Introduction: Gulf War illness (GWI) is an environmentally-triggered chronic multisymptom illness typified by protean symptoms, in which mitochondrial impairment is evident. It has been likened to accelerated aging. Nuclear genetics of detoxification have been linked to GWI.
View Article and Find Full Text PDFTime for post-exercise phosphocreatine-recovery (PCr-R), deemed a robust index of mitochondrial function in vivo, was previously reported to be elevated (signifying impaired ATP production) in veterans with Gulf War illness (GWI). Here we sought to replicate the finding and assess the impact of contravening previous eligibility requirements. The replication sample comprised white males.
View Article and Find Full Text PDFWe evaluated whether veterans with Gulf War illness (VGWI) report greater ionizing radiation adverse effects (RadAEs) than controls; whether radiation-sensitivity is tied to reported chemical-sensitivity; and whether environmental exposures are apparent risk factors for reported RadAEs (rRadAEs). 81 participants (41 VGWI, 40 controls) rated exposure to, and rRadAEs from, four radiation types. The relations of RadAE-propensity (defined as the ratio of rRadAEs to summed radiation exposures) to Gulf War illness (GWI) presence and severity, and to reported chemical-sensitivity were assessed.
View Article and Find Full Text PDFObjectives: SARS-CoV-2 infection ("COVID-19") and the hypoxemia that has attended some cases may predispose to rhabdomyolysis. We sought to identify reported cases of COVID-19-associated rhabdomyolysis, examining concurrent risk factors (RFs) and mortality outcomes.
Methods: We searched PubMed for articles conveying individual-level information on COVID-19-associated rhabdomyolysis, published between January 2020 and July 2022, with an English-language abstract.
A third of 1990-1 Gulf-deployed personnel developed drug/chemical-induced multisymptom illness, "Gulf War illness" (). Veterans with GWI () report increased drug/exposure adverse effects (). Using previously collected data from a case-control study, we evaluated whether the fraction of exposures that engendered AEs ("AE Propensity") is increased in VGWI (it was); whether AE Propensity is related to self-rated "chemical sensitivity" (it did); and whether specific exposures "predicted" AE Propensity (they did).
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