Introduction

Hookah use is increasingly common among U.S. college students, but little is known regarding the relationship between hookah and cigarette use. The purpose of this study was to test the hypothesis that the added nicotine exposure from hookah use may accelerate the uptake of cigarettes.

Methods

An ethnically diverse sample of college students (n = 256; 43% female) who had smoked cigarettes in the past month completed 2 in-person interviews over 6 months. This study was a secondary analysis of data collected for a longitudinal study of young adult cigarette smoking patterns. Analyses examined 6-month changes in past 30 day cigarettes smoked and number of days smoking, controlling for age, nicotine dependence, marijuana use, and the respective baseline variable for each outcome.

Results

Current hookah use (any use in past 30 days) was endorsed by 34% of participants at baseline, while 94% reported lifetime use. Change in past 30 day number of cigarettes (p = .043) and number of smoking days (p = .040) differed significantly between those who did or did not report recent hookah use at baseline. Hookah users reported a greater number of cigarettes smoked at the 6-month follow-up, while nonusers decreased their smoking quantity. For number of smoking days in the past 30, hookah users reported a smaller decrease than nonusers.

Conclusions

Recent hookah use predicted increased cigarette smoking over 6 months in a college sample. These are the first prospective data demonstrating this relationship, indicating the value of developing strategies to prevent hookah use among college students.

Abstract Background Individuals with posttraumatic stress disorder (PTSD) are more likely to undertake harmful health behaviors like substance use. Less is known about the association of PTSD with healthful behaviors such as healthy diet and exercise. The purpose of this study was to examine differences across physical health indicators and health behaviors in individuals with and without PTSD. Methods A cross-sectional, case–control study of health indicators and self-reported health behaviors in a community and military veteran sample was used. Results Based on a structured psychiatric interview, 25 participants had PTSD, and the remaining 55 without PTSD served as the comparison group. Participants were 40 years old on average and 45% were female. Multivariate analysis of variance analyses revealed that participants with PTSD had significantly higher body mass index (p = 0.004), had more alcohol use (p = 0.007), and reported fewer minutes of vigorous exercise (p = 0.020) than those without PTSD. Chi-square analysis of diet content and eating behavior constructs found that individuals with PTSD ate fewer fruits (p = 0.035) and had more guilt after overeating (p = 0.006). Conclusions These findings replicate prior research on the link between PTSD and negative health outcomes and engagement in harmful health behaviors and highlight the need for further examination of the association between PTSD and other health behaviors like diet content, eating behaviors, and exercise.

Ability to restrain one's dietary intake is a necessary skill for weight loss. However, dietary restraint has been shown to paradoxically increase disinhibited eating in certain populations, thereby negatively impacting weight loss and leading to worse overall health outcomes. The aim of this study was to address gaps in the literature regarding the relationships between separate facets of dietary restraint (intention; behavior) with weight loss and various types of disinhibited eating (binge eating, external eating, emotional eating) in overweight and obese adults who recently completed a weight loss intervention. A sample of mostly male Veterans with overweight and obesity (N = 88) self-reported their dietary restraint intention, restraint behavior, and current disinhibited eating following completion of an 8-week behavioral weight loss treatment. Greater dietary restraint intention was related to greater dietary restraint behavior, p < .05. Greater dietary restraint behavior was significantly related to greater recent weight loss, p < .05, while restraint intention was not, p > .05. Greater dietary restraint intention was related to greater current binge eating and external eating, while greater self-reported restraint behavior was related to less binge eating, p < .05. Thus, dietary restraint behavior appears to be adaptive for this population, whereas rigid dietary restraint intention may increase risk for disinhibited eating. To decrease disinhibited eating and improve weight loss outcomes in Veterans, interventions might specifically address rigid rule-following associated with abandonment of weight loss goals and help Veterans develop specific yet flexible eating plans. Future research should examine whether dietary restraint intention and behavior differentially predict disinhibited eating and weight loss outcomes prospectively.

Autonomic nervous system functioning, measured with heart rate variability (HRV), is associated with emotion regulation and likely contributes to binge eating. This study examined the link between HRV and binge eating severity and analyzed changes in HRV as a marker of emotion regulation in individuals with binge eating. Participants (n = 28) with obesity and loss of control eating reported overeating and loss of control episodes and completed an HRV assessment at rest and during a mental stressor. At rest, lower time-domain HRV was linked to more severe loss of control (SDNN B = -0.18, p = 0.03). Frequency-domain HRV was associated with more severe overeating (LFn B = 14.92, p = 0.03; HFn B = -14.81, p = 0.04). Frequency-domain HRV differed between resting and stressed conditions (p's < 0.001). Findings contribute to understanding emotion regulation in binge eating and guide future research and novel intervention development.

Objective

The relationship between sleep quality and pain has been studied in populations with chronic pain and in nonclinical populations using experimental paradigms. Little is known about the familial contributions to this relationship. This study examines self-reported sleep quality and pain in a nonclinical sample and to explore familial (i.e., shared genetic and common family environment) confounding in those relationships.

Design

Cross-sectional.

Subjects

Ninety nine community-based female twin pairs (N = 198) with a mean age of 29 years; 72% monozygotic.

Methods

The short form McGill Pain Questionnaire (McGill), a visual analog scale (VAS), a body map, and the Pittsburgh Sleep Quality Index (PSQI) measured self-reported pain and sleep quality. Mixed model regression adjusted for age was used to examine relationships between the pain indices and PSQI in overall and within-pair models.

Results

Higher PSQI total scores were significantly associated with higher scores across the McGill sensory (B = 0.37, p < 0.001), affective (B = 0.16, p < 0.001), total scores (B = 0.54, p < 0.001), the VAS (B = 2.41, p < 0.001), and number of sites with any pain on the body map (B = 0.42, p = 0.001). All of these associations were diminished and rendered nonsignificant in within-pair analyses that accounted for genetic and familial factors (all p's ≥ 0.01; Bonferroni α = 0.01).

Conclusions

These findings support an association between poor sleep quality and pain and suggest that this relationship may be confounded by shared genetic and environmental factors, which could elucidate biological mechanisms that underlie the development and maintenance of pain and sleep problems.

Background

Poor functional exercise capacity is common among those with obesity; however, objective measures of exercise capacity are rarely examined in behavioral treatments targeting obese individuals. We examined whether a 4-week acceptance and commitment therapy (ACT) intervention for disinhibited eating or a behavioral weight loss (BWL) intervention improved exercise capacity and explored demographic and disinhibited eating variables related to exercise capacity.

Methods

Veterans (n = 61), randomized to receive ACT or BWL, completed an assessment of exercise capacity via the 6-min walk test (6MWT) at baseline and 6-month follow-up. Measures of disinhibited eating patterns and body mass index (BMI), at baseline and post-treatment, were also collected. Change in 6MWT distance and treatment group differences were examined using mixed ANOVAs. Characteristics related to baseline 6MWT and predictors of improvement in 6MWT at 6 months were examined with hierarchical multiple regression.

Results

There were overall significant improvements on the 6MWT from baseline to 6-month follow-up (F(1,59) = 11.14, p = .001, η_p² = .159) but no differences between the ACT and BWL groups. Baseline BMI (β = - .33, p = .005) was the only variable related to baseline 6MWT. Improvements on the 6MWT were related to younger age (β = - .41, p = 0.001), female gender (β = .36, p = .001), and treatment-related increases in dietary restraint behaviors (β = .42, p = .001).

Conclusions

Functional exercise capacity improved among participants completing behavioral interventions for weight and disinhibited eating. Improvements in dietary behavior regulatory skills may have generalized to improved regulation in other behavioral domains associated with exercise capacity.

Background

Interventions targeting weight-related experiential avoidance (EA) and disinhibited eating (DE) may also improve diet quality. Participants with overweight/obesity and DE who recently completed a behavioral weight-loss program were randomized to receive acceptance and commitment therapy or continued behavioral weight-loss treatment. In this secondary analysis, we explored (1) change in diet quality from baseline to 6-month follow-up (FU) and (2) whether weight-related EA at baseline and (3) change in weight-related EA during treatment were related to change in diet quality from baseline to FU.

Method

Veterans (N = 68) completed food frequency questionnaires at baseline and FU, which were used to generate diet quality scores on the healthy eating index-15 (HEI-15). Weight-related EA was assessed using the Acceptance and Action Questionnaire for Weight-Related Difficulties-Revised (AAQW-R) at baseline, post-treatment, and FU. Aims were examined with mixed ANOVA analyses.

Results

Across both treatment groups, HEI-15 scores declined from baseline to FU. Women's HEI-15 decreased by about 5 times that of men. Baseline AAWQ-R was negatively associated with change in HEI-15. Neither AAWQ-R at post-treatment nor change in AAQW-R from baseline to post-treatment was significantly associated with change in HEI-15 at FU.

Conclusions

Greater weight-related EA at baseline was associated with lower diet quality at FU, but change in weight-related EA during treatment did not predict change in diet quality at FU. Interventions targeting DE and weight-loss may require specific components to improve and sustain healthy dietary intake in Veterans with obesity and DE.

Objectives

Hypothalamic-pituitary-adrenal (HPA) axis dysregulation is associated with chronic pain. Studying pain sensitivity and the HPA axis could elucidate the role of stress in chronic pain development, which might be influenced by familial factors, including genes.

Methods

Associations between pain sensitivity and salivary cortisol and familial confounding in these associations were examined in 88 female, community-based twin pairs (75% monozygotic, mean age 29 y). Cortisol was assessed after 0.25 mg dexamethasone (DEX), recovery from 0.25 mg DEX, and after 0.5 mg DEX. Cold pressor task (CPT) pain ratings were obtained at threshold and at tolerance. Conditioned pain modulation (CPM) was examined using thermal heat as the testing stimulus and hot water as the conditioning stimulus. Generalized estimating equation models were used and adjusted for baseline pain rating, age, and other relevant covariates.

Results

After controlling for baseline cortisol, greater cortisol suppression following DEX administration and lower recovery cortisol levels were associated with higher pain ratings at tolerance during the CPT (Bs=-2.42 to -17.82; Ps=0.031 to<0.001) as well as with reduced CPM (Bs=-0.92 to -1.68; Ps=0.003 to 0.046). Interestingly, familial confounding was evident in the CPT and CPM during recovery from DEX administration, but not immediately following DEX administration.

Discussion

These findings contribute to understanding possible mechanisms underlying chronic pain by demonstrating that HPA axis response to negative feedback is related to pain sensitivity.

Background

Despite substantial research on the comorbidity of anxiety disorders including posttraumatic stress disorder (PTSD) and chronic pain, little is known about the mechanisms underlying these conditions that might be potentially similar. Evoked pain sensitivity is one factor that has been associated with several pain conditions which might also have relevance to anxiety disorders and PTSD. The aim of this preliminary study was to examine evoked pain sensitivity in PTSD compared to other anxiety disorders and in control participants.

Method

The study used a cross-sectional case-control design in which participants completed a battery of questionnaires and structured interview and underwent cold pressor testing.

Results

Of 61 total participants, those in the PTSD (n =16) and other anxiety groups (n =12) endorsed significantly higher levels of psychological symptoms and poorer health functioning than control participants (n =33). The linear trend across baseline, threshold, and tolerance pain ratings from the cold pressor task significantly differed between participants with PTSD and the other anxiety and control groups suggesting lower pain sensitivity to a standardized stimulus of pain in individuals with PTSD.

Conclusions

These findings are similar to some of the prior research and suggest that individuals with PTSD may exhibit lower cold pain sensitivity compared to those with other anxiety disorders. There is a need for future research to determine explanatory mechanisms.

Background

There is a dearth of knowledge about the link between cortisol and pain sensitivity.

Purpose

We examined the association of salivary cortisol with indices of cold pain sensitivity in 198 female twins and explored the role of familial confounding.

Methods

Three-day saliva samples were collected for cortisol levels and a cold pressor test was used to collect pain ratings and time to threshold and tolerance. Linear regression modeling with generalized estimating equations examined the overall and within-pair associations.

Results

Lower diurnal variation of cortisol was associated with higher pain ratings at threshold (p = 0.02) and tolerance (p < 0.01). The relationship of diurnal variation with pain ratings at threshold and tolerance was minimally influenced by familial factors (i.e., genetics and common environment).

Conclusions

Understanding the genetic and non-genetic mechanisms underlying the link between HPA axis dysregulation and pain sensitivity may help to prevent chronic pain development and maintenance.