Background: Hypersensitivity to nickel is a very common cause of allergic contact dermatitis since this metal is largely present in industrial and consumer products as well as in some commonly consumed foods, air, soil, and water. In nickel-sensitized individuals, a cell-mediated delayed hypersensitivity response results in contact dermatitis due to mucous membrane coming in long-term contact with nickel-containing objects. This process involves the generation of reactive oxidative species and lipid peroxidation-induced oxidative damage. Immunologically, the involvement of T helper (h)-1 and Th-2 cells, as well as the reduced function of T regulatory cells, are of importance. The toxicity, mutagenicity, and carcinogenicity of nickel are attributed to the generation of reactive oxygen species and induction of oxidative damage via lipid peroxidation, which results in DNA damage. Objective: The aim of this research review is to identify nutritionally actionable interventions that can intercept nickel-induced cell damage due to their antioxidant capacities. Conclusion: Nutritional interventions, may be used to modulate immune dysregulation, thereby, intercepting nickel-induced cellular damage. Among these are a low-nickel diet and an antioxidant-rich diet that is sufficient in iron needed to minimize nickel absorption. These dietary approaches not only reduce the likelihood of nickel toxicity by minimizing nickel exposure, but also help prevent oxidative damage by supplying the body with antioxidants that neutralize free radicals.

Women of reproductive age experience higher rates of sleep disturbance than their male counterparts, leading to lack of restorative sleep and increasing risk for chronic disease. The objective of this review is to overlay the menstrual cycle with sleep regulation to develop an evidence-based theoretical model that directs clinical interventions for improved sleep in affected women. Utilizing the basic mechanisms for sleep and the menstrual cycle, in addition to evidence for sleep and hormonal dysregulation, hormonal fluctuations are mapped to variations in gamma-aminobutyric acid (GABA), melatonin, and cortisol levels. Effective interventions that may be included in individualized treatment plans – varying based on the scope of practice for each practitioner – are presented, along with the impetus for future research to explore the relationship between the menstrual cycle and sleep regulation.