Ph.D.

published_or_final_version / Pharmacology and Pharmacy / Doctoral / Doctor of Philosophy

Not available / text

published_or_final_version / Pharmacology / Doctoral / Doctor of Philosophy

published_or_final_version / Pharmacology / Doctoral / Doctor of Philosophy

No description available.

No description available.

Background: Celiac disease occurs worldwide in approximately 1% of the population, whereof the majority of cases are undiagnosed. Sweden experienced an epidemic (1984-1996) of clinically detected celiac disease in children below 2 years of age, partly attributed to changes in infant feeding. Whether the epidemic constituted a change in disease occurrence and/or a shift in the proportion of diagnosed cases remains unknown. Moreover, the cause of the epidemic is not fully understood. Objective: To increase the knowledge regarding the occurrence of celiac disease in Sweden, with focus on the epidemic period and thereafter, as well as the etiology of celiac disease in general, by investigating the Swedish epidemic and its potential causes. Methods: We performed a two-phased cross-sectional multicenter screening study investigating the total prevalence, including both clinically- and screening-detected cases, of celiac disease in 2 birth cohorts of 12-year-olds (n=13 279): 1 of the epidemic period (1993) and 1 of the post-epidemic period (1997). The screening strategy entailed serological markers analyses, with subsequent small intestinal biopsy when values were positive. Diagnosis was ascertained in clinical cases detected prior to screening. Infant feeding practices in the cohorts were ascertained via questionnaires. An ecological approach combined with an incident case-referent study (475 cases, 950 referents) performed during the epidemic were used for investigating environmental- and lifestyle factors other than infant feeding. Exposure information was obtained via register data, a questionnaire, and child health clinic records. All studies utilized the National Swedish Childhood Celiac Disease Register. Results: The total prevalences of celiac disease were 2.9% and 2.2% for the 1993 and 1997 cohorts, respectively, with 2/3 cases unrecognized prior to screening. Children born in 1997 had a significantly lower celiac disease prevalence compared to those born in 1993 (prevalence ratio, 0.75; 95% confidence interval [CI], 0.60-0.93). The cohorts differed in infant feeding; more specifically in the proportion of infants introduced to dietary gluten in small amounts during ongoing breastfeeding. Of the environmental and lifestyle factors investigated, no additional changes over time coincided with the epidemic. Early vaccinations within the Swedish program were not risk factors for celiac disease. Early infections (≥3 parental-reported episodes) were associated with increased risk for celiac disease (adjusted odds ratio [OR] 1.5; 95% CI, 1.1-2.0), a risk that increased synergistically if, in addition to having ≥3 infectious episodes, the child was introduced to gluten in large amounts, compared to small or medium amounts, after breastfeeding was discontinued (OR 5.6; 95% CI, 3.1-10). Early infections probably made a minor contribution to the Swedish epidemic through the synergistic effect with gluten, which changed concurrently. In total, approximately 48% of the epidemic could be explained by infant feeding and early infections. Conclusion: Celiac disease is both unexpectedly prevalent and mainly undiagnosed in Swedish children. Although the cause of the epidemic is still not fully understood, the significant difference in prevalence between the 2 cohorts indicates that the epidemic constituted a change in disease occurrence, and importantly, corroborates that celiac disease can be avoided in some children, at least up to 12 years of age. Our findings suggest that infant feeding and early infections, but not early vaccinations, have a causal role in the celiac disease etiology and that the infant feeding practice – gradually introducing gluten-containing foods from 4 months of age, preferably during ongoing breastfeeding – is favorable.

This study utilized both qualitative and quantitative procedures to examine the relationship between religiosity and eating disorders among a sample of nineteen eating disordered individuals who sought treatment at one of two college counseling centers, or at a hospital unit which specializes in treating eating disorders. Following theoretical works that point to asceticism as the link between religion and eating disorders, it was hypothesized that subject scores on the Shepherd Scale, a measure of religiosity from a Christian perspective, would positively correlate with scores on the Eating Disorder Inventory, a measure of eating disorder symptomatology, which includes a subscale that assesses asceticism. Analysis of subject scores shows no statistically significant correlation between religiosity and asceticism, though statistically significant negative correlations were found between religiosity and other Eating Disorder Inventory subscales. A marked difference in asceticism scores was found between subjects treated at the college counseling centers and those treated at the hospital unit. / Department of Counseling Psychology and Guidance Services

Background: Normative values of VO2max have been developed or updated based on the estimated VO2max, but measured normative values of VO2max have not been developed yet. VO2max has been reported to relate to coronary heart disease (CHD) risk factors, yet most of the studies have used estimated VO2max to compare CHD risk factors. Therefore, the purpose of this study was to develop norms for VO2max from the Ball State University (BSU) Adult Physical Fitness Program cohort that represented percentiles based on the measured VO2max. In addition, this study evaluated the relationship between measured VO2max and six coronary heart disease (CHD) risk factors, which include Body Bass Index (BMI), high density lipoprotein cholesterol (HDL-C), glucose, triglyceride (TG), total cholesterol (TC) and resting blood pressure (BP).Methods: Subjects were healthy men (N=1,867) and women (N=1,253), ranging in age from 19 to 75 years, who completed the standard BSU Adult Physical Fitness Program quiet and exercise testing sessions between 1971 and 2000, with the graded exercise testing (GXT) conducted with one of the following protocols including modified walking, running, Balke, Bruce, and BSU/Bruce ramp. To be included, subjects had to achieve respiratory exchange ratio (RER) >1.0 during their exercise test.Results: All subjects were classified into ten group determined by deciles of VO2max for each decade of age for males and females respectively. A linear regression showed that VO2max decreased 10.1% per decade (0.44 mi.kg'•min'•yr') for men and 9.7% per decade (0.32 ml•kg-l.min-l.yr') for women. There was no significant difference in the rate of agerelated decline in VO2max per decade between men and women or between deciles of VO2max. Also, the percent of subjects with an exercise history code >5 (regularly participate in exercise at least 3 days per week) was higher in the higher VO2max deciles. In addition, five positive CHD risk factors were inversely related to VO2max, and one negative CHD risk factor was directly related to VO2max. As expected, the higher CRF groups had a more favorable CHD risk factor profile. Also, the mean of VO2max decreased with the greater number of CHD risk factors.Conclusion: This study developed normative values of the VO2max based on measured VO2max. VO2max was significantly correlated to CHD risk factors. / School of Physical Education, Sport, and Exercise Science