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Abstract
Adolescence poses as both a transitional period in neurodevelopment and lifestyle practices. In particular, the developmental trajectory of the prefrontal cortex (PFC), a critical region for behavioral control and self-regulation, is enduring, not reaching functional maturity until the early 20 s in humans. Furthermore, the neurotransmitter dopamine is particularly abundant during adolescence, tuning the brain to rapidly learn about rewards and regulating aspects of neuroplasticity. Thus, adolescence is proposed to represent a period of vulnerability towards reward-driven behaviors such as the consumption of palatable high fat and high sugar diets. This is reflected in the increasing prevalence of obesity in children and adolescents as they are the greatest consumers of “junk foods”. Excessive consumption of diets laden in saturated fat and refined sugars not only leads to weight gain and the development of obesity, but experimental studies with rodents indicate they evoke cognitive deficits in learning and memory process by disrupting neuroplasticity and altering reward processing neurocircuitry. Consumption of these high fat and high sugar diets have been reported to have a particularly pronounced impact on cognition when consumed during adolescence, demonstrating a susceptibility of the adolescent brain to enduring cognitive deficits. The adolescent brain, with heightened reward sensitivity and diminished behavioral control compared to the mature adult brain, appears to be a risk for aberrant eating behaviors that may underpin the development of obesity. This review explores the neurodevelopmental changes in the PFC and mesocortical dopamine signaling that occur during adolescence, and how these potentially underpin the overconsumption of palatable food and development of obesogenic diet-induced cognitive deficits.
Highlights
Adolescence, Fast Food and Adverse Psychological ConditionsAdolescence represents a transitional developmental period between childhood and adulthood in the human lifespan
This study indicated that daily sucrose intake during adolescence led to decreased positive orofacial responses to sweet tastes when the rats were assessed as adults (Naneix et al, 2016) and this hedonic deficit was associated with lower c-Fos expression levels in the nucleus accumbens
A range of animal and human experimental literature specifies that adolescence is a period of vulnerability to engage in rewarding, yet potentially risky, behaviors, including overconsumption of high fat and high sugar foods
Summary
Adolescence represents a transitional developmental period between childhood and adulthood in the human (and animal) lifespan. Reports indicate that ADHD coincided with the expression of certain obesity-related genes in the pathways of dopaminergic neurocircuitry, such as fat mass–and obesity-associated variant (FTO; Albayrak et al, 2013) and melanocortin-4 receptor (MC4R; AgranatMeged et al, 2008). Polymorphisms of these genes have been linked with the incidence of obesity and dysregulated eating behaviors in humans (Frayling et al, 2007; Gerken et al, 2007; Cecil et al, 2008; Peng et al, 2011; Yilmaz et al, 2015). In particular the MC4R rs17782313 polymorphism is implicated in emotional eating and food cravings (Yilmaz et al, 2015) and the FTO rs1558902 polymorphism is associated with binge eating in adolescence (Micali et al, 2015)
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