The exact cause of food addiction is still unknown, and food addiction remains a highly debated topic. However, various hypotheses have been formulated both through preliminary in vivo animal and human studies.
It appears that drug and food stimuli impact similar regions of the brain (e.g., striatum, amygdala, and anterior insula), and share similar reward system pathways (e.g., dopaminergic, opioid, and cannabinoid systems). Notably, downregulating dopamine receptors (for example, by taking certain medications) might disrupt the reward system and trigger food addiction. The endocannabinoid system (ECS) also plays a role in modulating the brain's reward system and in regulating appetite. Conditions such as disrupted lipid metabolism, which is common in obesity, or an increased intake of polyunsaturated fatty acids (PUFAs), which is common in the western diet, can influence the production of endocannabinoids and the expression of cannabinoid type 1 receptors (CB1), which in turn promote both fat mass accumulation and appetite stimulation, the latter of which may lead to overeating. Obesity has been linked to a dysregulated ECS system, which may be influenced by food intake, and appears to be positively correlated with biomarkers of obesity. This suggests that food addiction in people with overweight or obesity could be linked to a heightened reward-system response to high-calorie/highly-palatable foods.[1][2][3]
Translating findings from animal studies to human conclusions is complex due to differing brain and body structures and the intricate human food and social environment, but animal studies can suggest pathways that might be involved in food addiction in people; these could then be explored and verified in clinical studies. For instance, rat studies exploring the potential addictive effect of sugar reported specific behavioral and neurochemical changes when sucrose consumption was stopped, including anxiety, nervousness, and an increase in body temperature, which are similar to the changes observed in drug-dependent rats when drug consumption is stopped.[1] Another rat study detected brain activity changes similar to those seen in drug addiction.[4]
Other studies found increasing evidence that food addiction may be connected to a disruption of the gut-brain axis and intestinal dysbiosis, which could have any one of a number of causes (e.g., prenatal and postnatal influences, breastfeeding, environmental factors, diet).[5]
Dysfunctional emotional coping mechanisms may also contribute to food addiction. One study showed that people with food addiction displayed significantly higher emotional eating scores, suggesting that eating excessively may be triggered by feelings such as loneliness, anger, fear, or sadness, in an attempt to overcome them.[6]