Humans have an intimate relationship with sugar — from birth to adulthood, we crave the sweet stuff more than almost any other food. But our love of sugar may go beyond that of a simple craving — maybe it’s time we looked at sugar like an addiction.
That’s the upshot of a recent research published in Scientific Reports. In an experiment done on mini-pigs, they found that sugar can affect the brain’s reward system in a “manner similar to that of drugs of abuse” the authors suggest.
Whether sugar is addictive in and of itself is not settled science, Anne Landau, the paper’s senior author, tells Inverse. Instead, the findings show it alters the brain in a way that places it in notorious company.
“Sugar alters brain circuitry in ways that are similar to, for example, cocaine, which is well known to alter the dopamine and opioid systems in the brain,” she says.
Sugar’s influence on reward
Sugar’s impact on the brain’s reward system boils down to how it affects two types of receptors in the brain.
The first set are dopamine receptors — dopamine is a central player in the brain’s reward system, released during pleasurable activities. The second set are opioid receptors, which are also found all over the brain, but are particularly found in areas involved in eating-related rewards.
In the study, the sensitivity of both receptors is dampened when pigs were allowed unrestricted access to sugar water for one hour each day for twelve days. The pigs were also fed a normal diet, so sugar consumption was superfluous to their caloric needs.
After the fist day, the scientists noted that sugar intake had lowered the “availability” of opioid and dopamine receptors in the pigs’ brains. Sugar essentially dampened the ability of these receptors to bind to their natural counterparts, the results suggest.
Overall, the availability of both types of receptors was reduced by 14 percent in the anterior cingulate cortex and the nucleus accumbent — both areas of the brain associated with reward.
At the end of the 12 days, the scientists found that the pattern held — the availability of both types of receptors continued to decrease significantly.
In a statement, Michael Winterdahl, the study’s first author, suggested that this change in receptor availability could hint at sugar’s addictive nature.
“If sugar can change the brain’s reward system after only twelve days, as we saw in the case of the pigs, you can imagine that natural stimuli such as learning or social interaction are pushed into the background and replaced by sugar and/or other ‘artificial’ stimuli,” Winderdahl said.
Is sugar really addictive?
The finding doesn’t reflect well on sugar, but there are some caveats. To image the pigs’ brains, the scientists had to sedate them with ketamine. Past studies in primates suggest ketamine can reduce the availability of dopamine receptors, and that effect may be reflected in these results.
Also, just because sugar can induce changes in that brain’s reward system, it may not be addictive in the same way as drugs like cocaine.
Cocaine is famous for blasting the brain full of dopamine. It blocks a transporter in the brain that clears dopamine away, allowing it to accumulate and create a euphoric high.
The study doesn’t look at any of the other hallmarks of addiction, which is why it may be too soon to place sugar with such nefarious company.
The results contradict other research suggesting sugar isn’t neurochemically addictive, and that binge-behavior related to sugar arises because animal studies often restrict access to the tasty treat.
“We don’t want to go as far as to say that sugar is addictive. We haven’t studied behavior in the pigs or looked at withdrawal,” Landau. says
For now, the study adds some solid footing to the anecdotal experiences of people who feel that their battle with sugar is a more than just a craving, but the science itself is far from settled.
Excessive sucrose consumption elicits addiction-like craving that may underpin the obesity epidemic. Opioids and dopamine mediate the rewarding effects of drugs of abuse, and of natural rewards from stimuli such as palatable food. We investigated the effects of sucrose using PET imaging with [11C]carfentanil (μ-opioid receptor agonist) and [11C]raclopride (dopamine D2/3 receptor antagonist) in seven female anesthetized Göttingen minipigs. We then gave minipigs access to sucrose solution for one hour on 12 consecutive days and performed imaging again 24 hours after the final sucrose access. In a smaller sample of five minipigs, we performed an additional [11C]carfentanil PET session after the first sucrose exposure. We calculated voxel-wise binding potentials (BPND) using the cerebellum as a region of non-displaceable binding, analyzed differences with statistical non-parametric mapping, and performed a regional analysis. After 12 days of sucrose access, BPND of both tracers had declined significantly in striatum, nucleus accumbens, thalamus, amygdala, cingulate cortex and prefrontal cortex, consistent with down-regulation of receptor densities. After a single exposure to sucrose, we found decreased binding of [11C]carfentanil in nucleus accumbens and cingulate cortex, consistent with opioid release. The lower availability of opioid and dopamine receptors may explain the addictive potential associated with intake of sucrose.