A study of statistics anxiety levels of graduate dental hygiene students.

PURPOSE: In light of increased emphasis on evidence-based practice in the profession of dental hygiene, it is important that today's dental hygienist comprehend statistical measures to fully understand research articles, and thereby apply scientific evidence to practice. Therefore, the purpose of this study was to investigate statistics anxiety among graduate dental hygiene students in the U.S. METHODS: A web-based self-report, anonymous survey was emailed to directors of 17 MSDH programs in the U.S. with a request to distribute to graduate students. The survey collected data on statistics anxiety, sociodemographic characteristics and evidence-based practice. Statistic anxiety was assessed using the Statistical Anxiety Rating Scale. Study significance level was α=0.05. RESULTS: Only 8 of the 17 invited programs participated in the study. Statistical Anxiety Rating Scale data revealed graduate dental hygiene students experience low to moderate levels of statistics anxiety. Specifically, the level of anxiety on the Interpretation Anxiety factor indicated this population could struggle with making sense of scientific research. A decisive majority (92%) of students indicated statistics is essential for evidence-based practice and should be a required course for all dental hygienists. CONCLUSION: This study served to identify statistics anxiety in a previously unexplored population. The findings should be useful in both theory building and in practical applications. Furthermore, the results can be used to direct future research.

Sex differences in lipoprotein metabolism and dietary response: basis in hormonal differences and implications for cardiovascular disease.

The transport of fat in the blood stream is approximately twice as fast in women as men. Disease states such as obesity and diabetes are associated with greater lipoprotein abnormalities in women compared with men. A greater increment in cardiovascular disease risk in women is linked to these abnormalities. A greater change in triglyceride level and a lesser change in low-density lipoprotein are observed in women than men with high-carbohydrate or high-fat feeding. Most consistent are greater changes in high-density lipoprotein (HDL), HDL(2), and apolipoprotein A-I levels in women compared with men with high-carbohydrate or high-fat feeding. Dietary fat restriction in women appears to have a less beneficial lipoprotein effect than in men. Dietary fat restriction for heart disease prevention may be less ideal in women than in men.

A moderate-fat diet for combined hyperlipidemia and metabolic syndrome.

A low-fat diet is recommended for hyperlipidemia. However, low-density lipoprotein (LDL) responses depend on the type of hyperlipidemia (ie, simple hypercholesterolemia or combined hyperlipidemia). In combined hyperlipidemia, which is typical of patients with metabolic syndrome, LDL levels are only one third as responsive to fat and cholesterol as simple hypercholesterolemia. The diminished dietary sensitivity of combined hyperlipidemia is explained by diminished intestinal absorption of cholesterol, a feature of metabolic syndrome. In turn, combined hyperlipidemia is caused by heightened lipid secretion by the liver. A moderate-fat, moderate-carbohydrate diet employing allowable fats has the promise of reducing endogenous lipoprotein production in combined hyperlipidemia. Triglyceride, LDL, and small-dense LDL should be lower, and high-density lipoprotein, apoprotein A-I, and buoyant LDL should be higher. A test of this dietary strategy on lipoproteins and downstream benefits on inflammatory mediators, oxidative stress, and vascular reactivity is now underway.

Gender differences in lipoprotein metabolism and dietary response: basis in hormonal differences and implications for cardiovascular disease.

The transport of fat in the blood stream is approximately twice as fast in women as men. Disease states such as obesity and diabetes are associated with greater lipoprotein abnormalities in women compared with men. A greater increment in cardiovascular disease risk in women is linked to these abnormalities. A greater change in triglyceride level and a lesser change in low-density lipoprotein are observed in women than men with high-carbohydrate or high-fat feeding. Most consistent are greater changes in high-density lipoprotein (HDL), HDL2, and apolipoprotein A-I levels in women compared with men with high-carbohydrate or high-fat feeding. Dietary fat restriction in women appears to have a less beneficial lipoprotein effect than in men. Dietary fat restriction for heart disease prevention may be less ideal in women than in men.

Effects of insulin resistance and obesity on lipoproteins and sensitivity to egg feeding.

OBJECTIVE: This study was undertaken to determine if insulin resistance without and with obesity influences LDL response to dietary cholesterol and saturated fat. METHODS AND RESULTS: We fed 0, 2, and 4 egg yolks per day to 197 healthy subjects in a 4-week, double-blind, randomized, crossover design. Subjects were dichotomized on body mass index (<27.5 and > or =27.5 kg/m2) and insulin sensitivity (insulin-sensitivity index > or =4.2x1.0(-4) and <4.2x1.0(-4) min(-1) microU/mL), yielding insulin-sensitive (IS, n=65), insulin-resistant (IR, n=75), and obese insulin-resistant (OIR, n=58) subjects. Mean fasting baseline LDL cholesterol (LDL-C) levels were higher in IR and OIR subjects (3.44+/-0.67 and 3.32+/-0.80 mol/L) than in IS subjects (2.84+/-0.75 mmol/L) (P<0.001). Progressive triglyceride elevations and HDL-C decreases were seen across the 3 groups. Ingesting 4 eggs daily yielded significant LDL-C increases of 7.8+/-13.7% (IS) and 3.3+/-13.2% (IR) (both P<0.05) compared with 2.4+/-12.6% for OIR (NS). HDL-C increases were 8.8+/-10.4%, 5.2+/-10.4%, and 3.6+/-9.4% in IS, IR, and OIR, respectively (all P<0.01). CONCLUSIONS: Insulin resistance without and with obesity is associated with elevated LDL-C as well as elevated triglyceride and low HDL-C. The elevated LDL-C cannot be explained by dietary sensitivity, because the LDL-C rise with egg feeding is less in IR persons regardless of obesity status, probably attributable to diminished cholesterol absorption. The results suggest that dietary management of insulin resistance and obesity can focus more on restricting calories and less on restricting dietary fat.

The atherogenic lipoprotein profile associated with obesity and insulin resistance is largely attributable to intra-abdominal fat.

Obesity and insulin resistance are both associated with an atherogenic lipoprotein profile. We examined the effect of insulin sensitivity and central adiposity on lipoproteins in 196 individuals (75 men and 121 women) with an average age of 52.7 years. Subjects were subdivided into three groups based on BMI and their insulin sensitivity index (S(I)): lean insulin sensitive (n = 65), lean insulin resistant (n = 73), and obese insulin resistant (n = 58). This categorization revealed that both obesity and insulin resistance determined the lipoprotein profile. In addition, the insulin-resistant groups had increased central adiposity. Increasing intra-abdominal fat (IAF) area, quantified by computed tomography scan and decreasing S(I), were important determinants of an atherogenic profile, marked by increased triglycerides, LDL cholesterol, and apolipoprotein B and decreased HDL cholesterol and LDL buoyancy (Rf). Density gradient ultracentrifugation (DGUC) revealed that in subjects who had more IAF and were more insulin resistant, the cholesterol content was increased in VLDL, intermediate-density lipoprotein (IDL), and dense LDL fractions whereas it was reduced in HDL fractions. Multiple linear regression analysis of the relation between the cholesterol content of each DGUC fraction as the dependent variable and IAF and S(I) as independent variables revealed that the cholesterol concentration in the fractions corresponding to VLDL, IDL, dense LDL, and HDL was associated with IAF, and that S(I) additionally contributed independently to VLDL, but not to IDL, LDL, or HDL. Thus an atherogenic lipoprotein profile appears to be the result primarily of an increase in IAF, perhaps via insulin resistance.

The concurrent accumulation of intra-abdominal and subcutaneous fat explains the association between insulin resistance and plasma leptin concentrations : distinct metabolic effects of two fat compartments.

Obesity is associated with insulin resistance, particularly when body fat has a central distribution. However, insulin resistance also frequently occurs in apparently lean individuals. It has been proposed that these lean insulin-resistant individuals have greater amounts of body fat than lean insulin-sensitive subjects. Alternatively, their body fat distribution may be different. Obesity is associated with elevated plasma leptin levels, but some studies have suggested that insulin sensitivity is an additional determinant of circulating leptin concentrations. To examine how body fat distribution contributes to insulin sensitivity and how these variables are related to leptin levels, we studied 174 individuals (73 men, 101 women), a priori classified as lean insulin-sensitive (LIS, n = 56), lean insulin-resistant (LIR, n = 61), and obese insulin-resistant (OIR, n = 57) based on their BMI and insulin sensitivity index (S(I)). Whereas the BMI of the two lean groups did not differ, the S(I) of the LIR subjects was less than half that of the LIS group. The subcutaneous and intra-abdominal fat areas, determined by computed tomography, were 45 and 70% greater in the LIR subjects (P < 0.001) and 2.5- and 3-fold greater in the OIR group, as compared with the LIS group. Fasting plasma leptin levels were moderately increased in LIR subjects (10.8 +/- 7.1 vs. 8.1 +/- 6.4 ng/ml in LIS subjects; P < 0.001) and doubled in OIR subjects (21.9 +/- 15.5 ng/ml; P < 0.001). Because of the confounding effect of body fat, we examined the relationships between adiposity, insulin sensitivity, and leptin concentrations by multiple regression analysis. Intra-abdominal fat was the best variable predicting insulin sensitivity in both genders and explained 54% of the variance in S(I). This inverse relationship was nonlinear (r = -0.688). On the other hand, in both genders, fasting leptin levels were strongly associated with subcutaneous fat area (r = 0.760) but not with intra-abdominal fat. In line with these analyses, when LIS and LIR subjects were matched for subcutaneous fat area, age, and gender, they had similar leptin levels, whereas their intra-abdominal fat and insulin sensitivity remained different. Thus, accumulation of intra-abdominal fat correlates with insulin resistance, whereas subcutaneous fat deposition correlates with circulating leptin levels. We conclude that the concurrent increase in these two metabolically distinct fat compartments is a major explanation for the association between insulin resistance and elevated circulating leptin concentrations in lean and obese subjects.