Objective To explore the relationship between benign prostatic hyperplasia (BPH)and obesity. Methods The 109 elder men were divided into two groups: BPH group (n=59) and non-BPH group (n= 50). The blood samples were collected for the detections of prostate specific antigen (PSA), triglyceride (TG), total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), fasting blood glucose (FBG), insulin,androgen, estrogen, sex hormone binding globulin (SHBG) and dehydroepiandrosterone(DHEA).The anthropometric indexes including height, body weigh, waist circumference (WC), hip circumference (HC), systolic blood pressure (SBP), diastolic blood pressure (DBP), body mass index (BMI), waist-to-height ratio (WHtR) and waist-to-hip ratio (WHR) were measured and calculated. The total prostate volume (TPV) were measured by transabdominal ultrasonography three times at least. Results The morbidity rate of BPH was significantly higher in obesity group and over weight group than in health control group (73.33% and 64.28% vs. 26. 67%, x2 = 13. 991 and 6. 836, both P＜0. 002). So was in central obesity group versus in health control group (71.19% vs.36.00%, x2 =12. 156, P＜0. 001). The waist-height index, waist circumference, body weight, BMI and hip circumference were significantly higher in BPH group than in non-BPH group [(0. 56±0. 05)vs. (0.52±0.06), (93. 6±8.8) cm vs. (87.0± 10. 1) cm; (72.6±9.7) kg vs. (64.5±9.3) kg;(25.7±3.4) kg/m2 vs. (23.1±2.9) kg/m2; (100.2±6.6) cm vs. (95.6±8. 1) cm; t=-3.3, -3. 65, -4.38, -4. 17 and -3.18, respectively, all P＜0.01]. The TPV was higher in obesity groupthan in normal group [ (40.8± 23.5 ) ml vs. (20. 1 ± 6.1 ) ml, t = - 2.82, P＜ 0. 002] and obviously higher in central obesity group than in non-central obesity group [(42.8±25.6)ml vs. (26. 9±11.2)ml, t= -3. 93, P＜0. 001]. The ratio of E2/TT and HOMA-IR were higher in central obesity group [(9. 06±4.36) and (2.81 ±2. 80)] than in non-central obesity group [(7. 38±3. 11) and (1. 55±0.76), t= -2.02 and -4.24, both P＜0. 05]. Inversely, the TT and SHBG were lower in central obesity group than in non-central obesity group [(4.54 ± 1.54) nmol/L vs. (5.20 ± 1.54) nmol/L,(45.8± 17.24) nmol/L vs. (59.6 ± 26.09) nmol/L, t = 2.16 and 2.79, both P＜ 0. 05]. Logistic regression analysis showed that waist circumference was a major factor affecting TPV (x2= 19.52, P=0. 000). The annual growth rate of TPV was significantly higher in obesity group and central obesity group than in health control group [(7. 14±8. 09)ml vs. (1. 49±5.14)ml, (7. 96±13.81)mlvs. (1. 35±5.36)ml, t=-2.19 and -3.28, both P＜0. 05]; The PSAD was significantly lower in central obesity group than in health control group [(0. 048±0. 036) vs. (0. 090±0. 093), t=2.02, P＜0. 05], and lower in obesity group than in health control group [(0. 052 ±0. 039) vs. (0. 091 ±0. 080), t= 3. 13, P＜0. 01]. Conclusions The occurrence of BPH is closely related to obesity,especially central obesity. Its mechanism may be related to sex hormone imbalance and the GH/IGF-1 axis disorders in obese patients.