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Reduced risk of prostate cancer in men who are childless as compared to those who have fathered a child: A population based case‐control study
Author(s) -
Giwercman Aleksander,
Richiardi Lorenzo,
Kaijser Magnus,
Ekbom Anders,
Akre Olof
Publication year - 2005
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.20963
Subject(s) - prostate cancer , medicine , odds ratio , offspring , gynecology , population , cancer registry , cancer , prostate , case control study , oncology , pregnancy , biology , environmental health , genetics
Androgens are believed to play a major role in the etiology of prostate cancer, but studies of sex‐hormone exposure in relation to risk for prostate cancer have been inconclusive. Male fertility may be an indicator of long‐term androgen status. To study the role of testicular function in prostate cancer development, we have assessed number of biological children in relation to risk for this malignancy. We carried out a population‐based case‐control study with retrospective ascertainment of cases occurring in Sweden between 1958–98. In total, 48,850 cases of prostate cancer were identified through the nation‐wide Cancer Registry. For each case, one control, matched by year of birth, was randomly selected from the Swedish population. Information on offspring was obtained from the Swedish Multi‐Generation Registry. We estimated odds ratios (OR) and 95% confidence intervals (CI) for the association between number of offspring and risk for subsequent prostate cancer. Being childless or having fathered one child only were associated with reduced risks for prostate cancer compared to having fathered 2 or more children (OR = 0.83; 95% CI = 0.81–0.86 and OR = 0.93; 95% CI = 0.90–0.96, respectively). There was no further change in risk associated with fathering of more than 2 children. The risk for prostate cancer is reduced among childless men. A dysfunctioning reproductive apparatus fueling to a lesser extent prostatic growth, could be a plausible mechanism of this association. © 2005 Wiley‐Liss, Inc.