• Sucrose is reinforcing and it promotes dopamine release independent of its taste.
• Drugs and sucrose have strong yet transient effects on the mesolimbic system.
• Addictive drugs severely disrupt brain plasticity after long-term exposure.
• No data currently suggest similar central adaptations following sucrose.
Obesity and obesity-related disorders are a major threat to public health. It has been suggested that food addiction is a valid clinical concept and that food addiction is a contributing factor to the obesity epidemic. Research involving restricted access ‘binge’ diets has shown that rodents will display sucrose-related behavior that is reminiscent of substance addiction, under certain conditions. A question that remains, however, is if food or certain components of food possess addictive qualities akin to drugs of abuse. The alternative is that ‘food addiction’ (or rather ‘eating addiction’) is not a substance use disorder in the sense that people are addicted to any specific substance or component of food, but rather an addictive disorder involving disinhibition of food intake in general that shares similarities with behavioral addictions such as problem gambling. Here we describe how sugar (a candidate addictive component of frequently consumed foods) has short and long term effects on the brain and compare this to how addictive substances functionally alter the mesolimbic dopamine system. We focus on this system since plasticity changes in the mesolimbic system have been implicated in the development of drug addiction. We conclude that sugar has a strong direct influence on the dopamine system, which underlies its profound reinforcing qualities. However, at present there is limited evidence to suggest that sugar intake induces plasticity changes comparable to those induced by drugs of abuse. Thus, based on current literature we propose that it is probably that the long term effects of sugar on the brain are both qualitatively as well as quantitatively different from those of addictive substances