510 perinsulinemia [17-19] or to the increased estrogen-to-an- drogen ratio [8]. It is noteworthy that the association be- tween obesity and BPH/LUTS was stronger for patients with severe symptoms requiring surgery (OR: 2.0-2.4) [8,9] than for those who reported moderate-to-severe LUTS (OR: 1.2-1.4) and may indicate a dose-response relation- ship. Finally, the relationship between obesity and BPH/ LUTS was observed in different races and ethnicities (i.e., American, European, and Asian), indicating its genera- lizability. 2. Dyslipidemia Similar to obesity, the relationship between BPH and dys- lipidemia has been documented in several studies. Rahman el al observed that prostate weight was sig- nificantly higher in hyperlipidemic rats than in controls (mean: 2.6 vs 1.4 g; p＜0.001) [20]. Vikram et al conducted a longitudinal study over 12 weeks and reported that rats fed a high-fat diet had a significantly higher prostate weight than did controls [21]. These observations were fur- ther corroborated by Escobar et al in another rat model [22]. 　In addition to animal models, the relationship between BPH and dyslipidemia has been documented in epidemio- logic studies. Hammarsten et al [14] examined the data of 158 men and reported that individuals with a low level of high-density lipoprotein (HDL) cholesterol (＜1.18 mmol/l) had a larger prostate volume (mean: 49.0 vs 39.0 ml; p=0.002) and a higher annual BPH growth rate (mean: 1.02 vs 0.78 ml/y; p=0.006) than did individuals with a high level of HDL cholesterol (≥1.18 mmol/l). In a subsequent report, Hammarsten and Högstedt corroborated these findings in a larger sample (n=307) [4]. Nandeesha et al observed that men with BPH had a significantly higher total cholesterol (mean: 4.5 vs 4.2 mmol/l; p＜0.05) and low-density lip- oprotein (LDL) cholesterol levels (mean: 2.8 vs 2.2 mmol/l; p＜0.001) than did men without BPH [23]. The same au- thors observed that the level of HDL cholesterol was sig- nificantly lower in men with BPH than in those without BPH (mean: 0.9 vs 1.2 mmol/l; p＜0.001). 　Conversely, in the Rancho Bernardo study, Parsons et al observed no overall association between LDL cholesterol and BPH (p=0.2) [24]. However, when men were stratified according to diabetes status, individuals with diabetes who had the highest LDL cholesterol had a 4-fold (95% con- fidence interval [CI]: 1.3-12.6; p=0.02) higher risk of report- ing BPH (defined as a history of prostate surgery other than for cancer or physician-diagnosed BPH) than did those with the lowest LDL cholesterol (＞133 mg/dl vs ＜110 mg/dl). This observation suggests that dyslipidemia may interact with other components of MetS to increase BPH risk [24]. This may at least partially explain why other in- vestigators observed no significant relationship between dyslipidemia and BPH/LUTS [25-27]. 3. Hypertension Hypertension was also associated with BPH/LUTS in sev- eral animal models and epidemiologic studies. Golomb et Korean J Urol 2011;52:507-516 Abdollah et al al reported that spontaneously hypertensive rats develop BPH-like features with aging in the absence of any in- ductive exogenous agents [28]. Conversely, their normo- tensive counterparts did not develop such features. Ham- marsten et al examined the data of 158 Swedish men re- ferred to one center [14]. They reported that individuals with treated hypertension had a larger prostate volume (mean: 51.0 vs 44.0 ml; p=0.003) and higher annual BPH growth rate (mean: 1.06 vs 0.90 ml/y; p=0.002) than did controls. Similarly, Joseph et al reported that men with a history of hypertension had a 1.5-fold (95% CI: 1.1-2.1) higher risk of moderate-to-severe LUTS (defined as an American Urological Association Symptom Index [AUASI] of ≥8) compared with their counterparts without a history of hypertension [15]. Rohrman et al examined the data from 2,372 participants in the Third National Health and Nutrition Examination Survey (NHANES III) [29]. They reported that men with a history of hypertension had sig- nificantly higher odds of LUTS than did their counterparts without such a history (OR: 1.8; 95% CI: 1.2-2.6). 4. Insulin resistance Insulin resistance represents another important compo- nent of MetS. To tackle the decreased responsiveness of in- sulin-sensitive tissues toward insulin, β-cells secrete more insulin and hence hyperinsulinemia is observed. These hormonal abnormalities may play an important role in the development of BPH/LUTS. Vikram et al reported an aug- mented prostatic epithelial cell proliferation in insulin-re- sistant rats [21]. The same authors showed that an induced status of hypoinsulinemia led to a dramatic decrease in the size of the prostate gland [30]. These observations were cor- roborated by Ikeda et al in another animal model [31]. 　At an epidemiologic level, Hammareston and Högstedt [4] addressed the relationship between fasting plasma in- sulin and BPH. In their cohort, men in the highest quartile of plasma fasting insulin (＞13 mU/l) had a significantly larger prostate volume (mean: 61.0 vs 45.0 ml; p=0.009) and higher annual BPH growth rate (mean: 1.49 vs 0.84 ml/y; p=0.01) than did men in the lowest quartile of plasma fasting insulin (＜7 mU/l). In the Flint Men’s Health Study, individuals with a history of diabetes had twice the risk (OR: 2.0; 95% CI: 1.5-2.6) of suffering from moder- ate-to-severe LUTS (defined as an AUASI ≥8) as did their counterparts without a history of diabetes [15]. Seim et al evaluated the data of 21,694 individuals who participated in the second Nord-Trondelag Health Study and reported that men with diabetes were more likely to have an IPSS ≥8 than were their nondiabetic counterparts (OR: 1.3; 95% CI: 1.1-1.5) [11]. Similarly, Nandeesha et al reported that the level of fasting serum insulin was significantly higher in men with BPH than in controls (mean: 237.4 vs 134.7 pmol/l; p＜0.001) [23]. In a recent report, Hammarsten et al confirmed the relationship between fasting serum in- sulin and prostate volume in a multicentric study (β co- efficient: 0.2; p=0.02) [13].