Obesity: Thompson IM

Wang C, Nieschlag E, Swerdloff R, Behre HM, Hellstrom WJ, Gooren LJ, Kaufman JM, Legros JJ, Lunenfeld B, Morales A, Morley JE, Schulman C, Thompson IM, Weidner W, Wu FC, Anonymous00084, Anonymous00085, Anonymous00086, Anonymous00087, Anonymous00088. · Division of Endocrinology, Department of Medicine, Harbor-UCLA Medical Center, and Los Angeles BioMedical Research Institute, Torrance, CA 90509, USA. · J Androl. · Pubmed #18772485 No free full text.

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Schenk JM, Kristal AR, Neuhouser ML, Tangen CM, White E, Lin DW, Thompson IM. · Fred Hutchinson Cancer Research Center, Cancer Prevention Program, Seattle, Washington 98109-1024, USA. · Prostate. · Pubmed #19475640 No free full text.

Abstract: BACKGROUND: Recent epidemiologic studies have identified obesity as a risk factor for benign prostatic hyperplasia (BPH). We examined whether adiponectin, leptin, and C-peptide were associated with incident, symptomatic BPH and whether these factors mediate the relationship between obesity and BPH risk. METHODS: Data are from Prostate Cancer Prevention Trial placebo arm participants who were free of BPH at baseline. Incident BPH (n = 698) was defined as treatment, two International Prostate Symptom Score (IPSS) values > 14, or an increase of >or=5 in IPSS from baseline documented on at least two occasions plus at least one score >or=12. Controls (n = 709) were selected from men reporting no BPH treatment or IPSS > 7 during the 7-year trial. Baseline serum was analyzed for adiponectin, C-peptide, and leptin concentrations. RESULTS: Neither C-peptide nor leptin was associated with BPH risk. The odds ratio [95% CI] contrasting highest to lowest quartiles of adiponectin was 0.65[0.47, 0.87] P(trend) = 0.004. Findings differed between levels of physical activity: there was a strong inverse association between adiponectin and BPH among moderately/very active men OR = 0.43 [0.29, 0.63], and no association among sedentary/minimally active men OR = 0.92 [0.65, 1.30] P(interaction) = 0.005. Adiponectin concentrations explained only a moderate amount of the relationship between obesity and BPH risk. CONCLUSIONS: High adiponectin concentrations were associated with reduced risk of incident, symptomatic BPH. This association was limited to moderately/very active men; suggesting the relationship between obesity and BPH involves a complex interaction between factors affecting glucose uptake and insulin sensitivity. However, adiponectin is likely not the only mechanism through which obesity affects BPH risk.

Kristal AR, Arnold KB, Schenk JM, Neuhouser ML, Weiss N, Goodman P, Antvelink CM, Penson DF, Thompson IM. · Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. · J Urol. · Pubmed #17382740 No free full text.

Abstract: PURPOSE: We examined risk factors for incident symptomatic benign prostate hyperplasia in 5,667 Prostate Cancer Prevention Trial placebo arm participants who were free of benign prostatic hyperplasia at baseline. MATERIALS AND METHODS: During 7 years benign prostatic hyperplasia symptoms were assessed annually using the International Prostate Symptom Score and benign prostatic hyperplasia treatment was assessed quarterly by structured interview. Total benign prostatic hyperplasia was defined as receipt of treatment or report of 2 International Prostate Symptom Score values greater than 14. Severe benign prostatic hyperplasia was defined as treatment or 2 International Prostate Symptom Score values of 20 or greater. Weight and body circumferences were measured by trained staff and demographic health related characteristics were collected by questionnaire. Cox proportional hazards models were used to calculate the covariate adjusted relative hazards of benign prostatic hyperplasia developing. RESULTS: The incidence of total benign prostatic hyperplasia was 34.4 per 1,000 person-years. The risk of total benign prostatic hyperplasia increased 4% (p <0.001) with each additional year of age. Risks for total benign prostatic hyperplasia were 41% higher for black (p <0.03) and Hispanic men (p <0.06) compared to white men, and for severe benign prostatic hyperplasia these increases were 68% (p <0.01) and 59% (p <0.03), respectively. Each 0.05 increase in waist-to-hip ratio (a measure of abdominal obesity) was associated with a 10% increased risk of total (p <0.003) and severe (p <0.02) benign prostatic hyperplasia. Neither smoking nor physical activity was associated with risk. CONCLUSIONS: Black race, Hispanic ethnicity and obesity, particularly abdominal obesity, are associated with increased benign prostatic hyperplasia risk. Weight loss may be helpful for the treatment or prevention of benign prostatic hyperplasia.

Gong Z, Neuhouser ML, Goodman PJ, Albanes D, Chi C, Hsing AW, Lippman SM, Platz EA, Pollak MN, Thompson IM, Kristal AR. · Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North M4-B402, Seattle, WA 98109-1024, USA. · Cancer Epidemiol Biomarkers Prev. · Pubmed #17035408 links to  free full text

Abstract: Studies on the relationship between obesity and prostate cancer incidence are inconsistent. In part, this inconsistency may be due to a differential effect of obesity on low-grade and high-grade cancer or confounding of the association of obesity with prostate cancer risk by diabetes. We investigated the associations of obesity and diabetes with low-grade and high-grade prostate cancer risk. Data were from 10,258 participants (1,936 prostate cancers) in the Prostate Cancer Prevention Trial who all had cancer presence or absence determined by prostate biopsy. Multiple logistic regression was used to model the risk of total prostate cancer, and polytomous logistic regression was used to model the risk of low-grade and high-grade prostate cancer. Compared with men with body mass index < 25, obese men (body mass index > or =30) had an 18% [odds ratio (OR), 0.82; 95% confidence interval (95% CI), 0.69-0.98] decreased risk of low-grade prostate cancer (Gleason <7) and a 29% (OR, 1.29; 95% CI, 1.01-1.67) increased risk of high-grade prostate cancer (Gleason > or =7) or, alternatively, a 78% (OR, 1.78; 95% CI, 1.10-2.87) increased risk defining high-grade cancer as Gleason sum 8 to 10. Diabetes was associated with a 47% (OR, 0.53; 95% CI, 0.34-0.83) reduced risk of low-grade prostate cancer and a 28% (OR, 0.72; 95% CI, 0.55-0.94) reduced risk of high-grade prostate cancer. Associations of obesity or diabetes with cancer risk were not substantially changed by mutually statistical controlling for each other. Obesity increases the risk of high-grade but decreases the risk of low-grade prostate cancer, and this relationship is independent of the lower risk for prostate cancer among men with diabetes.

Baillargeon J, Platz EA, Rose DP, Pollock BH, Ankerst DP, Haffner S, Higgins B, Lokshin A, Troyer D, Hernandez J, Lynch S, Leach RJ, Thompson IM. · Center for Epidemiology and Biostatistics, University of Texas Health Sciences Center at San Antonio, 78284-7802, USA. · Cancer Epidemiol Biomarkers Prev. · Pubmed #16835332 links to  free full text

Abstract: BACKGROUND: The purpose of this investigation was to examine the association of obesity and the adipokines leptin, adiponectin, and interleukin-6 (IL-6) with prostate cancer risk and aggressiveness. METHODS: One hundred twenty-five incident prostate cancer cases and 125 age-matched controls were sampled from among participants in the original San Antonio Center for Biomarkers of Risk of Prostate Cancer cohort study. The odds ratios (OR) of prostate cancer and high-grade disease (Gleason sum >7) associated with the WHO categories of body mass index (kg/m(2)) and with tertiles of serum concentrations of adiponectin, leptin, and IL-6 were estimated using multivariable conditional logistic regression models. RESULTS: Body mass index was not associated with either incident prostate cancer [obese versus normal; OR, 0.75; 95% confidence interval (95% CI), 0.38-1.48; P(trend) = 0.27] or high-grade versus low-grade disease (OR, 1.17; 95% CI, 0.39-3.52; P(trend) = 0.62). Moreover, none of the three adipokines was statistically significant associated with prostate cancer risk or high-grade disease, respectively: leptin (highest versus lowest tertile; OR, 0.77; 95% CI, 0.28-1.37; P(trend) = 0.57; OR, 1.20; 95% CI, 0.48-3.01; P(trend) = 0.85); adiponectin (OR, 0.87; 95% CI, 0.46-1.65; P(trend) = 0.24; OR, 1.93; 95% CI, 0.74-5.10; P(trend) = 0.85); IL-6 (OR, 0.84; 95% CI, 0.46-1.53; P(trend) = 0.98; OR, 0.84; 95% CI, 0.30-2.33; P(trend) = 0.17). CONCLUSIONS: Findings from this nested case-control study of men routinely screened for prostate cancer and who had a high prevalence of overweight and obesity do not provide evidence to support that prediagnostic obesity or factors elaborated by fat cells strongly influence prostate cancer risk or aggressiveness. However, due to the small sample population, a small or modest effect of obesity and adipokines on these outcomes cannot be excluded.

Thompson IM, Leach R, Troyer D, Pollock B, Naylor S, Higgins B. · Departments of Surgery and Pathology and Cellular and Structural Biology, University of Texas HSC at San Antonio, The San Antonio Center for Biomarkers of Risk of Prostate Cancer (SABOR), San Antonio Cancer Institute, TX 78229, USA. · Urol Oncol. · Pubmed #15082010 No free full text.

Abstract: This study was designed to use a prospectively analyzed, population-based, multiethnic cohort of men to determine if there is a relationship between one measure of obesity/overweight (Body Mass Index) and Prostate Specific Antigen (PSA). A total of 1565 men without a prior diagnosis of prostate cancer were prospectively enrolled in the San Antonio study of Biomarkers Of Risk (SABOR) Clinical and Epidemiologic Center of the Early Detection Research Network of the National Cancer Institute. Body Mass Index (BMI) was compared with serum PSA levels, stratifying by ethnic group. No relationship was found between BMI and PSA in any ethnic group or in the cohort as a whole. This study suggests that there is no increased risk of overdetection of prostate cancer among obese men due to an elevation in PSA.