**2. Nutrition**

Several products are thought to be associated with increased risk for developing prostate cancer, others are known to act protectively. To the first group we may include saturated fats, red meat and dairy products (Kondo et al., 1994; Shirai, et al., 1997; Torniainen et al., 2007). In the second group we will find vitamin A, D and E, selenium, lycopene, fitoestrogens and isoflavones (Clark et al., 1998; Heinonen et al., 1998; Imaida et al., 2001; Kato et al., 2000; Schwartz et al., 1990). Vitamin A, D, E, selenium, lycopene and fitoestrogens are the compounds of fruits, vegetables, soya and tea. Vitamin A is known to improve cell apoptosis (Pienta et al., 1993; Young et al., 1994). Vitamin D facilitates cell differentiation (Hedlund et al., 1997). It was hypothesized that it may increase PSA

The Influence of Obesity on Prostate Cancer Diagnosis and Treatment 23

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

Skeletal metastases are most common in advanced Pca. Metastases are known to be osteoblastic ones. Prostate cancer cells are absorbing lipids directly to develop and progress,

 It was also experimentally shown that bone marrow without adypocytes is less attractive for prostate cancer cells to residue (Brown et al., 2006). It was even suggested that lowering lipid levels with statins will impact the progression of prostate cancer, but this assumption

As stated in the introduction in obese levels of sex hormones are different from that observed in normal weight people. Prostate is hormone-sensitive gland and therefore

Also prostate cancer is hormone-sensitive and testosterone is known to accelerate its progression to advanced and metastatic form while estrogens inhibit such progress. This finding led us to application of castration (surgical or pharmacological) in the treatment of

However, the relation between dishormonese and prostate cancer is not so unequivocal. Testosterone also influences the differentiation of prostate cells (but not prostate cancer cells) to mature forms, while estrogens have contrary impact and therefore may lead to

It is also assumed that PCa in overweight people is more aggressive. Usually it was stated that Pca with Gleason score > 7 was significantly more frequent in obese patients. Not all authors agree with that hypothesis (Chyou et al., 1994; Major et al., 2011; Nilsen et al., 1999;

Authors emphasize that central obesity as the outcome of excessive fat accumulation results in glucose intolerance, high blood pressure, atherosclerosis, cardiovascular disease, insulin resistance, altered metabolic profile, metabolic syndrome, and obesity-related lipid

6. Unfavorable postoperative features especially higher rate of:

abovementioned study gave us only weak proof of such correlation.

poorly differentiated Pca (Massengill et al. 2003; Schatzl et al., 2001).

Rodriguez et al., 2007; Schuurman et al., 2000; Snowdon et al., 1984).

that is why bone marrow is so common place of metastases.

a. high grade disease b. positive surgical margins c. extraprostatic extension (pT3a) d. lymph node metastases (N+) e. biochemical recurrence

7. hemodilution (explained later)

**4. Prostate cancer cells and adipocytes** 

turned out not to be true (Platz et al., 2006).

androgens are needed for its development.

advanced or metastatic prostate cancer.

**6. Aggressive prostate cancer** 

f. fatal disease

**5. Sex hormones** 

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 Study Group, 1994).

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).
