New research reveals how junk food during adolescence rewires critical brain regions, increasing the risk for poor decision-making and obesity well into adulthood.
Study: Adolescent nutritional influences on the brain: implications for eating behaviors. Image Credit: Yuriy Golub / Shutterstock
Researchers have recently reviewed the existing literature to understand how an adolescent’s eating behavior affects the development of the prefrontal cortex (PFC) and hippocampus (HPC), as well as overall health. This narrative review synthesizes both animal and human studies to clarify these relationships and current knowledge gaps. The research is published in the journal Neuropharmacology.
Adolescence and food consumption
The transition from childhood to adolescence also involves a shift from dependence on direct control mechanisms linked to food and sensory receptors to an increasing reliance on indirect control mechanisms that facilitate adjustments in one's eating behavior.
In contrast to children whose eating behavior is primarily determined by hunger and fullness cues, adolescents’ eating behavior is significantly influenced by multiple external factors, including personal beliefs, media, food preferences, and peer pressure. The modern food environment features easy-to-access, highly palatable foods with high levels of fat, sugar, and salt, often directly marketed to adolescents. These ingredients typically increase food cravings by bypassing the normal regulatory controls.
Multiple studies have shown that compared to children, adolescents are more commonly inclined towards consuming hyper-palatable and ultra-processed foods (UPF), which are widely available in Western countries. These studies have also pointed out that adolescents are the highest consumers of high-fat, high-sugar (HFHS) foods, which cause obesity and metabolic disease. According to U.S. data, ultra-processed foods account for approximately 65% of total energy intake among adolescents, who also have the highest intake of added sugars. In the last three decades, a rapid increase in the prevalence of adolescent obesity has been recorded, with rates having quadrupled during this period.
Which part of the brain influences eating behavior?
The PFC region of the brain is involved in executive functions, including sustained attention, higher-order cognition, planning, decision-making, and inhibitory control. This part of the brain is not fully developed in humans until around the age of twenty-four. The PFC involves the integration of sensory signals to discriminate food palatability, responses to food cues, and discriminate food palatability. It also weighs the rewarding aspects of hyperpalatable foods against potential consequences as part of the brain's reward system.
The HPC is another region of the developing adolescent brain linked to feeding behavior. It regulates the episodic meal-related memories and conditional learned associations between food-related stimuli and post-ingestive signals. Impaired hippocampal activity leads to decreased memory of meals and increased response to food cues, resulting in elevated meal frequency, total energy intake, and weight gain. Animal studies suggest that the hippocampus’ structural and functional development during adolescence is especially sensitive to diet quality, with human research showing correlations between poor dietary habits and memory impairments.
The impact of adolescent eating behavior on the brain
Excessive consumption of calorically dense yet nutrient-poor foods throughout adolescence impacts the neurocognitive development of the PFC. Much of the mechanistic evidence for this comes from animal studies, with human evidence being largely correlational (e.g., brain imaging studies linking diet, PFC volume, and cognitive performance). This impaired development has a long-lasting impact on eating behavior, contributing to diet-induced obesity in adulthood.
Adolescent rats fed an HFHS diet for just a month exhibited a reduced number of fast-acting parvalbumin-positive (PV+) interneurons and perineuronal nets (PNNs) in the medial prefrontal cortex (mPFC), which disrupts neuroplasticity. Notably, adolescent rodents exposed to a Western diet for as little as one week exhibited rapid onset of anxiety-like and depression-like behaviors, a vulnerability not observed in adults.
HFHS foods were found to promote impulsivity, especially during adolescence. For example, animal studies have shown that adolescent rodents exposed to these diets exhibit increased impulsivity and reduced inhibitory control, and that baseline sex differences in these effects may exist, although further research is needed to confirm this in humans. The review highlights that males may experience greater and more persistent impulsivity, while females show a gradual emergence of these behaviors. Many animal-based studies have shown that GABAergic communication in the PFC is influenced by diet. For instance, adolescent rodents fed a high-fat and sucrose diet independently for two months showed a decreased GABA concentration and a reduced number of iGABAergic PV+ interneurons in the PFC and hippocampus. These changes in the brain regions are associated with impaired cognition and behavioral control.
Hyperpalatable foods activate the mesocorticolimbic pathway, encouraging further reward-seeking behavior. Experimental studies have shown that in comparison to control-fed rodents, those under a high-fat diet exhibited upregulation in D1 dopamine receptors and increased neuronal activation in the PFC, which increases reward-seeking behavior. In humans, elevated reward responsivity to food has been associated with increased body mass index. The review notes that over-engagement with such foods during adolescence may cause lasting changes in reward signaling, with some animal studies showing epigenetic changes that persist into adulthood.
Rodents fed with high-fat food demonstrated increased oxidative stress in the hippocampus, higher memory impairments, anxiety, and decreased social interaction. Similarly, rodents fed high-fructose corn syrup, a key ingredient in most soda drinks, exhibited impaired hippocampal-dependent spatial learning and memory in both male and female rats.
A previous study has also shown that the size and volume of the hippocampus are impacted by HFHS food consumption. Specifically, fat intake is associated with reductions in left hippocampal volume (linked to verbal memory), whereas increased dietary fructose is linked to increases in the right hippocampus (associated with spatial memory), reflecting possible lateralized hippocampal functions. Besides fat, higher dietary intake of fructose is associated with an increase in the volume of the right hippocampus, which could be due to delayed synaptic pruning or inflammation. However, the review cautions that the significance and consequences of such volume changes are not fully understood, and findings are sometimes contradictory (e.g., some studies find reduced hippocampal volume with fat intake, others see increases with fructose).
Many studies have confirmed that early life HFHS diet impairs the structural and functional signaling of the hippocampus, which negatively impacts hippocampal-dependent memory and learning. In comparison to control-fed rats, the HFHS diet increases hippocampal lesions, which in turn elevate meal frequency and appetitive responding, ultimately leading to obesity. Additionally, animal research indicates that a Western diet during adolescence can increase blood-brain barrier permeability in the hippocampus, thereby further impairing cognitive function.
Importantly, some of these diet-induced effects may not be fully reversible even after a healthy dietary intervention in adulthood, particularly when exposure occurs during critical periods of brain development in adolescence.
Taken together, the habitual feeding behaviors developed during adolescence may trigger long-lasting alterations in brain circuitry that could influence health throughout the lifespan. While much of the mechanistic evidence is derived from animal studies, human epidemiological and neuroimaging data are generally consistent with these findings; however, direct causal pathways require further investigation.