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Does weight affect prostate size?

Recent studies have shown that men with high body mass index (BMI) and central obesity, as denoted by waist circumference (WC) have bigger prostate volumes (PV) with subsequent increase in lower urinary tract symptoms (LUTS) than men with normal BMI.

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BPH is a prevalent condition with an estimated 90% of men in their 80 s demonstrating histologic evidence of the disease [14]. Previous studies have established a link between obesity and BPH [3, 7, 9, 15, 16]. Worldwide, obesity is on the rise even in countries with low socio-economic index implying it is no longer a disease of the affluent [17, 18]. This necessitated further research into the effects of obesity on PV, PSA levels and LUTS. A recent systematic review re-affirmed the aggravating effects of obesity on BPH [15]. BMI and Central obesity, as determined by the WC, are modifiable risk factors to the development of prostate disease—including BPH, prostatitis and prostate cancer [3, 10, 12, 19, 20]. Other studies have gone further and demonstrated that central obesity was the most significant predictor of PV than overall obesity [15, 21]. Our data suggest that there is no correlation between WC and PV (r = 0.131, p = 0.081). This was also true for the effect of BMI on PV whereby; obese patients generally had larger PV but the results were not statistically significant (5% CI, p = 0.195). Lee et al. and Kim et al. arrived at a similar conclusion, that there was no link between BMI and prostate volume, leading to the conclusion that central obesity as denoted by WC > 90 cm rather than overall obesity is a predictor of prostate growth and LUTS. These findings were a result of a multicentre, prospective, cross-sectional study at four urology centres in Korea from July 2007 to May 2008 recruiting 602 patients with BPH. Men with waist circumference > 90 cm had increased prostate volume; however, they had lower PSA values than men with WC < 90 cm [21, 22]. In contrast, Lee et al. showed that prostate volume was bigger in obese and central obesity patients than in those with normal BMI. The authors analysed 146 men over the age of 40 and separated them into three groups according to their BMI and into two groups according to their WC. Significantly increased prostate size was noticeable in the obesity group than in the normal group as well as in the central obesity group than in the group with normal waist size [7]. Similarly to this Matsuda et al. and Kim et al. showed a positive correlation between BMI and prostate size; however in both these studies there was a negative correlation between BMI and prostate specific antigen (PSA) levels, whereby men with high BMI had low PSA [8, 9]. The study showed that hypertension, diabetes and smoking were quite prevalent in our population. There was no statistically significant difference in PV between the hypertensive and the non-hypertensive (p = 0.454). Similarly to our study, Li-Peng showed no correlation between BPH and hypertension [11]. This is in contrast to the findings of a 2013 South Korean study in which men with hypertension had a higher International Prostate Symptom Score as well as larger PV putting them at an increased risk of LUTS compared to the non-hypertensive [23].

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Our data showed diabetic patients had slightly higher mean PV. However, the results were not statistically significant at 5% CI (p = 0.832). This finding differs with Ahmed Elabbady’s study findings in which diabetes was significantly associated with lower serum PSA and testosterone, but larger PV [24]. We did not include the correlation with ethnicity and testosterone levels as an endpoint in our study, which could explain the findings in Elabbady’s study. Smoking is a known trigger of prostate inflammation—a mechanism contributing to BPH [25]. However, previous studies have shown conflicting results on the effects of smoking on PV [23, 26]. This study demonstrated that smoking had no statistically significant effect on PV (5% CI, p = 0182) despite smokers having minimally larger prostates than non-smokers. This was corroborated by a study done by Platz et al. which showed that smoking had no correlation with PV, and that it may in fact reduce PV, thus protecting against BPH [27]. The current evidence trends towards the level of both total and free PSA being directly proportional to PV [28,29,30,31]. This study confirms this relationship as our data showed a direct correlation between the level of PSA and PV (r = 0.247, p = 0001). Our findings further suggest that increasing age was associated with increased PV (r = 0.195, p = 0.009) which was in keeping with evidence from previous studies [29]. However, not all previous studies agree with these findings. Stacy Loeb et. al., found that PV was highly variable in men with BPH and a good number of aging men had stable or decreasing prostate size [32]. Currently, the medical management of BPH related LUTS is hugely reliant on the prostatic smooth muscle relaxation effects of alpha-adrenergic receptor blockers [17, 33]. This has led to a hunt for alternate therapies that may aid LUTS improvement. With the previously established link between obesity and BPH, there have been proposals to promote and incorporate lifestyle modifications and appropriate medical management as an adjunct to diseases prevention, diagnosis and therapy [15, 17, 33].

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The findings of this study suggest that the routine/aggressive medical management of obesity would be of little to no benefit with regard to BPH/LUTS as there was no correlation between PV and any of hypertension, diabetes, BMI, and WC. This is supported by another study which showed that modest weight loss might not prevent the onset or progression of LUTS [34].

Study limitations

Like many other previous studies, some limitations of this study were a small sample size as well as the fact that it was a single centre study. Larger multicentre studies are required to establish the true effects of obesity on BPH as related to PV and LUTS.

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