Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2008. / Source: Dissertation Abstracts International, Volume: 69-11, Section: B, page: 6733. Adviser: Edward McAuley. Includes bibliographical references (leaves 101-117) Available on microfilm from Pro Quest Information and Learning.

Thesis (Ph.D.)--Indiana University, Dept. of Kinesiology, 2009. / Title from PDF t.p. (viewed on Jul 19, 2010). Source: Dissertation Abstracts International, Volume: 70-12, Section: B, page: 7486. Adviser: Timothy D. Mickleborough.

Thesis (Ph. D.)--University of Illinois at Urbana-Champaign, 2006. / Source: Dissertation Abstracts International, Volume: 67-07, Section: B, page: 3712. Advisers: Sharon M. Donovan; Kelly A. Tappenden. Includes bibliographical references (leaves 145-168). Available on microfilm from Pro Quest Information and Learning.

Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2006. / Source: Dissertation Abstracts International, Volume: 67-11, Section: B, page: 6317. Adviser: Karen Chapman-Novakofski. Includes bibliographical references. Available on microfilm from Pro Quest Information and Learning.

Food is a primary reinforcer. There is strong evidence that when animals are chronically deprived of calories, the reward of a food stimulus becomes more salient. Recently leptin has been implicated in food reward. Typically the rewarding value of food is separated into the "liking" or pleasure/palatability component generated by the stimulus, and into the "wanting" or appetitive/incentive component. The goal of this current study was examine whether plasma leptin concentrations were related to food hedonics and food reinforcement in humans and to investigate the effect of food deprivation on these variables. Fourteen apparently healthy obese adults (n=9 women and 5 men; age=33.5+/-7.8) with BMI (kg/m2) between 30-45 were subjected to 8 weeks of caloric deprivation (-700kcal/day). Plasma leptin (ELISA), body weight and composition (DEXA), food reinforcement and food hedonics were measured pre- and post-intervention. Post weight loss palatability was rated significantly higher for the food reinforcers than that measured pre weight loss (p<0.01). No significant effect of the chronic food deprivation was noted for the reinforcing value of food. A significant negative correlation was observed between changes in palatability and those in body weight expressed as relative changes (r=-.62; p<0.05). No significant correlations were noted between changes in leptin and those in palatability or the reinforcing value of food. However, in a subgroup that lost the greatest percent of initial body weight (7-8%), food was more reinforcing post intervention (p<0.05). These findings demonstrate that chronic caloric deprivation can increase the subjectively rated palatability of preferred food items. The subgroup may be a caveat illustrating that a greater relative weight loss can lead to food becoming more rewarding.

Doctor of Philosophy / Department of Human Nutrition / Weiqun Wang / Body weight control via increasing exercise and/or decreasing calorie intake has been linked to a reduced cancer risk in animal models. However, the underlying mechanisms are not clear. This study assessed the impact of exercise with or without limited dietary calorie intake on the overview profiling of phospholipids and gene expression in the skin tissues of weight controlled-mice. Mice were randomly assigned to three groups: ad libitum-fed sedentary control, ad libitum-fed treadmill exercise at 13.4 m/min for 60 min/d, 5 d/wk (Ex+AL), and exercise but pair-fed with the sedentary control (Ex+PF). After 10 wks, Ex+PF but not Ex+AL mice demonstrated a significant decrease in both body weight and percentage of body fat when compared to the sedentary controls. Among 338 phospholipids measured in the skin samples by electrospray ionization mass spectrometry, most classes of phosphatidylinositol (PI), phosphatidylcholine-containing lipids with ether linkage (ePC), and some lysophosphatidylcholine (lysoPC) significantly decreased in Ex+PF mice when compared to the controls. Furthermore, some species of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) containing omega-3 18:0-22:6 fatty acyl combinations increased significantly in Ex+PF mice. A total of 25 significantly-changed phospholipids were distinguishable between diet and exercise treatments by discriminant analysis. The reduced PI in Ex+PF mice was observed concomitantly with a significant reduction of PI3K protein expression. Among the 45,101 probe sets tested in skin tissues, expression of 839 genes was significantly changed by exercise with or without limited dietary calorie intake. The genes with impacted expression were involved in oxidative stress, inflammatory response, lipolysis, protein synthesis, and signaling pathway. Up-regulated expression of genes involved in elongation of long chain fatty acids in Ex+PF but not Ex+AL mice appears to partially account for increased level of 18:0-22:5PC/PE and 18:0-22:6 PC/PE. Taken together, these data indicate that controlling body weight via exercise with limited dietary calorie intake rather than exercise alone significantly modified phospholipid and gene expression profiles. The altered profiles may be associated with cancer preventive mechanisms; in particular, reduced PI and PI-related PI3K expression and altered expression of genes involved in protein kinase activity and lipid metabolism may prevent cancer.

Master of Science / Department of Human Nutrition / Mark D. Haub / BACKGROUND: Dietary supplements are increasing in popularity; individuals are looking beyond traditional methods of calorie restriction and exercise to improve health. Calcium is a critical nutrient for bone metabolism that has also been shown to enhance weight loss effects secondary to diet. PURPOSE: To determine whether eight months of calcium supplementation, in a liquid, shelf-stable form, increases bone mineral density or decreases body weight and/or body fat in free-living young adult women. METHODS: Volunteer subjects (n=42) were randomly assigned to a supplement group receiving 1,125 mg Ca2+/day (CA-BEV) or to a free-living control group (CON), which did not receive the supplement. At baseline and after the 8-month intervention (POST), dietary intake was assessed using 3-day diet records. Total body composition (body fat percentage, %FatTB; abdominal percentage fat, %FatAb; fat mass, FM; non-bone fat-free mass, FFM) and bone mineral density (lumbar spine and femoral neck; BMD) were measured via dual energy x-ray absorptiometry. Subjects also completed a sub-maximal treadmill exercise test to estimate respiratory fitness at baseline and POST. RESULTS: At POST, the CA-BEV group's calcium intake (1,868[plus or minus]941 mg/d) was significantly greater than (p<0.05) the CON group (867[plus or minus]405 mg/d) and the calcium:protein ratio of the CA-BEV group (29.5[plus or minus]17.1 mg/g) was greater than (p<0.05) the CON group (12.9 ±6.2 mg/g). Those differences in calcium did not lead to predicted differences (p<0.05) between groups for BMD, body weight, %FatTB, %FatAB, FM or FFM. CONCLUSION: Our findings do not support the hypothesis that increasing calcium intake increases BMD or decreases body weight or body fat in healthy young women over an 8-month period despite a nearly two-fold increase in calcium intake.

Obesity is a risk factor for several cancers, including colorectal cancer (CRC). I and my colleagues investigated adulthood weight change and body fat distribution and its change in relation to CRC risk in the Nurses’ Health Study and Health Professionals Follow-up Study. We also identified distinct trajectories of body fatness across the lifespan using a group-based modeling approach and then compared cancer risk across these trajectories. We found that weight gain from early adulthood to baseline was associated with an increased risk of CRC, whereas weight loss was associated with a lower risk. The association was stronger in men than in women. High waist circumference, hip circumference and waist-to-hip ratio were all associated with a higher risk of CRC in men, even after adjusting for body mass index. The associations were weaker in women. Ten-year gain of waist circumference, independent of weight change, was positively associated with CRC risk in men, but not in women. We identified 5 distinct adiposity trajectories across the lifespan: lean-stable, lean-moderate increase, lean-marked increase, medium-stable, and heavy-marked increase. Compared to women in the lean-stable group, those in the lean-marked increase and heavy-marked increase groups had a higher risk of esophageal adenocarcinoma and cancers of the colorectum, pancreas, kidney, and endometrium. Postmenopausal breast cancer risk was inversely associated with early-life adiposity, but was positively associated with late-life adiposity. In men, increased body fatness at any life period was associated with a higher risk of esophageal adenocarcinoma and colorectal cancer; compared to men in the lean-stable group, those in the heavy-marked increase group had a higher risk of pancreatic cancer, but lower risk of advanced prostate cancer. The trajectory-cancer associations were generally stronger for non-smokers and women who did not use menopausal hormone therapy. In conclusion, weight gain from early to middle adulthood was positively, and weight loss was negatively associated with CRC risk. Abdominal adiposity was positively associated with CRC risk and this association was stronger and independent of overall obesity in men than in women. Adiposity trajectories throughout life were associated with cancer risk and the pattern of associations varied by sex and cancer site. / Nutrition

Background: Fine particulate matter (PM2.5) pollution is a major risk factor for cardiovascular diseases. Identifying modifiable factors and preventative strategies to mitigate the cardiovascular effect of PM2.5 is essential to aid the development of personalized intervention. Method: Chapter one and two were based on a crossover human intervention trial using B vitamin supplementation (2.5 mg/d folic acid, 50 mg/d vitamin B6, and 1 mg/d vitamin B12). Ten volunteer received three two-hour controlled exposure experiments to medical air or PM2.5 (250μg/m3), in pre-determined order. Chapter three utilized the Normative Aging Study, a longitudinal cohort study with 573 elderly men. We used electrocardiogram to measure resting heart rate (HR) and heart rate variability (HRV), hematology analyzer to determine white blood cell (WBC) counts, and Infinium HumanMethylation450 BeadChip to measure DNA methylation in peripheral CD4+ T helper (Th) cells (pre-, post-, 24-hr post-exposure). Blood TLR2 methylation was analyzed using pyrosequencing. Daily flavonoid and methyl nutrients intakes were assessed through the Food Frequency Questionnaire. Results: Compared to medical air, PM2.5 exposure was associated with 3.8 beat/min (95% CI, 0.3, 7.4; P=0.04) higher resting HR, 57.5% (95% CI, 2.5%, 81.5%; P=0.04) lower low-frequency (LF) power, and altered DNA methylation landscape, following exposure. PM2.5 exposure was associated with 11.5% (95% CI, 0.3%, 24.0%; P=0.04) higher total WBC count and 12.9% (95% CI, 4.4%, 22.1%; P=0.005) higher lymphocyte count, at 24-hour post-exposure. These effects of PM2.5 were abrogated with B vitamins supplement. In the Normative Aging Study, every 10 µg/m3 increase in 48-hour PM2.5 moving average was associated with 7.74% (95%CI: -1.21%, 15.90%; P=0.09), 7.46% (95%CI: 0.99%, 13.50%; P=0.02), 14.18% (95%CI, 1.14%, 25.49%; P=0.03), and 12.94% (95%CI, -2.36%, 25.96%; P=0.09) reductions in root mean square of successive differences (rMSSD), standard deviation of normal-to-normal intervals (SDNN), LF power, and high-frequency (HF) power, respectively. Higher TLR2 methylation exacerbated the rMSSD, SDNN, LF, and HF reductions associated with heightened PM2.5 (Pinteraction=0.006, 0.03, 0.05, 0.04, respectively). Every interquartile-range increase in flavonoid intake was associated with 5.09% reduction in mean TLR2 methylation (95%CI, 0.12%, 10.06%; P=0.05) and counteracted the effects of PM2.5 on LF (Pinteraction=0.05). Conclusions: Ambient PM2.5 exposure peak has unfavorable effect on cardiac autonomic function, the immune system, and the epigenome – which, can be counteracted by B vitamins supplementation. In addition, the epigenetic regulation of TLR2-related immunity may determine vulnerability of older individuals when confronted with air pollution peaks.

The purpose of this study was to examine social physique anxiety (SPA) and disordered eating in female aesthetic athletes. Participants included 144 female competitive athletes (M = 19.0 years, SD = 2.08) from the four aesthetic sports of synchronized swimming, figure skating, jazz dance, and gymnastics. The participants completed the SPA scale (SPAS) and the Questionnaire for Eating Disorder Diagnoses (Q-EDD) (which is a new more accurate measure to assess disordered eating) that has not previously been used with female aesthetic athletes. Results revealed that 59.7% of the participants were classified in the asymptomatic category, 29.9% in the symptomatic category, and 10.4% in the eating disordered category. For the two Q-EDD subcategories, there were no participants classified in the chew/spitting category, and three participants classified in the exercise bulimia nervosa category. Also, it was shown that the eating disordered group and the symptomatic group had significantly higher SPA than the asymptomatic group. Thus, these results indicate that in this subpopulation of athletes, there are many who display eating disorder symptomatology, and suggest that interventions that target SPA and disordered eating in these athletes are needed.