The prevalence of obesity in the United States has dramatically increased in the past decade.¹ Increased body mass index (BMI) has been linked to death from colon, breast, and many other cancers.² Although there are biological bases for increased risk of certain cancers in obese persons,³ delayed diagnosis may provide an explanation for advanced stage of disease and poor outcome.

Purpose: Among patients with biochemical recurrence after radical prostatectomy, we found previously that postoperative prostate-specific antigen doubling time (PSADT) was associated with risk of prostate cancer death. However, given the small number of patients in the highest risk PSADT subgroup, it is unclear which PSADT subgroups contribute the greatest to prostate cancer–specific death and how this influences all-cause mortality. Patients and Methods: This study was a retrospective analysis of 379 patients treated with radical prostatectomy between 1982 and 2000 who had a biochemical recurrence and PSADT data available. Mean and median follow-up after surgery was 11.4 (standard deviation, 5.4) and 11.0 years, respectively (range, 1.6 to 23.0 years). Results: Shorter PSADT was significantly associated with prostate cancer–specific and all-cause mortality (P < .001). Although patients with a PSADT less than 3 months were at the greatest risk of death, because of the limited number of patients in this group, they accounted for only 13% of prostate cancer deaths at 15 years after biochemical recurrence, whereas patients with an intermediate PSADT (3.0 to 8.9 months) accounted for 58% of all prostate cancer deaths. Among patients with a PSADT less than 15 months, prostate cancer accounted for 90% of all deaths. Only patients in the slowest PSADT subgroup (≥ 15 months) had a greater risk of competing-causes mortality compared with that from prostate cancer. Conclusion: Among a select cohort of young, healthy patients with PSA recurrence after radical prostatectomy and a PSADT less than 15 months, prostate cancer accounted for an estimated 90% of all deaths by 15 years after recurrence. The majority of prostate cancer deaths occurred among patients with an intermediate PSADT (3.0 to 8.9 months).

Both obesity and prostate cancer are epidemic in Western society. Although initial epidemiologic data appeared conflicting, recent studies, especially large prospective studies published in the past 6–12 months, have clarified the association between obesity and prostate cancer. The aim of this paper is to review the epidemiologic data linking obesity and prostate cancer, with an emphasis on new data published since 2005. A PubMed search was done on the keywords, “prostate cancer” and “obesity.” Relevant articles and their references were reviewed for data on the association between obesity and prostate cancer. Recent data suggest that obesity is associated with reduced risk of nonaggressive disease but increased risk of aggressive disease. This may in part be explained by an inherent bias in our ability to detect prostate cancer in obese men (lower prostate-specific antigen values and larger sized prostates making biopsy less accurate for finding an existing cancer). Ultimately, this leads to increased risk of cancer recurrence after primary therapy and increased risk of prostate cancer mortality. The biologic causes of these associations are likely multifactorial, although the lower testosterone levels among obese men appear to be one of the most promising explanations. The association between obesity and prostate cancer is complex. Emerging data suggest a differential effect of obesity by disease aggressiveness: obesity may reduce the risk of nonaggressive disease while it may promote aggressive disease.