Division of Urologic Surgery, Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA.
Eur Urol. 2013 May;63(5):800-9. doi: 10.1016/j.eururo.2012.11.013. Epub 2012 Nov 15.
Obesity and prostate cancer (PCa) affect substantial proportions of Western society. Mounting evidence, both epidemiologic and mechanistic, for an association between the two is of public health interest. An improved understanding of the role of this modifiable risk factor in PCa etiology is imperative to optimize screening, treatment, and prevention.
To consolidate and evaluate the evidence for an epidemiologic link between obesity and PCa, in addition to examining the proposed underlying molecular mechanisms.
A PubMed search for relevant articles published between 1991 and July 2012 was performed by combining the following terms: obesity, BMI, body mass index and prostate cancer risk, prostate cancer incidence, prostate cancer mortality, radical prostatectomy, androgen-deprivation therapy, external-beam radiation, brachytherapy, prostate cancer and quality of life, prostate cancer and active surveillance, in addition to obesity, BMI, body mass index and prostate cancer and insulin, insulin-like growth factor, androgen, estradiol, leptin, adiponectin, and IL-6. Articles were selected based on content, date of publication, and relevancy, and their references were also searched for relevant articles.
Increasing evidence suggests obesity is associated with elevated incidence of aggressive PCa, increased risk of biochemical failure following radical prostatectomy and external-beam radiotherapy, higher frequency of complications following androgen-deprivation therapy, and increased PCa-specific mortality, although perhaps a lower overall PCa incidence. These results may in part relate to difficulties in detecting and treating obese men. However, multiple molecular mechanisms could explain these associations as well. Weight loss slows PCa in animal models but has yet to be fully tested in human trials.
Obesity appears to be linked with aggressive PCa. We suggest clinical tips to better diagnose and treat obese men with PCa. Whether reversing obesity slows PCa growth is currently unknown, although it is an active area of research.
肥胖症和前列腺癌(PCa)影响着西方社会的大部分人群。越来越多的流行病学和机制研究证据表明,两者之间存在关联,这与公共卫生息息相关。深入了解这一可改变的危险因素在 PCa 病因学中的作用,对于优化筛查、治疗和预防措施至关重要。
本文旨在综合评估肥胖与 PCa 之间的流行病学关联,并探讨潜在的分子机制。
通过组合以下术语,在 PubMed 上搜索了 1991 年至 2012 年 7 月发表的相关文章:肥胖、体重指数(BMI)、前列腺癌风险、前列腺癌发病率、前列腺癌死亡率、根治性前列腺切除术、雄激素剥夺疗法、外照射放疗、近距离放射治疗、前列腺癌与生活质量、前列腺癌与主动监测,以及肥胖、BMI、体重指数与前列腺癌和胰岛素、胰岛素样生长因子、雄激素、雌二醇、瘦素、脂联素、IL-6。文章的选择基于内容、发表日期和相关性,并对其参考文献进行了搜索,以查找相关文章。
越来越多的证据表明,肥胖与侵袭性 PCa 的发生率升高、根治性前列腺切除术和外照射放疗后生化失败的风险增加、雄激素剥夺疗法后并发症的发生率增加以及前列腺癌特异性死亡率增加相关,尽管总体上前列腺癌的发病率可能较低。这些结果可能部分与肥胖男性的诊断和治疗困难有关。然而,多种分子机制也可以解释这些关联。动物模型中减肥可减缓 PCa 的发展,但在人体试验中尚未得到充分验证。
肥胖似乎与侵袭性 PCa 相关。我们提出了一些临床建议,以更好地诊断和治疗患有 PCa 的肥胖男性。目前尚不清楚是否可以通过逆转肥胖来减缓 PCa 的生长,但这是一个活跃的研究领域。