**3. Obesity**

It is of paramount significance to distinguish between high-risk and low-risk patients depending on extent of obesity. There are many ways to determine the range of overweight and obesity. The most prevalent is body mass index developed by World Health Organization. However, it does not differentiate fat mass from muscle mass. That is why waist - hip ratio (WHR) is more commonly applied while assessing the central adiposity, and correlates much stronger with hormonal alterations (the importance of that finding is emphasized later in the text) than BMI.

There are various theories concerning the influence of obesity on the natural development, diagnostics or progression after radical treatment of Pca. The Health Professional Follow-Up Study was based on 47757 men who were observed for 14 years and showed that relative risk for developing prostate cancer was 0,52 in obese compared to non-obese men (Giovannucci et al., 2003).

The 5 times increased percentage of biochemical recurrence after radical prostatectomy observed in Afro-Americans, compared to Euro-Americans, is sometimes explained by 3 times more frequent presence of overweight or obesity among the former. It also may result from the polymorphism of the androgen receptor which causes higher PSA concentration in Afro-Americans. On the other hand two large studies failed to demonstrate disastrous impact of obesity on prostate cancer morbidity (Andersson et al., 1997; Rapp et al., 2005).

Not only the absolute value of BMI seems to be important when assessing the patient's risk. It was shown that also gaining weight at the greatest rate of ≥ 1.5 kg/year between 25 years of age and time of Pca diagnosis will result in more rapid biochemical failure after radical treatment (Strom et al., 2005).

The influence of obesity on Pca is definitely negative, including the following:

	- a. technical problems (larger hooks, smaller operational field)
	- b. larger prostates observed in obese patients (much problem while conducting nervesparing technique)
	- a. high grade disease
	- b. positive surgical margins
	- c. extraprostatic extension (pT3a)
	- d. lymph node metastases (N+)
	- e. biochemical recurrence
	- f. fatal disease

doubling time (PSA DT) (Beer et al., 2003). Selenium is a known antioxidant (Clark et al., 1996). In Asia, where soya and tea consumption (fitoestrogens) is higher in comparison to western countries, the prevalence of prostate cancer is lower (Adlercreutz et al., 1993; Fotsis et al., 1993). Several studies tried to prove the favorable impact of vitamin E in Pca prevention (Knekt et al., 1990; The Alpha-Tocopherol, Beta-Carotene Cancer Prevention

However, it has to be stressed that such influences are still rather hypothesis than evidence based facts. SELECT (Selenium and Vitamin E Comparison Trial) trial failed to demonstrate the favorable impact of selenium and vitamin E on Pca morbidity (Ledesma et al., 2011).

It is of paramount significance to distinguish between high-risk and low-risk patients depending on extent of obesity. There are many ways to determine the range of overweight and obesity. The most prevalent is body mass index developed by World Health Organization. However, it does not differentiate fat mass from muscle mass. That is why waist - hip ratio (WHR) is more commonly applied while assessing the central adiposity, and correlates much stronger with hormonal alterations (the importance of that finding is

There are various theories concerning the influence of obesity on the natural development, diagnostics or progression after radical treatment of Pca. The Health Professional Follow-Up Study was based on 47757 men who were observed for 14 years and showed that relative risk for developing prostate cancer was 0,52 in obese compared to non-obese men

The 5 times increased percentage of biochemical recurrence after radical prostatectomy observed in Afro-Americans, compared to Euro-Americans, is sometimes explained by 3 times more frequent presence of overweight or obesity among the former. It also may result from the polymorphism of the androgen receptor which causes higher PSA concentration in Afro-Americans. On the other hand two large studies failed to demonstrate disastrous impact of obesity on prostate cancer morbidity (Andersson et al.,

Not only the absolute value of BMI seems to be important when assessing the patient's risk. It was shown that also gaining weight at the greatest rate of ≥ 1.5 kg/year between 25 years of age and time of Pca diagnosis will result in more rapid biochemical failure after radical

1. dishormonose – abnormal hormone concentrations, which induces the intensification of

2. comorbidities, which pushes the prostate diagnostics into the background and

4. difficulties during transrectal ultrasound (TRUS) of the prostate and prostate biopsy

b. larger prostates observed in obese patients (much problem while conducting nerve-

The influence of obesity on Pca is definitely negative, including the following:

consequently patients suffer from more advanced forms of prostate cancer

diagnostics and at the same time postpones proper treatment

(due to larger prostates in obese patients) (Freedland et al., 2006). 5. difficulties during radical prostatectomy and radical radiotherapy due to: a. technical problems (larger hooks, smaller operational field)

3. difficulties in per rectum examination in obese patients,

Study Group, 1994).

emphasized later in the text) than BMI.

(Giovannucci et al., 2003).

1997; Rapp et al., 2005).

treatment (Strom et al., 2005).

sparing technique)

**3. Obesity** 

7. hemodilution (explained later)

Lastly it was proved that the unfavorable impact of obesity on Pca may be explained by genetic examinations. It was hypothesized that the AA genotype of rs9939609, which is associated with an increase in BMI, would protect against non-aggressive prostate tumors whilst increasing the risk of aggressive prostate tumors (Lewis et al., 2010). The abovementioned study gave us only weak proof of such correlation.
