Excessive sugar consumption and neurocognitive problems

Aşırı şeker tüketimi ve nörobilişsel problemler

In today’s world, sugar has become an indispensable ingredient for food and beverages. This has led to excessive sugar consumption in children, adolescents and adults in more than 60 countries, as a result of the use that is four times higher (>100g/person/day) than what is recommended by the World Health Organization (25g/person/day).

Is sugar an addiction?

The concept of “sugar addiction” and sugar being categorized as a substance of abuse are still under discussion. On the other hand, there is a growing number of evidences in regards to the congruence in the relevant brain circuits and molecular signal pathways in the use of sugar and drugs. People consume sugar and food for regulating the homeostatic energy balance, and also for pleasure. This hedonistic desire towards delicious food is reward-oriented, and overeating can result in a maladaptive/negative neuroplasticity that invalidates the homeostatic regulation. In humans, sugar can induce a secretion of dopamine as much as that which is caused by addictive drugs, while stimulating the urge of reward. This situation claims that sugar changes the reward signals and circuits of the brain in a similar way that other misused drugs can do.

Sugar and neurocognitive problems

In a series of studies carried out on rodents, it was shown that high-sugar and/or high-fat diets accelerated psychiatric phenotypes similar to addiction. A growing number of evidences show that the consumption of food and beverages with high sugar content in the western diet can be associated with the increasing obesity epidemic. Moreover, another strong correlation was revealed between attention deficit/hyperactivity disorders (ADHD) and excessive weigh/obesity. High sugar consumption is associated with hyperactivity in children, and with carelessness and impulsiveness in adults.

Surprisingly, high intake of sucrose during pregnancy revealed increased locomotor (locomotor: the ability to move by using the musculoskeletal systems) activity, reduced attention/learning and impulsiveness, as well as ADHD-like behavioral phenotypes, in rodent offspring. Anxiety, depression, and cognitive deficiencies are strongly correlated with deteriorated hippocampal neurogenesis in animal models; however, there is a lack of evidence for a causal correlation. Indeed, hippocampal neurogenesis and changes in physiology accompany the anxiety and spatial memory disorders caused by long-term sucrose consumption.

Recent evidences show that obesity and impulsiveness, which are caused by weak eating habits, lead to even more consumption of processed food and beverages.

Sucrose (saccharose) has become indispensable for modern food and beverages. The fact that excessive sugar consumption causes obesity, increased locomotor activity, as well as emotional and cognitive disorders, puts forward that sugar meets all the criteria needed to categorize it as a misused drug. On the other hand, it was still uncertain whether a chronic excessive sucrose consumption that started in adolescence would affect the locomotor behavior, emotions, and cognition throughout the adulthood. Therefore, using a rodent model, attempts were made to understand the effects of a long-term intake of sucrose in order to determine its impact on mobility, anxiety, memory, and hippocampal neurogenesis. For the very first time, the results show that long-term consumption of sucrose leads to a substantial weight gain, and that it causes permanent hyperactivity and learning disorders in adult rodents in association with reduced hippocampal neurogenesis. These results suggest that long-term intake of sugar in the western diet can play a part in the pathogenesis of the disorders associated with attention deficit and hyperactivity.

Beecher, K., Alvarez Cooper, I., Wang, J., Walters, S. B., Chehrehasa, F., Bartlett, S. E., & Belmer, A. (2021). Long-term overconsumption of sugar starting at adolescence produces persistent hyperactivity and neurocognitive deficits in adulthood. Frontiers in neuroscience, 15, 567.