Context: Widespread digital retouching of advertising imagery in the fashion, beauty, and other consumer industries promotes unrealistic beauty standards that have harmful effects on public health. In particular, exposure to misleading beauty imagery is linked with greater body dissatisfaction, worse mood, poorer self-esteem, and increased risk for disordered eating behaviors. Moreover, given the social, psychological, medical, and economic burden of eating disorders, there is an urgent need to address environmental risk factors and to scale up prevention efforts by increasing the regulation of digitally altered advertising imagery. Methods: This manuscript summarizes the health research literature linking digital retouching of advertising to increased risk of eating disorders, disordered weight and appearance control behaviors, and body dissatisfaction in consumers, followed by a review of global policy initiatives designed to regulate digital retouching to reduce health harms to consumers. Next, we turn to the US legal context, reporting on findings generated through legal research via Westlaw and LexisNexis, congressional records, federal agency websites, law review articles, and Supreme Court opinions, in addition to consulting legal experts on both tax law and the First Amendment, to evaluate the viability of various policy initiatives proposed to strengthen regulation on digital retouching in the United States. Findings: Influencing advertising practices via tax incentives combined with corporate social responsibility initiatives may be the most constitutionally feasible options for the US legal context to reduce the use of digitally alternated images of models' bodies in advertising. Conclusions: Policy and corporate initiatives to curtail use of digitally altered images found to be harmful to mental and behavioral health of consumers could reduce the burden of eating disorders, disordered weight and appearance control behaviors, and body dissatisfaction and thereby improve population health in the United States.

Inhibition of prostaglandin (PG) biosynthesis has been used to relieve pain for thousands of years. Today non-steroidal anti-inflammatory drugs (which largely inhibit PG synthesis) are widely used to treat pain. Four main types of prostaglandins (PGD2, PGE2, PGF2 and PGI2) are synthesized from arachidonic acid during inflammation and have been demonstrated to impact nociception. PGE2 has been the most studied and utilized for its pain producing properties and has been demonstrated to increase hypersensitivity in rodent nociceptive behavioral models when applied centrally and/or peripherally. Surprisingly, there are no published reports that use withdrawal from radiant light beam (Hargreaves apparatus) to examine the dose response effect of peripherally applied PGE2 on thermal nociceptive hypersensitivity. To address this gap in the literature, we performed a dose response study examining the effect of PGE2 on thermal hypersensitivity (assessed using a Hargreaves apparatus) where rats were injected with 0.003–30 μg of PGE2, intradermally into the hindpaw. Thermal hypersensitivity was assessed by measuring withdraw latency from a radiant light beam (Hargreaves test) and our primary objective was to determine the dose of PGE2 causing the most pronounced increase in thermal hypersensitivity (i.e. lowest withdraw latency). A secondary objective was to determine the minimum dose of PGE2 required to cause statistically significant decreases in thermal withdrawal latency as compared to rats injected with vehicle. We found that rats injected with the 30 μg dose of PGE2 exhibited the most pronounced thermal nociceptive hypersensitivity though secondary analysis showed that rats injected with PGE2 doses of 0.03–30 μg had lower withdrawal latencies as compared to rats injected with vehicle. This work fills an evidence gap and provides context to guide dose selection in future rodent pain behavior studies.

Deficiency in retinoid acid receptor-related orphan receptor alpha (RORα) of staggerer mice results in extensive granule and Purkinje cell loss in the cerebellum as well as in learned motor deficits, cognition impairments and perseverative tendencies that are commonly observed in autistic spectrum disorder (ASD). The effects of RORα on brain lipid metabolism associated with cerebellar atrophy remain unexplored. The aim of this study is to examine the effects of RORα deficiency on brain phospholipid fatty acid concentrations and compositions. Staggerer mice (Rora sg/sg) and wildtype littermates (Rora +/+) were fed n-3 polyunsaturated fatty acids (PUFA) containing diets ad libitum. At 2 months and 7 or more months old, brain total phospholipid fatty acids were quantified by gas chromatography-flame ionization detection. In the cerebellum, all fatty acid concentrations were reduced in 2 months old mice. Since total fatty acid concentrations were significantly different at 2-monthold, we examined changes in fatty acid composition. The composition of ARA was not significantly different between genotypes; though DHA composition remained significantly lowered. Despite cerebellar atrophy at >7months-old, cerebellar fatty acid concentrations had recovered comparably to wildtype control. Therefore, RORα may be necessary for fatty acid accretions during neurodevelopment. Specifically, the effects of RORα on PUFA metabolisms are region-specific and age-dependent.

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