TY - JOUR
T1 - Anthropometric Measures at Multiple Times Throughout Life and Prostate Cancer Diagnosis, Metastasis, and Death
AU - Gerdtsson, Axel
AU - Poon, Jessica B.
AU - Thorek, Daniel L.
AU - Mucci, Lorelei A.
AU - Evans, Michael J.
AU - Scardino, Peter
AU - Abrahamsson, Per Anders
AU - Nilsson, Peter
AU - Manjer, Jonas
AU - Bjartell, Anders
AU - Malm, Johan
AU - Vickers, Andrew
AU - Freedland, Stephen J.
AU - Lilja, Hans
AU - Ulmert, David
N1 - Funding Information:
Funding/Support and role of the sponsor: This study was supported by the strategic research area (SRA) Epidemiology for Health (EpiHealth) at Lund University and Uppsala University, Sweden.
Funding Information:
Financial disclosures: David Ulmert certifies that all conflicts of interest, including specific financial interests and relationships and affiliations relevant to the subject matter or materials discussed in the manuscript (eg, employment/affiliation, grants or funding, consultancies, honoraria, stock ownership or options, expert testimony, royalties, or patents filed, received, or pending), are the following: Daniel L. Thorek was supported by a Steve Wynne Young Investigator Award from the Prostate Cancer Foundation (PCF). Michael J. Evans was supported by the Imaging and Radiation Sciences Bridge Program of Memorial Sloan-Kettering Cancer Center (MSKCC), the Experimental Therapeutics Center of MSKCC, William H. and Alice Goodwin and the Commonwealth Foundation for Cancer Research, the David H. Koch Young Investigator Award PCF, and the National Cancer Institute (K99CA172695, R01CA176671). Andrew Vickers was supported by a National Institutes of Health/National Cancer Institute Cancer Center Support Grant to MSKCC (P30 CA008748). Stephen J. Freedland was supported by NIH 1K24CA160653. Hans Lilja and Andrew Vickers were supported by NIH (R01 CA160816, R33 CA 127768-03, and P50-CA92629); Swedish Cancer Society (11-0624 and 14-0722); the Sidney Kimmel Center for Prostate and Urologic Cancers; David H. Koch through the PCF; the National Institute for Health Research Oxford Biomedical Research Centre based at Oxford University Hospitals NHS Trust and University of Oxford, UK; FiDIPro-program award from TEKES (Finland) and Fundación Federico SA. David Ulmert was supported by the Tegger Foundation, the Gunnar Nilsson Cancer Foundation, the Bertha Kamprad Foundation, and the David H. Koch Young Investigator Award from the PCF.
Funding Information:
David Ulmert certifies that all conflicts of interest,including specific financial interests and relationships and affiliationsrelevant to the subject matter or materials discussed in the manuscript(eg, employment/affiliation, grants or funding, consultancies, honoraria,stock ownership or options, expert testimony, royalties, or patents filed,received, or pending), are the following: Daniel L. Thorek was supportedby a Steve Wynne Young Investigator Award from the Prostate CancerFoundation (PCF). Michael J. Evans was supported by the Imaging andRadiation Sciences Bridge Program of Memorial Sloan-Kettering CancerCenter (MSKCC), the Experimental Therapeutics Center of MSKCC,William H. and Alice Goodwin and the Commonwealth Foundation forCancer Research, the David H. Koch Young Investigator Award PCF, andthe National Cancer Institute (K99CA172695, R01CA176671). Andrew Vickers was supported by a National Institutes of Health/National CancerInstitute Cancer Center Support Grant to MSKCC (P30 CA008748).Stephen J. Freedland was supported by NIH 1K24CA160653. Hans Liljaand Andrew Vickers were supported by NIH (R01 CA160816, R33 CA127768-03, and P50-CA92629); Swedish Cancer Society (11-0624 and14-0722); the Sidney Kimmel Center for Prostate and Urologic Cancers;David H. Koch through the PCF; the National Institute for HealthResearch Oxford Biomedical Research Centre based at Oxford UniversityHospitals NHS Trust and University of Oxford, UK; FiDIPro-programaward from TEKES (Finland) and Fundacio´n Federico SA. David Ulmertwas supported by the Tegger Foundation, the Gunnar Nilsson CancerFoundation, the Bertha Kamprad Foundation, and the David H. KochYoung Investigator Award from the PCF.Funding/Support and role of the sponsor: This study was supported bythe strategic research area (SRA) Epidemiology for Health (EpiHealth) atLund University and Uppsala University, Sweden.
Publisher Copyright:
© 2015 European Association of Urology.
PY - 2015
Y1 - 2015
N2 - Background Previous studies of prostate cancer (PCA) risk and anthropometrics (ie, body measurements) were based on single measurements or obtained over limited time spans. Objective To study the association between anthropometrics measured at multiple time points in life and their relation to later diagnosis, metastasis, or death from PCA. Design, setting, and participants This case-control study includes 27 167 Swedish men enrolled in two population-based projects from 1974 to 1996. PCA diagnosis up to December 31, 2006, disease information, gestation time, and anthropometrics at birth, military conscript testing, and adulthood were collected. A total of 1355 PCA cases were matched with 5271 controls. Outcome measurements and statistical analysis Univariate conditional logistic regression was used to determine whether clinical diagnosis, metastasis, or PCA death was associated with low birth weight (weight <2500 g); with small size for gestational age; or with weight, length, or body mass index (BMI) at birth, adolescence (aged 16-22 yr), or early middle age (aged 44-50 yr). Results and limitations Apart from weight at adolescence, which was associated with an increased risk of PCA diagnosis (odds ratio [OR] per 5 kg: 1.05; 95% confidence interval [CI], 1.01-1.09; p = 0.026), preadulthood measurements were not associated with any PCA end point. Adulthood parameters were not associated with diagnosis. In contrast, weight and BMI at early middle age were significantly associated with metastasis (OR per 5 kg: 1.13; 95% CI, 1.06-1.20; p < 0.0001, and OR: 1.09; 95% CI, 1.05-1.14; p < 0.0001) and death (OR per 5 kg: 1.11 (95% CI, 1.03-1.19; p = 0.005, and OR: 1.08; 95% CI, 1.03-1.13; p = 0.003), respectively. It remains unclear whether these results apply to men of nonwhite origin, to populations with active PCA screening programs, or to countries without socialized health care. Conclusions The analyses of these large data sets demonstrate that significant effects of body characteristics (with links to metabolic syndrome) measured at early middle age are associated with PCA disease severity, metastatic progression, and outcome. Conversely, measurements at birth and adolescence are not associated with PCA prevalence or outcome. Patient summary Increased weight and body mass index in adults is associated with a higher risk of prostate cancer metastasis and death.
AB - Background Previous studies of prostate cancer (PCA) risk and anthropometrics (ie, body measurements) were based on single measurements or obtained over limited time spans. Objective To study the association between anthropometrics measured at multiple time points in life and their relation to later diagnosis, metastasis, or death from PCA. Design, setting, and participants This case-control study includes 27 167 Swedish men enrolled in two population-based projects from 1974 to 1996. PCA diagnosis up to December 31, 2006, disease information, gestation time, and anthropometrics at birth, military conscript testing, and adulthood were collected. A total of 1355 PCA cases were matched with 5271 controls. Outcome measurements and statistical analysis Univariate conditional logistic regression was used to determine whether clinical diagnosis, metastasis, or PCA death was associated with low birth weight (weight <2500 g); with small size for gestational age; or with weight, length, or body mass index (BMI) at birth, adolescence (aged 16-22 yr), or early middle age (aged 44-50 yr). Results and limitations Apart from weight at adolescence, which was associated with an increased risk of PCA diagnosis (odds ratio [OR] per 5 kg: 1.05; 95% confidence interval [CI], 1.01-1.09; p = 0.026), preadulthood measurements were not associated with any PCA end point. Adulthood parameters were not associated with diagnosis. In contrast, weight and BMI at early middle age were significantly associated with metastasis (OR per 5 kg: 1.13; 95% CI, 1.06-1.20; p < 0.0001, and OR: 1.09; 95% CI, 1.05-1.14; p < 0.0001) and death (OR per 5 kg: 1.11 (95% CI, 1.03-1.19; p = 0.005, and OR: 1.08; 95% CI, 1.03-1.13; p = 0.003), respectively. It remains unclear whether these results apply to men of nonwhite origin, to populations with active PCA screening programs, or to countries without socialized health care. Conclusions The analyses of these large data sets demonstrate that significant effects of body characteristics (with links to metabolic syndrome) measured at early middle age are associated with PCA disease severity, metastatic progression, and outcome. Conversely, measurements at birth and adolescence are not associated with PCA prevalence or outcome. Patient summary Increased weight and body mass index in adults is associated with a higher risk of prostate cancer metastasis and death.
KW - Exposure windows
KW - Long-term risk predictions
KW - Metabolic syndrome-associated anthropometrics
KW - Prostate cancer
KW - Risk factors
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U2 - 10.1016/j.eururo.2015.03.017
DO - 10.1016/j.eururo.2015.03.017
M3 - Article
C2 - 25794458
AN - SCOPUS:84953838000
SN - 0302-2838
VL - 68
SP - 1076
EP - 1082
JO - European Urology
JF - European Urology
IS - 6
ER -