Understanding the interface of HIV, trauma, post-traumatic stress disorder, and substance use and its implications for health outcomes.

Many individuals living with HIV have been exposed to some type of traumatic event during their lives and may be living with symptoms of post-traumatic stress disorder (PTSD). A substantial number of these individuals are also likely to show evidence of a co-morbid substance use disorder (SUD). There is reason to believe that the co-occurrence of HIV and PTSD or co-morbid PTSD and SUD (PTSD/SUD) may predict poorer health outcomes. There are several pathways through which PTSD or PTSD/SUD might adversely impact the health of individuals living with HIV, including participation in negative health behaviours, low levels of adherence to antiretroviral medications, and/or a direct, deleterious effect on immune function. Psychological interventions are needed to treat PTSD and PTSD/SUD in HIV-positive individuals, and reduce the negative impact of these conditions on health outcomes. This article will explore data on the prevalence of trauma exposure, PTSD, and PTSD/SUD among individuals living with HIV, the pathways through which these conditions might affect health, possible interventions for PTSD and PTSD/SUD for individuals living with HIV, and methods for integrating care for individuals with these disorders. Future directions for research related to HIV, PTSD, and PTSD/SUD will also be discussed.

Spouse support and long-term adherence to lipid-lowering diets.

Social support is inversely associated with heart disease risk. Support may influence heart disease by encouraging health behavior change in high-risk individuals. This study examined the association between spouse support and maintenance of low-fat diets in men with hypercholesterolemia. Participants were 254 men enrolled in a 24-month randomized trial of lipid-lowering diets initiated in 1985 in Seattle, Washington. The Evaluation of Spouse Support, which assesses the extent to which spouses supported maintenance of lipid-lowering diets, was administered after the last of eight dietary classes and at 3, 12, and 24 months postinstruction. Attainment of dietary goals was determined from food records completed at the end of the class and at 3, 12, and 24 months. Compared with those in the lowest quartile, those in the highest quartile of support were more likely to attain dietary goals at 3 months (odds ratio (OR) = 4.5, 95% confidence interval (CI) 1.9-10.4), 12 months (OR = 5.5, 95% CI 2.4-12.5), and 24 months (OR = 3.9, 95% CI 1.7-9.3). Support was not associated with end-of-class dietary goal achievement. Social support may be an important factor in the maintenance of low-fat diets.

Relationship of self-effecacy to cholesterol lowering and dietary change in hyperlipidemia.

This study examined whether self-efficacy was associated with lipid lowering and dietary change among men undergoing dietary counseling to lower cholesterol levels. Twenty-five hyperlipidemic men (total cholesterol ≧220 mg/dL) participated in four weeks of dietary instruction. Plasma lipids were measured prior to treatment, at posttreatment, and at three- and twelvemonth follow-up. Dietary intake and self-efficacy as measured by the revised Eating Self-Efficacy Scale (ESES-R) were assessed at pretreatment, posttreatment, and three-month follow-up. Pre-treatment to posttreatment increases in self-efficacy in situations characterized by negative affect were related to extent of lipid lowering and dietary change. Although subjects showed significant reductions in cholesterol levels following treatment, by one year, lipid levels had returned to pretreatment values. Factors related to long-term maintenance of dietary change and lipid lowering among hyperlipidemics merit further research.

Intraventricular neuropeptide Y injections stimulate food intake in lean, but not obese Zucker rats.

We examined the effect of acute third intraventricular (IVT) injections of either saline or NPY (0.95, 3.0, 9.5, or 30.0 micrograms in 1 microliter) on the 1-, 4-, and 22-hour postinjection food and water intake of female obese (fa/fa), heterozygous lean (Fa/fa), and homozygous lean (Fa/Fa) Zucker rats. None of the doses of NPY had an effect on either food or water intake of fa/fa rats. A significant increase of food intake was seen in Fa/Fa rats at 1 and 4 hours after the 3.0 micrograms injection of NPY and at 1, 4, and 22 hours after the 9.5 micrograms injection of NPY. Both 3.0 and 9.5 micrograms of NPY also stimulated 1- and 4-hour postinjection food intake of Fa/fa rats, although this effect was significant only at 4 hours after the 3.0 micrograms dose. NPY had a less reliable effect on water intake; 3.0 micrograms of NPY stimulated 1-hour postinjection water intake of Fa/fa rats and 4-hour postinjection water intake of Fa/Fa rats. These results indicate that lean, but not obese Zucker rats, respond by eating more to centrally administered NPY. This deficit is similar to the effects seen with IVT insulin injections and may be a result of a common receptor-mediated mechanism.

Neuropeptide Y paradoxically increases food intake yet causes conditioned flavor aversions.

Neuropeptides have been implicated in the short-term regulation of food intake and the long-term control of body weight. Previous studies have shown that central administration of neuropeptide Y (NPY), the most abundant of these peptides in the brain, produces robust increases of food intake. We now report that NPY, at doses that stimulate food intake when administered intraventricularly, also causes the formation of robust conditioned flavor aversions when given via the same cannula and at the same dose. This apparently paradoxical effect may be indicative of different populations of central NPY receptors having dissimilar effects on ingestive behaviors. The results also suggest that the use of conditioned aversions to investigate drug-induced malaise may not be appropriate when applied to ingestive behaviors.

The role of arginine vasopressin in the development of tolerance to ethanol in normal and Brattleboro rats.

Administration of AVP and related peptide fragments following ethanol (EtOH) administration has been shown to enhance retention of tolerance to ethanol. The present studies were designed specifically to: (1) examine the influence of AVP given concurrently with EtOH on the development of tolerance to the ataxic and hypothermic effects of EtOH in Long-Evans rats, and (2) to determine if tolerance to these effects develops in Brattleboro rats which are deficient in AVP. In Experiment 1, EtOH (2.5 g/kg, 15% v/v) was administered IP to 2 groups of rats in combination with a SC injection of either AVP (6 micrograms/kg) or an equal volume of saline. Two additional control groups received IP saline injections in combination with either saline or AVP. After 13 days, EtOH-treated rats were significantly more tolerant than saline-treated animals. AVP significantly increased the hypothermic and ataxic effects of EtOH and failed to enhance tolerance development. AVP delayed the extinction of tolerance to the hypothermic (but not the ataxic) effects of ethanol when administered during the extinction phase to rats previously treated with EtOH. In Experiment 2, Brattleboro rats were injected with EtOH or an equivalent volume of saline and tested for ataxia and hypothermia. Rats receiving EtOH failed to demonstrate significant tolerance to either effect of ethanol after 12 treatment days.

Reduction of food intake and body weight by chronic intraventricular insulin infusion.

This study examined the effect of chronic infusions of insulin in one of three doses (5, 7.5 or 10 mU/day) into the third ventricle, on food and water intake and body weight in the rat. Solutions were infused via osmotic minipumps at a rate of 1 microliter/hour for seven days. The two highest doses of insulin produced a dose-related suppression of food intake and weight loss, which was greater than the effect produced by 5 mU/day or a control infusion of Ringers solution. The effect of 5 mU/day on food and water intake and body weight was similar to the effect of the control infusion. All groups treated with insulin decreased food intake during the day and night, although only differences in nighttime food intake were statistically significant. Ten mU/day also produced a significantly greater reduction in water intake than each of the other solutions. Weight loss in the animals infused with insulin could not be explained by a decrease in caloric intake alone. Food intake returned to normal in all groups by the end of a seven day post-infusion period, with recovery being slowest among the animals receiving the highest doses of insulin. All animals recovered body weight at approximately the same rate. These results provide further evidence for the view that brain insulin plays a role in the regulation of food intake and body weight.

Glycerol reduces food intake in diabetic rats.

Streptozotocin diabetic rats received four daily subcutaneous injections of glycerol or a glycerol solution in place of water for a seven day period. Both night and total food intake in the subcutaneous glycerol group were significantly suppressed below untreated diabetic controls. The oral glycerol group showed a nonsignificant decrease in night foot intake and a significant reduction in day and total food intake. Consumption of additional fluid calories by the oral glycerol group contributed to the suppression of food intake in this group, but suppression in the subcutaneous group was unrelated to calculated calories obtained from glycerol. The oral glycerol group also consumed more of the glycerol solution than the other diabetic groups did of water. Results of this study support previous findings that subcutaneous and oral glycerol suppress food intake in normal rats although suppression with oral glycerol may have related to caloric intake, and suggest that low plasma concentrations of insulin do not interfere with the effects obtained with glycerol in normal animals.

Diabetes enhances the palatability of glycerol and glucose.

Male rats were provided with flavored solutions (0.3 M glucose, 0.3 M glycerol or 0.6 M glycerol) or water before and after the induction of diabetes by streptozotocin. Normal animals given 0.3 M glucose showed a significant increase in fluid intake but normal animals offered the glycerol solutions did not show an increase in intake compared to animals given water. After the onset of diabetes, exposure to the same flavored solutions resulted in significant increases in fluid intake by animals offered both the glycerol and glucose solutions. The animals offered glucose consumed significantly more than did the animals offered the glycerol solutions. The animals offered 0.6 M glycerol consumed significantly more than did the animals offered 0.3 M glycerol on 8 out of the 10 days of exposure. Therefore, while diabetes does not appear to modify the palatability of glucose it seems to produce an enhanced palatability for glycerol not seen in normal rats.