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Eating disorders have potential to significantly impact growth and sexual development, particularly when associated with malnutrition. The hypothalamic-pituitary-gonadal axis, which dictates puberty and sexual maturation, including bone growth, is sensitive to metabolic changes such as those in eating disorders. Consequences may include pubertal delay/arrest, stunted growth, weakened bones, menstrual changes, impotence, sexual dysfunction, infertility, or adverse pregnancy outcomes. The physical and psychological impacts of eating disorders can also affect intimate relationships and sexual satisfaction. Visits to mental health providers offer an opportunity to assess the development and reproductive health concerns of patients with eating disorders. The purpose of this article is to review the epidemiology, pathophysiology, and morbidities of the reproductive sequelae of eating disorders and to educate mental health providers on when to refer patients for further medical evaluation.

Allergic (Th2 high immunophenotype) asthmatics have a heightened susceptibility to common respiratory viral infections such as human rhinovirus. Evidence suggests that the innate interferon response is deficient in asthmatic/atopic individuals, while other studies show no differences in antiviral response pathways. Unsensitized and OVA-sensitized/challenged Th2 high (BN rats) and Th2 low immunophenotype (PVG rats) animals were inoculated intranasally with attenuated mengovirus (vMC 0 ). Sensitized animals were exposed/unexposed during the acute viral response phase. Cellular and transcriptomic profiling was performed on bronchoalveolar lavage cells. In unsensitized PVG rats, vMC 0 elicits a prototypical antiviral response (neutrophilic airways inflammation, upregulation of Th1/type I interferon-related pathways). In contrast, response to infection in the Th2 high BN rats was associated with a radically altered intrinsic host response to respiratory viral infection, characterized by macrophage influx/Th2-associated pathways. In sensitized animals, response to virus infection alone was not altered compared to unsensitized animals. However, allergen exposure of sensitized animals during viral infection unleashes a notably exaggerated airways inflammatory response profile orders of magnitude higher in BN versus PVG rats despite similar viral loads. The co-exposure responses in the Th2 high BN incorporated type I interferon/Th1, alternative macrophage activation/Th2 and Th17 signatures. Similar factors may underlie the hyper-susceptibility to infection-associated airways inflammation characteristic of the human Th2 high immunophenotype.