrontal areas of the brain than is seen when leaner people are presented with that same meal and other studies have demonstrated that showing food cues to obese subjects will induce activation of the prefrontal cortex and the experience of food cravings.
When brain changes result in increased food cravings and an increased drive to get food and when this occurs in parallel with a high expectation for pleasure through conditioned memories, a decrease in the ability to weigh possible negative consequences and a decreased ability to inhibit eating , it is not surprising that food cravings often lead to compulsive eating and it explains in part why some food addicts will continue to eat even when they no longer describe the behavior as pleasurable.1