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      Children’s Environmental Health in the Digital Era: Understanding Early Screen Exposure as a Preventable Risk Factor for Obesity and Sleep Disorders


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          The quantity, accessibility and focus on child-targeted programming has exponentially increased since it entered American households in the early 1900s. It may have started with the television (TV), but technology has evolved and now fits in our pockets; as of 2017, 95% of American families own a smartphone. Availability and child-tailored content has subsequently led to a decrease in the age at initial screen exposure. The negative effects that accompany the current culture of early screen exposure are extensive and need to be considered as technology continues to enter the home and inundate social interactions. Increased levels of early screen exposure have been associated with decreased cognitive abilities, decreased growth, addictive behavior, poor school performance, poor sleep patterns, and increased levels of obesity. Research on the adverse effects of early screen exposure is mounting, but further epidemiological studies are still needed to inform prevention and regulation policies.

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          Most cited references35

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          Do obese children become obese adults? A review of the literature.

          Obese children may be at increased risk of becoming obese adults. To examine the relationship between obesity in childhood and obesity in adulthood, we reviewed the epidemiologic literature published between 1970 and July 1992. Comparison between studies was complicated by differences in study design, definitions of obesity, and analytic methods used. Although the correlations between anthropometric measures of obesity in childhood and those in adulthood varied considerably among studies, the associations were consistently positive. About a third (26 to 41%) of obese preschool children were obese as adults, and about half (42 to 63%) of obese school-age children were obese as adults. For all studies and across all ages, the risk of adult obesity was at least twice as high for obese children as for nonobese children. The risk of adult obesity was greater for children who were at higher levels of obesity and for children who were obese at older ages. The wide range of estimates in this literature are, in part, due to differences in study designs, definitions of obesity, ages at which participants were measured, intervals between measurements, and population and cultural differences.
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            Obesity and obstructive sleep apnea: pathogenic mechanisms and therapeutic approaches.

            Obstructive sleep apnea is a common disorder whose prevalence is linked to an epidemic of obesity in Western society. Sleep apnea is due to recurrent episodes of upper airway obstruction during sleep that are caused by elevations in upper airway collapsibility during sleep. Collapsibility can be increased by underlying anatomic alterations and/or disturbances in upper airway neuromuscular control, both of which play key roles in the pathogenesis of obstructive sleep apnea. Obesity and particularly central adiposity are potent risk factors for sleep apnea. They can increase pharyngeal collapsibility through mechanical effects on pharyngeal soft tissues and lung volume, and through central nervous system-acting signaling proteins (adipokines) that may affect airway neuromuscular control. Specific molecular signaling pathways encode differences in the distribution and metabolic activity of adipose tissue. These differences can produce alterations in the mechanical and neural control of upper airway collapsibility, which determine sleep apnea susceptibility. Although weight loss reduces upper airway collapsibility during sleep, it is not known whether its effects are mediated primarily by improvement in upper airway mechanical properties or neuromuscular control. A variety of behavioral, pharmacologic, and surgical approaches to weight loss may be of benefit to patients with sleep apnea, through distinct effects on the mass and activity of regional adipose stores. Examining responses to specific weight loss strategies will provide critical insight into mechanisms linking obesity and sleep apnea, and will help to elucidate the humoral and molecular predictors of weight loss responses.
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              Associative learning mediates dynamic shifts in dopamine signaling in the nucleus accumbens.

              The ability to predict favorable outcomes using environmental cues is an essential part of learned behavior. Dopamine neurons in the midbrain encode such stimulus-reward relationships in a manner consistent with contemporary learning models, but it is unclear how encoding this translates into actual dopamine release in target regions. Here, we sampled dopamine levels in the rat nucleus accumbens on a rapid (100 ms) timescale using electrochemical technology during a classical conditioning procedure. Early in conditioning, transient dopamine-release events signaled a primary reward, but not predictive cues. After repeated cue-reward pairings, dopamine signals shifted in time to predictive cue onset and were no longer observed at reward delivery. In the absence of stimulus-reward conditioning, there was no shift in the dopamine signal. Consistent with proposed roles in reward prediction and incentive salience, these results indicate that rapid dopamine release provides a reward signal that is dynamically modified by associative learning.

                Author and article information

                Children (Basel)
                Children (Basel)
                23 February 2018
                February 2018
                : 5
                : 2
                : 31
                [1 ]Larner College of Medicine, University of Vermont, Burlington, VT 05405-0068, USA; candice.wolf@ 123456med.uvm.edu (C.W.); seth.wolf@ 123456med.uvm.edu (S.W.)
                [2 ]Sleep Medicine Department, Children’s National Medical Center, Washington, DC 20010, USA; miweiss@ 123456childrensnational.org
                Author notes
                [* ]Correspondence: gnino@ 123456childrensnational.org ; Tel.: +1-202-476-5000
                © 2018 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                : 29 December 2017
                : 20 February 2018

                sleep,obesity,screen exposure,technology,pediatric,addiction,cognitive deficit,bmi,development


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