Having quite a large sweet tooth myself, I feel a bit hypocritical writing on the subject of excessive sugar consumption. However the importance of this message, not to mention the sheer fascinating nature of the topic, has prompted me to press on. There are reasons to believe that certain hedonic foods, namely those high in sugar, can qualify as substances that are at risk for addictive abuse, not just in the colloquial but also in the clinical sense of the term. Psychologists at Princeton University, lead by Dr. Nicole Avena, research sugar addiction using a sucrose solution in rats, and they have discovered several similarities between the neurochemical effects of sugar and addictive drugs on the brain. Researchers fed rats on an intermittent feeding schedule, depriving them for 12 hours before allowing them to eat from a sucrose solution in addition to their regular food chow. After a month of this schedule rats began to show binge, craving and withdrawal-like behaviors for the sucrose, whereas rats who had received only the food chow on this intermittent schedule, or had unrestricted access to food and sucrose, did not show these effects. The scheduling of the sucrose availability is crucial as it prompts them to develop binge-like behaviors, and is similar to the schedule used to develop cocaine dependency in rats. This means that after being deprived of the food or drug the rat will self-administer extremely large quantities of the substance once it is available again. This behavior tapers off once the animals are sated, but these binges will consistently occur after each period of deprivation.
Due to these sucrose binges adaptations similar to those that occur in cocaine addicted animals were seen in the rats' brains. The binges resulted in surges of dopamine being released in the nucleus accumbens, a key facet of drug addiction, and one that is linked to feelings of reward and novelty. Over time mutations can occur in these dopamine receptors, increasing the sensitivity of some types (D1 and D3) while simultaneously decreasing the sensitivity and overall levels of others (D2). This results in larger doses of the substance being required to achieve the same level of arousal and decreases the sensitivity of this region to other types of natural rewards. This occurs after abuse of both sugar and drugs and seems to be linked to the bingeing nature of compulsive consumption.
An increase in craving was also seen in the test animals, demonstrated by an increase in sucrose-seeking in rats deprived of the solution. This behavior was resistant to extinction, remaining over a month after the last exposure to sucrose, and was also maintained in the face of adverse consequences, a principle criterion for compulsive behaviors.
In addition to craving, researchers discovered that mice seemed to go through withdrawal-like symptoms when deprived of sugar. These included tremors, head shakes, and signs of anxiety and aggression, all symptoms seen in animals going through opiate withdrawal. These effects stem from a crash in striatal dopamine, accompanied by decreases in opioid receptor activation, as well as an increase in acetylcholine, a neurochemical that has been linked to depression. One explanation for the similarity between sugar and opiate withdrawal is the activation of the opioid system by both substances. High fat/high sugar foods have been found to stimulate the release of endogenous opioids in the brain, which is thought to be due to their rewarding and pleasurable characteristics and causes effects similar to the administration of synthetic opiates, though on a much smaller scale.
This overlap between opiates and sugary foods has also been seen in abstinent heroin users, who often quickly develop a strong affinity for sweets while in recovery. Candy and junk food come to replace heroin as recovering users' preferred drug of abuse, indirectly activating the opioid system, and ex-heroin users are known to hoard, binge, and go to extremes to seek out sweets after going off drugs. This phenomenon is referred to as "consummatory cross-sensitization", and occurs when dependence upon one substance leads to the rapid acquisition of increased intake or dependence on another. It suggests that the brain and these neurotransmitter receptors can become primed after frequent activation, and will therefore become increasingly responsive to other sorts of excitatory stimuli.
After the New York Time's recent embarrassing op-ed publication on "iPhone addiction" and the resulting backlash, I'm reluctant to use the term in reference to anything other than drugs. However, given the evidence above, I believe there is a convincing argument that our brains and bodies process large quantities of sugar in much the same way as we do drugs of abuse. This does not mean that anyone who eats a slice of cake will develop sugar cravings, just as not everyone who takes drugs becomes addicted to them. However, for individuals who suffer from binge eating disorder or other eating problems it may be possible that their brains and bodies have adapted to put them at a disadvantage for trying to cut back on unhealthy foods or lose weight.