Safety and psychological impact of sailing adventure therapy among Veterans with substance use disorders.

OBJECTIVES: Many Veterans suffer from substance use disorders (SUDs). Treatment challenges include poor treatment engagement and high relapse rates. Complementary interventions have the potential to enhance both. This study was a preliminary evaluation of sailing adventure therapy (SAT) for this population. DESIGN: Retrospective chart review. Participants in the intervention were 22 Veterans (20 male, 2 female) aged 22-65 who entered a Veterans Administration residential SUD treatment program. All subjects had two or more SUDs, and many had psychiatric (95%) and/or medical (77%) comorbidities. The age, gender and diagnosis-matched control group (n = 22) received residential SUD treatment as usual (TAU) in the same program but without SAT. SETTING: Residential SUD treatment program at a Veterans Administration Medical Center. INTERVENTION: Sailing adventure therapy. MAIN OUTCOME MEASURES: Positive and Negative Affect Schedule (PANAS), State Trait Anxiety Inventory six-item short form (STAI: Y-6 item), Acceptance and Action Questionnaire II (AAQ II), Five Facet Mindfulness Questionnaire (FFMQ) and a locally developed patient survey. Outcome comparison among SAT plus TAU group versus TAU - only group included measures of successful completion of residential SUD treatment program as well as psychiatric hospitalizations and/or residential SUD treatment program readmissions within 12 months. RESULTS: Neither physical injuries nor increases in anxiety or negative affect occurred, as measured by the PANAS (positive change, p = 0.351; negative change, p = 0.605) and the STAI: Y-6 item (p = 0.144) respectively. There was no significant change in FFMQ (p = 0.580) but a significant increase occurred in AAQ II scores (p = 0.036) indicating an increase in psychological flexibility. Survey responses indicated the participants perceived the experience to be both pleasurable and calming. The preliminary outcome evaluation revealed a significant between-group difference (X2 = 5.34, DF = 1, p = 0.02, r = 0.35) indicating participating in SAT was associated with a greater likelihood of successfully completing residential SUD treatment. However, there were no significant between-group differences in number of psychiatric hospitalizations (X2 = 1.09, DF = 1, p = 0.29, r = 0.16) or residential substance abuse treatment program readmissions (X2 = 0.23, DF = 1, p = 0.64, r = 0.07) in the 12 months after discharge from the program. CONCLUSIONS: Preliminary evidence suggests that SAT is physically safe and not associated with increased anxiety or negative affect. Participant's perceptions of the experience were positive. Preliminary outcome measures suggest associations between participation in SAT and increased psychological flexibility as well as successful completion of a residential SUD treatment program. Further research is indicated to determine whether SAT may be developed as an effective complementary intervention for Veterans with SUDs.

High glycemic index carbohydrate diet alters the diurnal rhythm of leptin but not insulin concentrations.

Morning serum leptin values in humans are inconsistently altered by diet, and the molecular mechanisms controlling the diurnal leptin pattern remain unexplained. We determined whether leptin values after meals or the leptin diurnal pattern was altered by the type of carbohydrate (CHO) ingested in diets containing either 20% or 30% fat. In a randomized, crossover study design, nine healthy lean adults ate one of four isocaloric diets for 8 days. Diets contained 15% protein: A, high glycemic index (GI) CHO, 30% fat; B, low GI CHO, 30% fat; C, high GI CHO, 20% fat; and D, low GI CHO, 20% fat. Serum glucose, insulin, and leptin were measured at intervals on Day 8 for 24 hr, and on Day 9 during an oral glucose tolerance test (GTT). Although the 24-hr glucose and insulin profiles did not differ with the diets, diets A and C altered the serum leptin diurnal pattern. In contrast to the usual evening rise in leptin concentration, which begins after 2200 hr, diets A and C caused a rise in leptin beginning at 1300 hr. The area under the curve for leptin between 1230 and 2400 hr was 17% greater for diets A and C. During the GTT, leptin concentrations were similar for each diet. These results suggest that the pattern and amount of leptin secretion may be altered by high GI CHO or the simple sugar content of the diet, unrelated to differences in insulin concentration, that high GI foods may have little or no effect on serum insulin in the context of a mixed meal, and that a single 0800-hr leptin value may not be sufficient to reveal a diet-induced change in leptin secretion

Prolonged periods without food intake during pregnancy increase risk for elevated maternal corticotropin-releasing hormone concentrations.

OBJECTIVE: Fasting during pregnancy stimulates preterm delivery in animals and increases women's risk for preterm delivery. Fasting stimulates hypothalamic corticotropin-releasing hormone production in animals. Elevated maternal corticotropin-releasing hormone concentrations are associated with preterm birth. We hypothesized that prolonged periods without food during pregnancy increase maternal corticotropin-releasing hormone concentrations, which lead to preterm delivery. STUDY DESIGN: In the Behavior in Pregnancy Study, we examined prolonged periods without eating during pregnancy and corticotropin-releasing hormone concentrations and gestational age at delivery with multivariate logistic regression analysis (n = 237). RESULTS: Prolonged periods without food lasting 13 hours or longer were associated with elevated maternal corticotropin-releasing hormone concentrations compared with prolonged periods without food lasting less than 13 hours at two time points during pregnancy, controlling for pregravid body mass index, energy intake, income, race, smoking, and maternal age (18-20 weeks: adjusted odds ratio, 2.5; 95% CI, 0.9-7.1; 28-30 weeks: adjusted odds ratio, 1.7; 95% CI, 0.7-4.2). There was an inverse, linear relationship between maternal corticotropin-releasing hormone concentrations and gestational age at delivery. CONCLUSIONS: Prolonged periods without food intake during pregnancy are associated with elevated maternal corticotropin-releasing hormone concentrations and with preterm delivery.

Frequency of eating during pregnancy and its effect on preterm delivery.

Frequency of eating or meal patterns during pregnancy may be a component of maternal nutrition relevant to pregnancy outcome. To identify meal patterns of pregnant women and investigate the relation between these meal patterns and preterm delivery, the authors performed an analysis using data from the Pregnancy, Infection, and Nutrition Study (n = 2,065). Women recruited from August 1995 to December 1998 were categorized by meal patterns on the basis of their reported number of meals (breakfast, lunch, and dinner) and snacks consumed per day during the second trimester. An optimal pattern was defined according to the Institute of Medicine recommendation of three meals and two or more snacks per day. In this population, 72 percent of the women met this recommendation, and 235 delivered preterm. Women who consumed meals/snacks less frequently were slightly heavier prior to pregnancy, were older, and had a lower total energy intake. In addition, these women had a higher risk of delivering preterm (adjusted odds ratio = 1.30, 95 percent confidence interval: 0.96, 1.76). There was no meaningful difference in the risk by early versus late preterm delivery, but those who delivered after premature rupture of the membranes (adjusted odds ratio = 1.87, 95 percent confidence interval: 1.02, 3.43) had a higher risk than those who delivered after preterm labor (adjusted odds ratio = 1.11, 95 percent confidence interval: 0.64, 1.89). This study supports previous animal model work of an association between decreased frequency of eating and preterm delivery.

Nutritional regulation of leptin in humans.

Although leptin was first discussed as an "adipostat" that regulated food intake in accordance with triglyceride stores, it has become clear that leptin's role is much more complex and that a great many unanswered questions persist. Human studies have not shown that serum leptin concentrations can be changed rapidly by meals. Insulin seems to have a modest but immediate effect in attenuating the morning nadir of serum leptin as well as a greater effect manifested after 4-6 h. These changes in serum leptin, like the decreases that occur with fasting, are not accompanied by corresponding changes in adipose leptin mRNA, suggesting regulation by translational control or changes in the rate of leptin degradation, secretion or clearance. There is convincing evidence that insulin increases leptin synthesis and secretion, probably through an insulin-dependent effect on glucose metabolism. This effect of insulin is possibly mediated by the hexosamine pathway. What adipocytes seem to be communicating to the brain is not how much triglyceride they contain but whether they are currently synthesizing or hydrolysing triglyceride. Confounding many studies is the problem of leptin's diurnal rhythm. Because many studies only measured leptin during its morning nadir or examined the effects of insulin or specific nutrients provided after an overnight fast, important information on regulation may have been lost.