Introduction

Food addiction is a disorder in which impairments in dopaminergic pathways in the central nervous system lead to feeding behavior disruptions that contribute to overweight and obesity. Currently it is unknown which compounds may cause the neurobiological impairments related to food addiction. Objective: to analyze the relationship between the endocannabinoid system and food addiction from the prism of neurobiological and behavioral changes related to psychoactive substances.

Material and Methods

A scoping review of the available literature was conducted in database such as Cochrane, PubMed, Embase and Google Scholar, using MeSH terms such as: food addiction, endocannabinoids, nutrition, nucleus accumbens, hypothalamus, cannabinoid receptor type 1 and feeding behavior, from which sixty nine bibliographic resources were included.

Results

The endocannabinoid system activation can modulate the neuroendocrine regulation of appetite and satiety in the hypothalamus and thus increasing food intake, the activity of this system over the nucleus accumbens can intensify the sensorial properties of palatable food (high fat and high sugar), besides enhancing dopamine release in mesolimbic and mesocortical dopaminergic pathways, which may be related to behavior disruptions as impulsivity, craving, abstinence syndrome, tolerance and others, identified in food addiction and substance use disorders.

Conclusions

Food intake shown in people with food addiction may be associated with an increase of plasmatic levels of endocannabinoids agonists of cannabinoid receptor type 1, which would unravel a vicious circle that reinforce the palatable food intake originated in the stimulation of cerebral structures involved in dopaminergic pathways, and thus it would maintain an overactivation of the endocannabinoid system and would promote weight gain.

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