Linking drug and food addiction via compulsive appetite

Abstract

Background and Purpose ‘Food addiction’ is the subject of intense public and research interest. However, this nosology based on neurobehavioural similarities among obese individuals, patients with eating disorders and those with substance use disorders (drug addiction) remains controversial. We thus sought to determine which aspects of disordered eating are causally linked to preclinical models of drug addiction. We hypothesized that extensive drug histories, known to cause addiction‐like brain changes and drug motivation in rats, would also cause addiction‐like food motivation. Experimental Approach Rats underwent extensive cocaine, alcohol, caffeine or obesogenic diet histories and were subsequently tested for punishment‐resistant food self‐administration or ‘compulsive appetite’, as a measure of addiction‐like food motivation. Key Results Extensive cocaine and alcohol (but not caffeine) histories caused compulsive appetite that persisted long after the last drug exposure. Extensive obesogenic diet histories also caused compulsive appetite, although neither cocaine nor alcohol histories caused excess calorie intake and bodyweight during abstinence. Hence, compulsive appetite and obesity appear to be dissociable, with the former sharing common mechanisms with preclinical drug addiction models. Conclusion and Implications Compulsive appetite, as seen in subsets of obese individuals and patients with binge‐eating disorder and bulimia nervosa (eating disorders that do not necessarily result in obesity), appears to epitomize ‘food addiction’. Because different drug and obesogenic diet histories caused compulsive appetite, overlapping dysregulations in the reward circuits, which control drug and food motivation independently of energy homeostasis, may offer common therapeutic targets for treating addictive behaviours across drug addiction, eating disorders and obesity.

Food Addiction: a Deep Dive into ‘Loss of Control’ and ‘Craving’

“…Investigation into the neurobiological mechanisms involved in compulsive behaviour driven by drugs and obesogenic diets using animal models found overlapping neuroadaptations [53]. In humans, neuroimaging studies have demonstrated that both food and drugs of abuse can stimulate dopamine-based reward pathways [54], providing support that FA may operate similarly to substance use disorders.…”

Sex differences in cocaine self-administration by Wistar rats after predator odor exposure

“…It has been suggested that increases in mesolimbic dopamine may suppress food consumption, similar to what is seen following administration of the dopamine type-2 receptor agonist, bromocriptine (Thanos et al, 2011). However, following acute cocaine-induced appetite suppression, rats display increased motivation for high-calorie food which may lead to “binge eating” in cocaine-experienced rats (Laque et al, 2022). Clinical and preclinical work suggests that subjects with a history of cocaine use consume more calories and more high-fat food, but they do not gain more weight than non-cocaine users (Ersche et al, 2013; Bane et al, 1993).…”

Pramipexole restores behavioral inhibition in highly impulsive rats through a paradoxical modulation of frontostriatal networks

“…Alongside their apparent reliance on aberrant dopaminergic mechanisms, the compulsive nature of ICDs, which is not without similarities with that of substance use disorders [11][12][13][14][15][16][17][18], has led to their conceptualization as a form of behavioral addiction [19][20][21]. Similarly to psychostimulant use disorder, the vulnerability to develop ICDs has been shown to be associated with a high impulsivity trait [14,17,[21][22][23][24], which is characterized by a tendency to act prematurely, without forethought or concerns for adverse upcoming consequences [25].…”