Food Addiction Model

Question 1

Arguments against food addiction

Answer 1

1. Not well-supported by strong evidence
2. Food addiction and eating disorders may not be distinct entities because there is overlap between them
3. Hypothesized neurobiological changes underlying food addiction have not been consistently demonstrated in humans
4. While rodent studies show addiction-like eating patterns in response to palatable diets, translating these findings to human behavior is challenging

Question 2

Arguments in favor of food addiction

Answer 2

1. Similarities between use of food and drugs for comfort/soothing/stress relief/etc, suggesting a parallel between food consumption and addictive behavior
2. Human functional imaging data has shown how energy-dense, palatable food can impact brain structures and circuits associated with reward, similar to drugs of abuse
3. Addiction should not be viewed as a single disorder related solely to the substance of choice, but use disorders should be a constellation of related syndromes
4. Clinical features shared between SUDs and difficulties in controlling food intake (eg. feelings of deprivation, relapse during abstinence, continued consumption despite negative consequences)

Question 3

How to move the field forward (6)

Answer 3

1. Dysregulation of striatal glutamate homeostasis by drugs, leading to synaptic changes and vigorous drug-seeking, might also occur with excessive food consumption.
2. Deficits in brain reward function seen with drug overconsumption might similarly occur with overeating, potentially involving common neuromolecular mechanisms.
3. Habitual-like and compulsive consumption patterns seen in drug addiction may also be relevant to overeating.
4. “Hypofrontality,” or reduced cortical control seen in drug addiction, might also occur with overeating, though its significance in obesity is unclear.
5. Overeating should be studied as a disorder of decision-making, similar to drug addiction, considering the value placed on different types of food.
6. Genetic studies indicate that genetic variants associated with substance use and obesity may be largely distinct, suggesting different underlying mechanisms.