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Caitlin Mason,
Catherine M Alfano,
Ashley Wilder Smith,
Ching-Yun Wang, Marian L Neuhouser,
Catherine Duggan,
Leslie Bernstein,
Kathy B Baumgartner,
Richard N Baumgartner,
Rachel Ballard-Barbash,
Anne McTiernan
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ABSTRACT: BACKGROUND: Physical activity is associated with reduced mortality and higher quality of life in breast cancer survivors; however, limited data on the prevalence of activity and long-term trends after diagnosis are available. METHODS: A multi-ethnic cohort of 631 women (18-64 years) with stage 0-IIIA breast cancer were followed for 10 years. Recreational aerobic activity (MET-hrs/week) was ascertained for the year before diagnosis (baseline), 24 months, 5 and 10 years after enrollment. Women were classified according to U.S. physical activity guidelines (≥150 mins/week moderate or ≥75 mins/week vigorous activity). The odds ratios (OR) for meeting guidelines at 5 and 10 years according to baseline factors was estimated using logistic regression. The change in MET-hrs/wk was predicted using linear regression. RESULTS: Pre-diagnosis, 34% of women met physical activity guidelines; 34.0%, 39.5%, and 21.4% met guidelines at 24 months, 5 years, and 10 years post-enrollment, respectively. Fewer than 8% of survivors met guidelines at all follow-up periods. Over 10 years, recreational aerobic activity decreased by a mean(SD) 4.3(16.2) MET-hrs/wk. . Meeting guidelines pre-diagnosis was strongly associated with meeting guidelines at 5 years [OR (95% CI): 2.76 (1.85-4.1)] and 10 years [OR (95% CI): 3.35 (2.13-5.28)]. No other demographic or prognostic factors were significantly associated with the 10-year change in MET-hrs/wk. CONCLUSIONS: The majority of early breast cancer survivors do not meet national exercise recommendations 10 years post-diagnosis. Impact:Physical activity levels are low in breast cancer survivors across the 10 years post-diagnosis, yet the predictors of activity in this population remain poorly understood.
Cancer Epidemiology Biomarkers & Prevention 04/2013; · 4.12 Impact Factor
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ABSTRACT: The authors investigated associations of serum phospholipid n-3 and n-6 polyunsaturated fatty acids (PUFAs) and trans-fatty acids with prostate cancer risk, and whether myeloperoxidase G-463A (rs2333227) modified the associations in the Carotene and Retinol Efficacy Trial (CARET) (Seattle, Washington; Irvine, California; New Haven, Connecticut; San Francisco, California; Baltimore, Maryland; and Portland, Oregon, 1985-2003). Prerandomization sera were assayed for fatty acids among 641 men with incident prostate cancer (368 nonaggressive and 273 aggressive (stage III/IV or Gleason score ≥7)) and 1,398 controls. Overall, dihomo-γ-linolenic (quartiles 4 vs. 1: odds ratio (OR) = 0.66, 95% confidence interval (CI): 0.49, 0.95; Ptrend = 0.024) and docosatetraenoic (OR = 0.69, 95% CI: 0.46, 1.02; Ptrend = 0.011) acids were inversely associated with nonaggressive and aggressive prostate cancer risks, respectively. Among men with MPO GG, the genotype upregulating oxidative stress, quartiles 4 versus 1 eicosapentaenoic plus docosahexaenoic acids were suggestively associated with an increased risk of aggressive prostate cancer (OR = 1.66, 95% CI: 0.95, 2.92; Ptrend = 0.07). However, the association was the inverse among men with MPO GA/AA genotypes (Pinteraction = 0.011). Interactions were also observed for docosapentaenoic acid, total n-3 PUFAs, and arachidonic acid. MPO GA/AA vs. GG was associated with a 2-fold increase in aggressive prostate cancer risk among men with low (quartile 1) n-3 PUFAs. This study adds important evidence linking oxidative stress with prostate carcinogenesis.
American journal of epidemiology 03/2013; · 5.59 Impact Factor
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Heather M Ochs-Balcom,
Leah Preus,
Jean Wactawski-Wende,
Jing Nie,
Nicholas A Johnson,
Fouad Zakharia,
Hua Tang,
Chris Carlson,
Cara Carty,
Zhao Chen, [......],
Li Li,
Song Liu, Marian L Neuhouser,
Ulrike Peters,
John Robbins,
Michael F Seldin,
Timothy A Thornton,
Cheryl L Thompson,
Charles Kooperberg,
Lara E Sucheston
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ABSTRACT: Context:Both genes and environment have been implicated in determining the complex body composition phenotypes in individuals of European ancestry; however, few studies have been conducted in other race/ethnic groups.Objective:We conducted a genome-wide admixture mapping study in an attempt to localize novel genomic regions associated with genetic ancestry.Setting/Participants:We selected a sample of 842 African-American women from the Women's Health Initiative single nucleotide polymorphism (SNP) Health Association Resource for whom several dual-energy X-ray absorptiometry (DXA)-derived bone mineral density (BMD) and fat mass phenotypes were available.Methods:We derived both global and local ancestry estimates for each individual from Affymetrix 6.0 data and analyzed the correlation of DXA phenotypes with global African ancestry. For each phenotype, we examined the association of local genetic ancestry (number of African ancestral alleles at each marker) and each DXA phenotype at 570 282 markers across the genome in additive models with adjustment for important covariates.Results:We identified statistically significant correlations of whole-body fat mass, trunk fat mass, and all 6 measures of BMD with a proportion of African ancestry. Genome-wide (admixture) significance for femoral neck BMD was achieved across 2 regions ∼3.7 MB and 0.3 MB on chromosome 19q13; similarly, total hip and intertrochanter BMD were associated with local ancestry in these regions. Trunk fat was the most significant fat mass phenotype showing strong, but not genomewide significant associations on chromosome Xp22.Conclusions:Our results suggest that genomic regions in postmenopausal African-American women contribute to variance in BMD and fat mass existence and warrant further study.
The Journal of clinical endocrinology and metabolism 02/2013; · 6.50 Impact Factor
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Marian L Neuhouser,
Chongzhi Di,
Lesley F Tinker,
Cynthia Thomson,
Barbara Sternfeld,
Yasmin Mossavar-Rahmani,
Marcia L Stefanick,
Stacy Sims,
J David Curb,
Michael Lamonte,
Rebecca Seguin,
Karen C Johnson,
Ross L Prentice
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ABSTRACT: We used a biomarker of activity-related energy expenditure (AREE) to assess measurement properties of self-reported physical activity and to determine the usefulness of AREE regression calibration equations in the Women's Health Initiative. Biomarker AREE, calculated as the total energy expenditure from doubly labeled water minus the resting energy expenditure from indirect calorimetry, was assessed in 450 Women's Health Initiative participants (2007-2009). Self-reported AREE was obtained from the Arizona Activity Frequency Questionnaire (AAFQ), the 7-Day Physical Activity Recall (PAR), and the Women's Health Initiative Personal Habits Questionnaire (PHQ). Eighty-eight participants repeated the protocol 6 months later. Reporting error, measured as log(self-report AREE) minus log(biomarker AREE), was regressed on participant characteristics for each instrument. Body mass index was associated with underreporting on the AAFQ and PHQ but overreporting on PAR. Blacks and Hispanics underreported physical activity levels on the AAFQ and PAR, respectively. Underreporting decreased with age for the PAR and PHQ. Regressing logbiomarker AREE on logself-reported AREE revealed that self-report alone explained minimal biomarker variance (R(2) = 7.6, 4.8, and 3.4 for AAFQ, PAR, and PHQ, respectively). R(2) increased to 25.2, 21.5, and 21.8, respectively, when participant characteristics were included. Six-month repeatability data adjusted for temporal biomarker variation, improving R(2) to 79.4, 67.8, and 68.7 for AAFQ, PAR, and PHQ, respectively. Calibration equations "recover" substantial variation in average AREE and valuably enhance AREE self-assessment.
American journal of epidemiology 02/2013; · 5.59 Impact Factor
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ABSTRACT: BACKGROUND: Inflammation underlies the etiology of colorectal cancer (CRC). Hyperhomocysteinemia is associated with inflammation and may be a risk marker for CRC. Cysteine is a metabolic product of homocysteine and a precursor of the antioxidant glutathione. It is unknown whether cysteine is associated with CRC. OBJECTIVE: The objective was to assess the associations between homocysteine and cysteine and CRC incidence in postmenopausal women. DESIGN: Associations between homocysteine and cysteine and incident CRC in the Women's Health Initiative observational cohort were assessed by using a nested case-control design. Cases and controls (n = 988/group) were matched for age (mean ± SD age: 67 ± 7 y), ethnicity (85.2% white, 8.9% black, 2.2% Hispanic/Latina, and 3.6% other), hysterectomy status, and date of blood draw. Homocysteine and cysteine were measured by HPLC with postcolumn fluorimetric detection. RESULTS: Multivariate-adjusted ORs (95% CIs) for CRC were 1.46 (1.05, 2.04) for the highest quartile of homocysteine (>9.85 μmol/L) compared with the lowest quartile (≤6.74 μmol/L) (P = 0.02) and 0.57 (0.40, 0.82) for the highest quartile of cysteine (>309 μmol/L) compared with the lowest quartile (≤260 μmol/L) (P = 0.01). The association with homocysteine was significant for proximal colon tumors (P = 0.008) but not for distal or rectal tumors, whereas the association with cysteine was significant for rectal tumors (P = 0.02), borderline for proximal tumors (P = 0.06), and not significant for distal tumors. The associations with both homocysteine and cysteine were significant for localized tumors (P ≤ 0.01) but not for metastases. CONCLUSION: High plasma homocysteine is associated with increased risk of CRC, whereas high cysteine is associated with decreased risk. This trial was registered at clinicaltrials.gov as NCT 00000611.
American Journal of Clinical Nutrition 02/2013; · 6.67 Impact Factor
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ABSTRACT: PURPOSE: Tea and coffee contain bioactive compounds and both beverages have recently been associated with a reduced risk of prostate cancer (PCa). METHODS: We studied associations of tea and coffee consumption with PCa risk in a population-based case-control study from King County, Washington, USA. Prostate cancer cases were diagnosed in 2002-2005 and matched to controls by 5-year age groups. Logistic regression was used to generate odds ratios (ORs) and 95 % confidence intervals (CIs). RESULTS: Among controls, 19 and 58 % consumed at least one cup per day of tea and coffee, respectively. The analysis of tea included 892 cases and 863 controls, and tea consumption was associated with a reduced overall PCa risk with an adjusted OR of 0.63 (95 % CI: 0.45, 0.90; P for trend = 0.02) for men in the highest compared to lowest category of tea intake (≥2 cups/day vs. ≤1 cup/week). Risk estimates did not vary substantially by Gleason grade or disease stage. Coffee consumption was not associated with risk of overall PCa or PCa in subgroups defined by tumor grade or stage. CONCLUSIONS: Our results contribute further evidence that tea consumption may be a modifiable exposure that reduces PCa risk.
Cancer Causes and Control 02/2013; · 2.88 Impact Factor
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ABSTRACT: PURPOSE: Despite limited evidence on the association of vitamin D with outcomes in breast cancer survivors, some clinicians advise breast cancer patients to use vitamin D supplements. More evidence is needed to inform these recommendations. METHODS: In the Health, Eating, Activity, and Lifestyle study, we examined associations of post-treatment serum concentrations of 25-hydroxyvitamin D (25(OH)D) on overall and breast cancer-specific mortality in 585 breast cancer survivors from western Washington State, New Mexico, and Los Angeles County. 25(OH)D was measured in stored blood collected 2 years post-enrollment. Outcomes were ascertained from the Surveillance, Epidemiology, and End Results registries and medical records. Cox proportional hazards models were fit to assess associations of serum 25(OH)D with overall and breast cancer-specific mortality. RESULTS: After a median follow-up of 9.2 years; 110 women died, including 48 from breast cancer. Standard cut points classified 211 (31.6 %) women as serum 25(OH)D deficient (<20 ng/mL), 189 (32.2 %) as insufficient (20-30 ng/mL), and 185 (36.2 %) as sufficient (>30 ng/mL). Compared to women with deficient 25(OH)D, those in the sufficient ranges had a decreased risk of overall mortality (age-adjusted HR = 0.58; 95 % CI 0.36-0.96); however, multivariate adjustments attenuated the association (HR = 0.90; 95 % CI 0.50-1.61). No association was found between serum 25(OH)D and breast cancer-specific mortality (sufficient: HR = 1.21; 95 % CI 0.52-2.80) in multivariate models. CONCLUSION: In this breast cancer cohort, higher serum 25(OH)D may be associated with improved survival, but results were not statistically significant and must be interpreted with caution. The potential prognostic effect of vitamin D from diet, supplements, or both should be evaluated in future larger studies with additional endpoints from breast cancer patients.
Cancer Causes and Control 01/2013; · 2.88 Impact Factor
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ABSTRACT: BACKGROUND: Evidence suggests that high-heat cooking methods may increase the risk of prostate cancer (PCa). The addition of oil/fat, as in deep-frying, may be of particular concern, and has not specifically been investigated in relation to PCa. Potential mechanisms include the formation of potentially carcinogenic agents such as aldehydes, acrolein, heterocyclic amines, polycyclic aromatic hydrocarbons, and acrylamide. METHODS: We estimated odds ratios (OR) and 95% confidence intervals (CI) for the association between tertiles of intake of deep-fried foods from a food frequency questionnaire (French fries, fried chicken, fried fish, doughnuts and snack chips) and PCa risk, adjusted for potential confounders, among 1,549 cases and 1,492 controls. We additionally examined associations with more aggressive PCa (defined as regional/distant stage, elevated Gleason score or prostate-specific antigen level). RESULTS: Compared with <1/week, there was a positive association with PCa risk for intake ≥1/week of French fries (OR = 1.37; 95% CI, 1.11-1.69), fried chicken (OR = 1.30; 95% CI, 1.04-1.62), fried fish (OR = 1.32; 95% CI, 1.05-1.66), and doughnuts (OR = 1.35; 95% CI, 1.11-1.66). There was no association for snack chips (OR = 1.08; 95% CI, 0.89-1.32). Most of the estimates were slightly stronger for more aggressive disease (OR = 1.41; 95% CI, 1.04-1.92 for fried fish). CONCLUSION: Regular consumption of select deep-fried foods is associated with increased PCa risk. Whether this risk is specific to deep-fried foods, or whether it represents risk associated with regular intake of foods exposed to high heat and/or other aspects of the Western lifestyle, such as fast food consumption, remains to be determined. Prostate © 2013 Wiley Periodicals, Inc.
The Prostate 01/2013; · 3.48 Impact Factor
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Marian L Neuhouser,
Elizabeth A Platz,
Cathee Till,
Catherine M Tangen,
Phyllis J Goodman,
Alan Kristal,
Howard L Parnes,
Yuzhen Tao,
William D Figg,
M Scott Lucia,
Ashraful Hoque,
Ann W Hsing,
Ian M Thompson,
Michael Pollak
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ABSTRACT: The role of the insulin-like growth factor (IGF) axis and whether IGFs interact with androgen-suppressing agents in relation to prostate carcinogenesis is unclear. This nested case-control study (n = 1,652 cases/1,543 controls) examined whether serum IGF1, IGF2, IGFBP2, IGFBP3, and the IGF1:IGFBP3 ratio were associated with prostate cancer in the Prostate Cancer Prevention Trial (PCPT), a randomized, placebo-controlled trial of finasteride for prostate cancer prevention. Presence or absence of cancer was determined by prostate biopsy. Baseline serum was assayed for IGF-axis analytes using ELISA. Logistic regression estimated ORs and 95% confidence intervals for risk of total, low-grade (Gleason 2-6) and high-grade (Gleason 7-10) cancers. Results were stratified by intervention assignment. In both the placebo and finasteride arms, serum IGF1, IGF2, IGFBP3, and the IGF1:IGFBP3 ratio were not associated with prostate cancer. However, men in the highest versus lowest quartile of serum IGFBP2 had a 48% (P(trend) = 0.02) and 55% (P(trend) = 0.01) increased risk for total and low-grade cancers, respectively. These IGFBP2 associations were attenuated and no longer statistically significant in the finasteride arm. Our results suggest that in general, serum IGF-axis analytes were not associated with prostate cancer risk in the PCPT in which presence or absence of all cancers was biopsy-determined. The exception was the finding that high serum IGFBP2 is a risk factor for low-grade disease, which was attenuated for men on finasteride. Further research is needed to understand better the risk incurred by high IGFBP2 and whether androgen-suppressing agents such as finasteride influence aspects of IGFBP2 physiology relevant to prostate carcinogenesis. Cancer Prev Res; 1-9. ©2012 AACR.
Cancer Prevention Research 01/2013; · 4.91 Impact Factor
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ABSTRACT: Many carcinogens in tobacco smoke cause DNA damage, and some of that damage can be mitigated by the actions of DNA repair enzymes. In a case-control study nested within the Beta-Carotene and Retinol Efficacy Trial, a randomized chemoprevention trial in current and former heavy smokers, we examined whether lung cancer risk was associated with variation in 26 base excision repair, mismatch repair, and homologous recombination repair genes. Analyses were limited to Caucasians (744 cases, 1477 controls), and logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for individual SNPs and common haplotypes, with adjustment for matching factors. Lung cancer associations were observed (p<0.05) with SNPs in MSH5 (rs3131379, rs707938), MSH2 (rs2303428), UNG (rs246079), and PCNA (rs25406). MSH5 rs3131379 is a documented lung cancer susceptibility locus in complete linkage disequilibrium with rs3117582 in BAT3, and we observed associations similar in magnitude to those in prior studies (per A allele OR 1.37, 95% CI 1.13-1.65). UNG was associated with lung cancer risk at the gene level (p=0.02), and the A allele of rs246079 was associated with an increased risk (per A allele OR 1.15, 95% CI1.01-1.31). We observed stronger associations with UNG rs246079 among individuals who carried the risk genotypes (AG/AA) for MSH5 rs3131379 (pinteraction= 0.038). Our results provide additional evidence to suggest that the MSH5/BAT3 locus is associated with increased lung cancer risk among smokers, and that associations with other SNPs may vary depending upon MSH5/BAT3 genotype. Future studies to examine this possibility are warranted.
International Journal of Molecular Epidemiology and Genetics 01/2013; 4(1):11-34.
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Stefanie Zschäbitz,
Ting-Yuan David Cheng, Marian L Neuhouser,
Yingye Zheng,
Roberta M Ray,
Joshua W Miller,
Xiaoling Song,
David R Maneval,
Shirley Aa Beresford,
Dorothy Lane,
James M Shikany,
Cornelia M Ulrich
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ABSTRACT: BACKGROUND: The role of one-carbon metabolism nutrients in colorectal carcinogenesis is not fully understood. Associations might be modified by mandated folic acid (FA) fortification or alcohol intake. OBJECTIVE: We investigated associations between intakes of folate, riboflavin, vitamin B-6, and vitamin B-12 and colorectal cancer (CRC) in the Women's Health Initiative Observational Study, stratified by time exposed to FA fortification and alcohol intake. DESIGN: A total of 88,045 postmenopausal women were recruited during 1993-1998; 1003 incident CRC cases were ascertained as of 2009. Quartiles of dietary intakes were compared; HRs and 95% CIs were estimated by Cox proportional hazards models. RESULTS: Dietary and total intakes of vitamin B-6 in quartile 4 compared with quartile 1 (HR: 0.80; 95% CI: 0.66, 0.97 and HR: 0.80; 95% CI: 0.66, 0.99, respectively) and total intakes of riboflavin (HR: 0.81; 95% CI: 0.66, 0.99) were associated with reduced risk of CRC overall and of regionally spread disease. In current drinkers who consumed <1 drink (13 g alcohol)/wk, B vitamin intakes were inversely associated with CRC risk (P-interaction < 0.05). Dietary folate intake was positively associated with CRC risk among women who had experienced the initiation of FA fortification for 3 to <9 y (P-interaction < 0.01). CONCLUSIONS: Vitamin B-6 and riboflavin intakes from diet and supplements were associated with a decreased risk of CRC in postmenopausal women. Associations of B vitamin intake were particularly strong for regional disease and among women drinkers who consumed alcohol infrequently. Our study provides new evidence that the increased folate intake during the early postfortification period may have been associated with a transient increase in CRC risk.
American Journal of Clinical Nutrition 12/2012; · 6.67 Impact Factor
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Caitlin Mason,
Liren Xiao,
Ikuyo Imayama,
Catherine R Duggan,
Karen E Foster-Schubert,
Angela Kong,
Kristin L Campbell,
Ching-Yun Wang,
Adriana Villasenor, Marian L Neuhouser,
Catherine M Alfano,
George L Blackburn,
Anne McTiernan
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ABSTRACT: PURPOSE: To investigate the effects of 12 months of dietary weight loss and/or aerobic exercise on lean mass and the measurements defining sarcopenia in postmenopausal women, and to examine the potential moderating effect of serum 25-hydroxyvitamin D (25(OH)D) and age. METHODS: 439 overweight and obese postmenopausal women were randomized to: diet modification (N=118); exercise (N=117), diet+exercise (N=117), or control (N=87). The diet intervention was a group-based program with a 10% weight loss goal. The exercise intervention was 45 mins/day, 5 days/week of moderate-to-vigorous intensity aerobic activity. Total and appendicular lean mass were quantified by dual Xray absorptiometry (DXA) at baseline and 12 months. A skeletal muscle index (SMI=appendicular lean mass (kg)/m) and the prevalence of sarcopenia (SMI<5.67 kg/m) were calculated. Serum 25(OH)D was assayed using a competitive chemiluminescent immunoassay. RESULTS: Dietary weight loss resulted in a significant decrease in lean mass, and a borderline significant decrease in appendicular lean mass and SMI compared to controls. In contrast, aerobic exercise significantly preserved appendicular lean mass and SMI. Diet + exercise attenuated the loss of appendicular lean mass and SMI compared to diet alone, and did not result in significant loss of total- or appendicular lean mass compared to controls. Neither serum 25(OH)D nor age were significant moderators of the intervention effects. CONCLUSIONS: Aerobic exercise added to dietary weight loss can attenuate the loss of appendicular lean mass during weight loss, and may be effective for the prevention and treatment of sarcopenia among overweight and obese postmenopausal women.
Medicine and science in sports and exercise 11/2012; · 3.71 Impact Factor
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Adetunji T Toriola,
Ting-Yuan D Cheng, Marian L Neuhouser,
Mark H Wener,
Yingye Zheng,
Elissa Brown,
Joshua W Miller,
Xiaoling Song,
Shirley Aa Beresford,
Marc J Gunter,
Marie A Caudill,
Cornelia M Ulrich
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ABSTRACT: Initial studies have investigated the association between inflammation and colorectal cancer (CRC) using C-reactive protein (CRP) as a pro-inflammatory biomarker and have noted inconsistent results among women. We here report findings from a large prospective study with repeat measurements of CRP, as well as serum-amyloid A (SAA), an additional biomarker of inflammation, and risk of CRC. In the Women's Health Initiative Observational Study, we examined associations of CRP and SAA with CRC using repeat assessments (baseline and 3-year follow-up) among 953 matched case-control pairs for CRP and 966 pairs for SAA. Multivariate-adjusted conditional-logistic regression models were used with two-sided tests of significance. Receiver operating characteristic (ROC) curve analysis assessed their utility as early detection markers. Colon cancer risk (odds ratio, OR, and 95% confidence intervals) among women in the highest quintiles of CRP or SAA compared to those in the lowest quintiles was OR(colon/CRP) =1.37 (0.95-1.97, p-trend=0.04) and OR(colon/SAA) =1.26 (0.88-1.80, p-trend=0.10), respectively. Women with elevated concentrations of both CRP and SAA had an increased risk of OR(colon) =1.50 (1.12-2.00, p-value=0.006) compared to those with low concentrations. No positive associations were observed with rectal cancer and weaker associations for CRC overall. Temporal changes in biomarkers over 3-years did not predict risk. The area under the 6-month ROC curve for CRP+SAA was 0.62 (95%CI 0.55-0.68). Elevated inflammatory biomarkers are associated with an increased risk of CRC, mainly colon cancer. Nevertheless, changes in the biomarkers over time do not suggest that they merit consideration as early-detection markers for CRC. © 2012 Wiley Periodicals, Inc.
International Journal of Cancer 11/2012; · 5.44 Impact Factor
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Stephanie Whisnant Cash,
Huiyan Ma,
Pamela L Horn-Ross,
Peggy Reynolds,
Alison J Canchola,
Jane Sullivan-Halley,
Shirley A A Beresford, Marian L Neuhouser,
Thomas L Vaughan,
Patrick J Heagerty,
Leslie Bernstein
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ABSTRACT: Purpose: Little is known about the relationship between physical activity and thyroid cancer risk, and few cohort data on this association exist. Thus, the present study aimed to prospectively examine long-term activity and risk of papillary thyroid cancer among women. Methods: 116,939 women in the California Teachers Study, aged 22-79 years with no history of thyroid cancer at cohort entry, were followed from 1995-1996 through 2009; 275 were diagnosed with invasive papillary thyroid cancer. Cox proportional-hazards regression provided relative risk (RR) estimates and 95% confidence intervals (CI) for associations between thyroid cancer and combined strenuous and moderate recreational physical activity both in the long-term (high school through age 54 years or current age if younger than 54 years) and recently (during the three years prior to joining the cohort). Results: Overall, women whose long-term recreational physical activity averaged at least 5.5 MET-hours/week (i.e. were active) had a non-significant 23% lower risk of papillary thyroid cancer than inactive women (RR=0.77, 95% CI: 0.57, 1.04). RR estimates were stronger among normal weight or underweight women (body mass index, BMI<25.0kg/m(2), trend p=0.03) than among overweight or obese women (trend p=0.35; homogeneity-of-trends p=0.03). A similar pattern of risk was observed for recent activity (BMI<25kg/m(2), trend p=0.11; BMI≥25kg/m(2), trend p=0.16; homogeneity-of-trends p=0.04). Associations for long-term activity did not appear to be driven by activity in any particular life period (e.g. youth, adulthood). Conclusions: Long-term physical activity may reduce papillary thyroid cancer risk among normal weight and underweight women.
Cancer epidemiology. 10/2012;
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Brenda M Birmann, Marian L Neuhouser,
Bernard Rosner,
Demetrius Albanes,
Julie E Buring,
Graham G Giles,
Qing Lan,
I-Min Lee,
Mark P Purdue,
Nathaniel Rothman, [......],
Kenneth C Anderson,
Michael Pollak,
Nader Rifai,
Patricia Hartge,
Ola Landgren,
Lawrence Lessin,
Jarmo Virtamo,
Robert B Wallace,
Joann E Manson,
Graham A Colditz
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ABSTRACT: Insulin-like growth factor (IGF)-1, insulin, and interleukin (IL)-6 are dysregulated in multiple myeloma pathogenesis and may also contribute to multiple myeloma etiology. To examine their etiologic role we prospectively analyzed concentrations of serologic markers in 493 multiple myeloma cases and 978 controls from eight cohorts in the Multiple Myeloma Cohort Consortium. We computed odds ratios (OR) and 95% confidence intervals (CI) for multiple myeloma per one-standard deviation (SD) increase in biomarker concentration using conditional logistic regression. We examined heterogeneity by time since blood collection (≤3, 4 to ≤6, and >6 years) in stratified models. Fasting IGF binding protein (IGFBP)-1 concentration was associated with multiple myeloma risk within three years (OR, 95% CI per 1-SD increase: 2.3, 1.4-3.8, p=0.001) and soluble IL-6 receptor (sIL6R) level was associated within six years after blood draw (OR(≤3years), 95% CI: 1.4, 1.1-1.9, p = 0.01; OR(4-≤6years), 95% CI: 1.4, 1.1-1.7, p=0.002). No biomarker was associated with longer-term multiple myeloma risk (i.e., >6 years). Interactions with time were statistically significant (IGFBP-1, p-heterogeneity=0.0016; sIL6R, p-heterogeneity=0.016). The time-restricted associations likely reflect the bioactivity of tumor and microenvironment cells in transformation from monoclonal gammopathy of undetermined significance or smoldering multiple myeloma to clinically manifest multiple myeloma.
Blood 10/2012; · 9.90 Impact Factor
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ABSTRACT: PURPOSE: This study aimed to determine the prevalence of sarcopenia and examine whether sarcopenia was associated with overall and breast-cancer-specific mortality in a cohort of women diagnosed with breast cancer (stages I-IIIA). METHODS: A total of 471 breast cancer patients from western Washington State and New Mexico who participated in the prospective Health, Eating, Activity, and Lifestyle Study were included in this study. Appendicular lean mass was measured using dual X-ray absorptiometry scans at study inception, on average, 12 months after diagnosis. Sarcopenia was defined as two standard deviations below the young healthy adult female mean of appendicular lean mass divided by height squared (<5.45 kg/m(2)). Total and breast-cancer-specific mortality data were obtained from Surveillance Epidemiology and End Results registries. Multivariable Cox proportional hazard models assessed the associations between sarcopenia and mortality. RESULTS: Median follow-up was 9.2 years; 75 women were classified as sarcopenic, and among 92 deaths, 46 were attributed to breast cancer. In multivariable models that included age, race-ethnicity/study site, treatment type, comorbidities, waist circumference, and total body fat percentage, sarcopenia was independently associated with overall mortality (hazard ratio (HR) = 2.86; 95 % CI, 1.67-4.89). Sarcopenic women had increased risk of breast-cancer-specific mortality, although the association was not statistically significant (HR = 1.95, 95 % CI, 0.87-4.35). CONCLUSION: Sarcopenia is associated with an increased risk of overall mortality in breast cancer survivors and may be associated with breast-cancer-specific mortality. The development of effective interventions to maintain and/or increase skeletal muscle mass to improve prognosis in breast cancer survivors warrants further study. IMPLICATIONS FOR CANCER SURVIVORS: Such interventions may help breast cancer patients live longer.
Journal of Cancer Survivorship 10/2012; · 2.63 Impact Factor
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Josephina G Kuiper,
Amanda I Phipps, Marian L Neuhouser,
Rowan T Chlebowski,
Cynthia A Thomson,
Melinda L Irwin,
Dorothy S Lane,
Jean Wactawski-Wende,
Lifang Hou,
Rebecca D Jackson,
Ellen Kampman,
Polly A Newcomb
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ABSTRACT: BACKGROUND AND PURPOSE: Previous studies have shown that physical inactivity and obesity are risk factors for the development of colorectal cancer. However, controversy exists regarding the influence of these factors on survival in colorectal cancer patients. We evaluated the impact of recreational physical activity and body mass index (BMI) before and after colorectal cancer diagnosis on disease-specific mortality and all-cause mortality. PATIENTS AND METHODS: This prospective cohort study included 1,339 women enrolled in the Women's Health Initiative study who were diagnosed with colorectal cancer subsequent to study enrollment. BMI and recreational physical activity were measured before cancer diagnosis at study entry (pre-diagnostic) and after diagnosis at study follow-up interviews (post-diagnostic). We used Cox regression to estimate the association between pre- and post-diagnostic exposures and survival after colorectal cancer diagnosis. RESULTS: Among women diagnosed with colorectal cancer, 265 (13 %) deaths occurred during a median study follow-up of 11.9 years, of which 171 (65 %) were attributed to colorectal cancer. Compared with women reporting no pre-diagnostic recreational physical activity, those reporting activity levels of ≥18 MET-h/week had significantly lower colorectal cancer-specific mortality (hazard ratio (HR) = 0.68; 95 % confidence interval (CI): 0.41-1.13) and all-cause mortality (HR = 0.63; 95 % CI: 0.42-0.96). Similar inverse associations were seen for post-diagnostic recreational physical activity. Neither pre- nor post-diagnostic BMI were associated with mortality after colorectal cancer diagnosis. CONCLUSION: Recreational physical activity before and after colorectal cancer diagnosis, but not BMI, is associated with more favorable survival.
Cancer Causes and Control 10/2012; · 2.88 Impact Factor
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ABSTRACT: OBJECTIVE: Low-glycemic load diets lower post-prandial glucose and insulin responses; however, the effect of glycemic load on circulating incretin concentrations is unclear. We aimed to assess effects of dietary glycemic load on fasting and post-prandial glucose, insulin and incretin (i.e., glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1)) concentrations and to examine for effect modification by adiposity. MATERIALS AND METHODS: We conducted a single-center, randomized controlled crossover feeding trial in which a subset of participants had post-prandial testing. Participants were recruited from the local Seattle area. We enrolled 89 overweight-obese (BMI 28.0-39.9kg/m(2)) and lean (BMI 18.5-25.0kg/m(2)) healthy adults. Participants consumed two 28-day, weight-maintaining high- and low-glycemic load controlled diets in random order. Primary outcome measures were post-prandial circulating concentrations of glucose, insulin, GIP and GLP-1, following a test breakfast. RESULTS: Of the 80 participants completing both diet interventions, 16 had incretin testing and comprise the group for analyses. Following each 28-day high- and low-glycemic load diet, mean fasting concentrations of insulin, glucose, GIP and GLP-1 were not significantly different. Mean integrated post-prandial concentrations of glucose, insulin and GIP were higher (1504±476mg/dL/min, p<0.01; 2012±644μU/mL/min, p<0.01 and 15517±4062pg/mL/min, p<0.01, respectively) and GLP-1 was lower (-81.6±38.5 pmol/L/min, p<0.03) following the high-glycemic load breakfast as compared to the low-glycemic load breakfast. Body fat did not significantly modify the effect of glycemic load on metabolic outcomes. CONCLUSIONS: High-glycemic load diets in weight-maintained healthy individuals lead to higher post-prandial GIP and lower post-prandial GLP-1 concentrations. Future studies evaluating dietary glycemic load manipulation of incretin effects would be helpful for establishing diabetes nutrition guidelines.
Metabolism: clinical and experimental 09/2012; · 2.59 Impact Factor
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ABSTRACT: PURPOSE: Animal and laboratory studies suggest that long-chain omega-3 (n-3) fatty acids, a type of polyunsaturated fat found in fatty fish, may protect against carcinogenesis, but human studies on dietary intake of polyunsaturated fats and fish with endometrial cancer risk show mixed results. METHODS: We evaluated the associations between endometrial cancer risk and intake of fatty acids and fish in a population-based sample of 556 incident cancer cases and 533 age-matched controls using multivariate unconditional logistic regression methods. RESULTS: Although total n-3 fatty acid intake was not associated with endometrial cancer risk, higher intakes of eicosapentaenoic (EPA 20:5) and docosahexaenoic (DHA 22:6) fatty acids were significantly associated with lower risks (OR = 0.57, 95 % CI: 0.39-0.84; OR = 0.64, 95 % CI: 0.44-0.94; respectively) comparing extreme quartiles. The ratio of n-3:n-6 fatty acids was inversely associated with risk only on a continuous scale (OR = 0.84, 95 % CI: 0.71-0.99), while total fish intake was not associated with risk. Fish oil supplement use was significantly associated with reduced risk of endometrial cancer: OR = 0.63 (95 % CI: 0.45-0.88). CONCLUSIONS: Our results suggest that dietary intake of the long-chain polyunsaturated fatty acids EPA and DHA in foods and supplements may have protective associations against the development of endometrial cancer.
European Journal of Nutrition 08/2012; · 2.75 Impact Factor
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Alan R Kristal,
Cathee Till,
Catherine M Tangen,
Phyllis J Goodman, Marian L Neuhouser,
Frank Z Stanczyk,
Lisa W Chu,
Sherfaraz K Patel,
Ian M Thompson,
Juergen K Reichardt,
Ashraful Hoque,
Elizabeth A Platz,
William D Figg,
Adrie Van Bokhoven,
Scott M Lippman,
Ann W Hsing
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ABSTRACT: Finasteride, an inhibitor of 5α-reductase (type II), lowers intraprostatic dihydrotestosterone (DHT), which is reflected in serum as reduced 5α-androstane-3α,17β-diol glucuronide (3α-dG). It also modestly increases serum testosterone (T), estrone (E(1)), and estradiol (E(2)). In this altered hormonal milieu, it is unknown whether serum concentrations of these hormones are associated with prostate cancer risk.
In this nested case-control study of men in the finasteride arm of the Prostate Cancer Prevention Trial, sex steroid hormones and sex hormone binding globulin were measured at baseline and approximately 3-year posttreatment in 553 prostate cancer cases and 694 controls.
Median posttreatment changes in concentrations of 3α-dG, T, E(1), and E(2) were -73.8%, +10.1%, +11.2%, and +7.5% (all P < 0.001), respectively. Neither the pre- nor posttreatment concentrations of 3α-dG, nor its change, were associated with risk. Pretreatment, high concentrations of E(1) and low concentrations of T were associated with increased cancer risk [OR; 95% confidence interval (CI) quartile 4 vs. 1: 1.38 (0.99-1.93) P(trend) = 0.03; 0.64 (0.43-0.93) P(trend) = 0.07, respectively]. Posttreatment, high concentrations of both E(1) and E(2) were associated with increased cancer risk [OR; 95% CI quartile 4 vs. 1: 1.54 (1.09-2.17) P(trend) = 0.03; 1.49 (1.07-2.07) P(trend) = 0.02, respectively].
Among finasteride-treated men, concentrations of 3α-dG were not associated with total or Gleason grades 2 to 6, 7 to 10, or 8 to 10 cancer. High serum estrogens may increase cancer risk when intraprostatic DHT is pharmacologically lowered. Impact: Low posttreatment serum estrogens may identify men more likely to benefit from use of finasteride to prevent prostate cancer. Cancer Epidemiol Biomarkers Prev; 21(10); 1823-32. ©2012 AACR.
Cancer Epidemiology Biomarkers & Prevention 08/2012; 21(10):1823-32. · 4.12 Impact Factor
