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Sugar: sweet, tempting but dangerous

Only a really small fraction of us gets through a normal day without adding sugar to its standard meal. Just think about it for a second… Soft drinks, candies, cakes, cookies, pies, fruit drinks, desserts and milk products (ice cream, sweetened yogurt), even pasta…we are submerged by sugar-enriched food. Although obesity is undoubtedly a complex and a multifactorial metabolic disorder, increased sugar intake is considered one of the fundamental and principal factors of the current worldwide obesity epidemic.
A compelling body of evidence strongly suggests that high-sugar consumption results in profound neural alterations in critical brain regions involved in reinforcement and determining incentive salience of palatable food. In fact, the rewarding properties of sugar can modulate the activity of the brain reward system, the same neural pathway which is activated by drugs such as cocaine and amphetamine. The mesolimbic reward circuit is a collection of highly interconnected brain nuclei including the nucleus accumbens (NAc), the ventral tegmental area (VTA) and the amygdala that encodes emotional states such as anticipation of reward and motivation. Long-term consumption of highly palatable food can cause maladaptive modifications within the brain reward pathway. Modified cell morphology, altered synaptic plasticity and imbalanced neuronal homeostasis have been described following consumption of palatable food.

Intermittent access to sugar alters the amygdala

Among several brain regions, the basolateral amygdala (BLA), a specific nucleus of the amygdaloid complex, is known to influence reward learning and the association with adaptive, goal-directed and emotional behaviors. The BLA receives dopaminergic input from the VTA and sends glutamatergic projections to the medium spiny neurons in the NAc, a key structure of the mesolimbic reward circuit. In a recent study published in PLOS One, Shariff and colleagues (Queensland University of Technology, Brisbane, Australia) decided to examine the effect of short- and long-term binge-like sucrose consumption on the morphology of the BLA principal neurons using an intermittent-access two-bottle choice paradigm. Two bottles, one containing water and the second one containing 5% (w/v) sucrose, were presented simultaneously to the animals using a binge-access protocol. Surprisingly, the authors found that the total spine densities of BLA principal cells were not affected by binge-like consumption of sucrose.

Thus the authors sought to investigate whether sugar consumption was able to alter the general structure of the dendritic components of the BLA principal neurons. “Given that BLA principal cell apical dendrites receive distal glutamatergic inputs that play a pivotal role in the formation of emotional and associative memories, it is interesting to note that our study revealed significant restructuring of apical distal branches”, point out Dr. Bartlett, the senior author of the paper. In fact, decreased dendritic arbor length of principal neurons from the basolateral amygdala was detected in both short- and long-term sucrose consuming rats, thus suggesting a structural remodeling of BLA circuits. However, “whether long-term sucrose induced reductions in dendritic length and branching of BLA principal neurons (…) are associated with reductions in their excitatory activity and neuronal output is an interesting possibility that warrants further investigation”, report the authors.

Sugar and drugs of abuse

The same laboratory has previously reported that sugar consumption triggers a reduction of total dendritic length and an increase in distal spine density in the medium spiny neurons of the nucleus accumbens (Klenowski et al., 2016). This kind of cellular and morphological hallmarks have been also observed in response to chronic exposure to drugs of abuse such as alcohol, cocaine and amphetamines. Interestingly, different studies have also shown that not only drugs of abuse but also a high-fat diet attenuates dendritic spine density as well as decreased inhibitory synaptic transmission in the prefrontal cortex, a key region intricately involved with processing reward and motivation (Dingess et al., 2017; Thompson et al., 2017). “Taken together”, report the authors, “this suggests the possibility of overlapping neural pathways for drugs of abuse and certain foods types”.


It must be pointed out that comparing sugar to drugs of abuse is a simplistic short-cut. Indeed, natural rewards (sugar) and drugs of abuse (cocaine, amphetamine, etc) may share some common neuronal features, but the big picture is much more complex. In fact, it is also noteworthy that exposure to various drugs of abuse as well as various types of stress can cause an increase in distal spine density in the BLA principal neurons. This difference between sugar- and drug-induced structural modifications may indicate that both rewards (sugar vs drugs) may impact different aspects of the neuronal homeostasis.

Future studies are definitely needed to fully elucidate the mechanisms underlying food reward, thus hopefully leading to a better understanding of food-related maladaptive behaviors such as obesity.

Image credit Reese Wilson, 

Any views expressed are those of the author, and do not necessarily reflect those of PLOS. 

Peppe-BWGiuseppe Gangarossa received his PhD in Biomedical Sciences, specialty Neuroscience, from the University of Bologna. He has been a visiting fellow at the Karolinska Institutet (Sotckholm, Sweden), the French Inserm (Montpellier, France) and the Collège de France (Paris, France). Giuseppe is currently Assistant Professor of Physiology at the University Paris Diderot. His main research topic is dopamine-related brain disorders. You can follow him on twitter @PeppeGanga

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