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Background: Post-traumatic stress disorder (PTSD) and chronic pain are highly prevalent comorbid conditions. Veterans dually burdened by PTSD and chronic pain experience more severe outcomes compared to either disorder alone. Few studies have enrolled enough women Veterans to test gender differences in pain outcomes [catastrophizing, intensity, interference] by the severity of PTSD. Aim: Examine gender differences in the association between PTSD symptoms and pain outcomes among Veterans enrolled in a chronic pain clinical trial. Methods: Participants were 421 men and 386 women Veterans with chronic pain who provided complete data on PTSD symptoms and pain outcomes. We used hierarchical linear regression models to examine gender differences in pain outcomes by PTSD symptoms. Results: Adjusted multivariable models indicated that PTSD symptoms were associated with higher levels of pain catastrophizing (0.57, 95% CI [0.51, 0.63]), pain intensity (0.30, 95% CI [0.24, 0.37]), and pain interference (0.46, 95% CI [0.39, 0.52]). No evidence suggesting differences in this association were found in either the crude or adjusted models (all interaction p-values<0.05). Conclusion: These findings may reflect the underlying mutual maintenance of these conditions whereby the sensation of pain could trigger PTSD symptoms, particularly if the trauma and pain are associated with the same event. Clinical implications and opportunities testing relevant treatments that may benefit both chronic pain and PTSD are discussed.
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Background: Binge drinking and binge eating are prevalent, frequently co-occurring, high-risk behaviors among emerging adult women, each with physical and psychological consequences. The mechanisms driving their co-occurrence are not well understood, though a history of adverse childhood experiences (ACEs) may increase the risk for both binge behaviors. Objective: To assess the association between ACE subtypes and individual and co-occurring binge drinking and eating in emerging adult women. Participants and Setting: A diverse sample of women participating in the population-based study EAT 2018: Eating and Activity over Time (N = 788; aged 18-30; 19% Asian, 22% Black, 19% Latino, and 36% White). Methods: Multinomial logistic regression estimated associations among ACE subtypes (i.e., sexual abuse, physical abuse, emotional abuse, household dysfunction), and binge drinking, binge eating, and their co-occurrence. Results are reported as predicted probabilities (PP) of each outcome. Results: Over half of the sample (62%) reported at least one ACE. In models mutually adjusted for other ACEs, physical and emotional abuse showed the strongest associations with binge behaviors. Experiences of physical abuse had the strongest association with a ten-percentage point higher predicted probability of binge drinking (PP = 37%, 95% [CI 27-47%]) and seven-percentage point higher PP of co-occurring binge eating and drinking (PP = 12%, 95% CI [5-19%]). Emotional abuse had the strongest association with an 11-percentage point higher PP binge eating only (PP = 20%, 95% CI [11-29%]). Conclusions: This study found childhood physical and emotional abuse to be particularly relevant risk factors for binge drinking, binge eating, and their co-occurrence among emerging adult women.
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Sleep apnea (SA), defined as intermittent respiratory arrest during sleep, is associated with increased incidence of hypertension, peripheral vascular disease, stroke, and sudden cardiac death. We have shown that intermittent hypoxia with CO2 supplementation (IH), a model for SA, increases blood pressure and circulating ET-1 levels, upregulates lung pre-pro ET-1 mRNA, increases vasoconstrictor reactivity to ET-1 in rat small mesenteric arteries (MA) and increases vascular reactive oxygen species (ROS). NFAT activity is increased in the aorta (AO) and MA of mice exposed to IH in an ET-1-dependent manner, and the genetic ablation of the isoform NFATc3 prevents IH-induced hypertension. We hypothesized that IH causes an increase in arterial ROS generation, which activates NFATc3 to increase vasoconstrictor reactivity to ET-1. In support of our hypothesis, we found that IH increases ROS in AO and MA. In vivo administration of the SOD mimetic tempol during IH exposure prevents IH-induced increases in NFAT activity in mouse MA and AO. We found that IH causes an NFATc3-dependent increase in vasoconstrictor reactivity to ET-1, accompanied by an increase in vessel wall [Ca²âº]. Our results indicate that IH exposure causes an increase in arterial ROS to activate NFATc3, which then increases vasoconstrictor reactivity and Ca²âº response to ET-1. These studies highlight a novel regulatory pathway, and demonstrate the potential clinical relevance of NFAT inhibition to prevent hypertension in SA patients.
