The Nature of the Association between Anxiety Sensitivity and Pain-Related Anxiety: Evidence from Correlational and Intervention Studies.

High anxiety sensitivity (AS) has been associated with elevated pain-related anxiety in anxiety and pain samples. The present study investigated (a) the associations among the lower order dimensions of AS and pain-related anxiety, using a robust measure of AS, and (b) the pain-related anxiety outcomes of a telephone-delivered cognitive behavioural treatment (CBT) designed to reduce high AS. Participants were 80 anxiety treatment-seeking participants with high AS (M age = 36 years; 79% women). After providing baseline data on AS and pain-related anxiety, participants were randomly assigned to an eight-week telephone CBT or a waiting list control. At baseline, bivariate correlations showed AS physical and cognitive, but not social, concerns were significantly associated with pain-related fear and arousal but not escape/avoidance behaviours. Multiple regression revealed that after accounting for emotional distress symptoms, AS physical, but not cognitive or social, concerns uniquely predicted pain-related anxiety. Multilevel modelling showed that the AS-targeted CBT reduced pain-related anxiety and treatment-related changes in global AS and AS physical concerns mediated changes in pain-related anxiety. Results suggest that an AS-targeted intervention may have implications for reducing pain-related anxiety. Further research is needed in a chronic pain sample.

Evidence-based review on the effect of normal dietary consumption of fructose on blood lipids and body weight of overweight and obese individuals.

Although some investigators have hypothesized that ingestion of fructose from foods and beverages is responsible for the development of hyperlipidemia or obesity, a recent evidence-based review demonstrated that there was no relationship between the consumption of fructose in a normal dietary manner and the development of hyperlipidemia or increased weight in normal weight individuals. Because overweight and obese individuals may exhibit metabolic abnormalities such as insulin resistance, impaired glucose tolerance, hyperlipedemia, and/or alterations in gut hormones involved in appetite regulation, the findings of fructose studies performed in normal weight subjects may not be particularly relevant for overweight or obese subjects. A systematic assessment of the strength and quality of the studies and their relevance for overweight or obese humans ingesting fructose in a normal dietary manner has not been performed. The purpose of this review was to critically evaluate the existing database for a causal relationship between the ingestion of fructose in a normal, dietary manner and the development of hyperlipidemia or increased body weight in overweight or obese humans, using an evidence-based approach. The results of the analysis indicate that there is no evidence which shows that the consumption of fructose at normal levels of intake causes biologically relevant changes in triglycerides (TG) or body weight in overweight or obese individuals.

Evidence-based review on the effect of normal dietary consumption of fructose on development of hyperlipidemia and obesity in healthy, normal weight individuals.

In recent years, there has been episodic speculation that an increase in consumption of fructose from foods and beverages is an underlying factor responsible for the relatively recent increase in obesity and obesity-related diseases such as diabetes. Reports in support of this hypothesis have been published, showing that concentrations of triglycerides (TG) are higher and concentrations of insulin and hormones associated with satiety are lower in animals following the ingestion of fairly large quantities of fructose, compared to other carbohydrates. However, results from human studies are inconsistent. A possible reason for the inconsistent results is that they are dependent on the particular study population, the design of the studies, and/or the amount of fructose administered. A systematic assessment of the strength and quality of the studies and their relevance for healthy, normal weight humans ingesting fructose in a normal dietary manner has not been performed. The purpose of this review was to critically evaluate the existing database for a causal relationship between the ingestion of fructose in a normal, dietary manner and the development of hyperlipidemia or increased body weight in healthy, normal weight humans, using an evidence-based approach. The results of the analysis indicate that fructose does not cause biologically relevant changes in TG or body weight when consumed at levels approaching 95th percentile estimates of intake.

Effect of novel maize-based dietary fibers on postprandial glycemia and insulinemia.

BACKGROUND: Postprandial hyperglycemia has been associated with increased oxidative stress and the development of diabetes, heart disease and all-cause mortality. OBJECTIVE: To assess the effect of novel maize-based dietary fibers on postprandial glycemia and to assess the correlation between a rapid in vitro digestibility system and the blood glucose response. METHODS: In a clinical study, 12 healthy volunteers were fed seven test beverages containing maize-based fiber ingredients (25g total carbohydrate) along with 2 control meals on separate occasions in random order. Capillary blood samples were obtained and the relative glycemic and insulinemic responses were assessed by calculating the incremental area under the 2 h blood response curves. In vitro digestibility studies of the test fibers and control were also undertaken to determine if these correlated with the clinical findings. RESULTS: All test fibers resulted in significantly lower glycemic and insulinemic responses for the incremental area under the curve (iAUC) and at all time points compared with the control (P < 0.05). The in vitro digestibility curves were comparable to the cumulative in vivo iAUCs. In vitro data expressed as percent digestion correlated significantly with the in vivo iAUC for the first 30min of the test meal (P < 0.05). CONCLUSION: These novel maize-based dietary fibers all produce lower postprandial glycemic and insulinemic responses than the control. While further assessment is necessary in beverage and foods containing these fibers, they may be effective in applications for dietary strategies to control diabetes and other chronic diseases. In addition, the in vitro digestibility assay correlated well with in vivo data and may be useful in guiding product development.

Dietary soy beta-conglycinin (7S globulin) inhibits atherosclerosis in mice.

Although beta-conglycinin (7S globulin), a major soy storage protein, stimulates the expression of LDL receptors and the degradation of LDL by hepatocytes in vitro, the in vivo effects of dietary beta-conglycinin on the cardiovascular system are unknown. We assessed the effects of dietary beta-conglycinin and other soy peptide fractions on the development of atherosclerosis in atherosclerosis-susceptible mice. At 6 wk of age, male and ovariectomized female apolipoprotein (apo) E-null mice and LDL receptor-null, apoB transgenic mice were assigned randomly to treatment groups that differed only in the source of dietary protein: 1) casein/lactalbumin, 2) isoflavone-containing soy protein isolate, 3) beta-conglycinin, 4) glycinin (11S globulin, another major soy storage protein), 5) beta-conglycinin-devoid soy protein, and 6) W008 (a peptide fraction produced by hydrolysis and precipitation of soy protein isolate). After 4 mo, aortic atherosclerosis (cholesteryl ester content) and plasma lipoprotein cholesterol concentrations were quantified using GLC. Relative to mice fed casein/lactalbumin-based diets, the extent of atherosclerosis was reduced in ovariectomized female mice fed all soy protein-containing diets. Relative to mice fed isoflavone-containing soy protein isolate, atherosclerosis was reduced only in mice fed the beta-conglycinin-containing diet. Mean reductions were 39 and 67% (all P <0.05) in male and ovariectomized female apoE null mice and 66% (P < 0.05) in male LDL receptor null mice. These effects were unrelated to variation in isoflavone content of the protein source and only minimally related to plasma lipoprotein cholesterol concentrations. We conclude that a diet rich in beta-conglycinin has atheroprotective effects that greatly exceed those of isoflavone-containing soy protein isolate and do not depend on LDL receptors or influences on plasma lipoproteins.

Dietary soy and soy isoflavones have gender-specific effects on plasma lipids and isoflavones in golden Syrian f(1)b hybrid hamsters.

The specific components of soy responsible for its beneficial effects on plasma lipids are unknown. Golden Syrian F(1)B Hybrid hamsters (75 male, 74 female) were evaluated for the effect of dietary soy and soy isoflavones on plasma lipids. They were fed the following diets for 16 wk: casein/lactalbumin (C/L), soy protein with isoflavones [Soy(+)], soy protein with isoflavones removed [Soy(-)], Soy(-) plus isoflavone extract (IF), and C/L + IF. At necropsy, plasma total cholesterol, HDL cholesterol (HDLC), LDL + VLDL cholesterol (LDL + VLDLC), isoflavones, and uterine and accessory gland weights were measured. Male hamsters fed the three soy-containing diets had lower LDL + VLDLC concentrations than those fed the two C/L diets (P < 0.01), and those fed Soy(-) + IF did not differ from those fed Soy(+). In females, diet did not affect plasma LDL + VLDLC concentration. Females fed Soy(+) or Soy(-) had higher HDLC (P < 0.05) than those fed C/L. HDLC was not affected by diet in males. Due to higher equol production (P < 0.01), males had greater plasma isoflavone concentrations (P < 0.01) than females. There was a positive association between plasma total isoflavones and LDL + VLDLC (r = 0.65, P < 0.05) in females. These data suggest gender differences in plasma lipid and isoflavone responses to soy- based diets in Syrian F(1)B Hybrid hamsters, which offer an opportunity to explore effects of sex hormones on isoflavone metabolism and the effects of isoflavones on lipid metabolism.