Ethnicity |
PCa incidence, morbidity, and mortality rates vary significantly by race and ethnicity. African-American, Black, and Caribbean men show the highest PCa rates worldwide. These disparities are mostly related to differences in access to screening and treatment, exposure to PCa risk factors, and variations in genomic susceptibility (e.g., risk loci found at chromosome 8q24), among other biological factors. |
[15,16,17,18,19,20] |
Family history and genetic factors |
According to estimates, around 5 to 15% of PCa cases have been related to hereditary factors. In genome-wide association studies, almost 170 loci of susceptibility for hereditary PCa (about 33% of familial PCa risks) have been identified. Many genes show a strong association with hereditary PCa risk, including BRCA1, BRCA2, ATM, CHEK2, and PALB2, and Lynch syndrome MLH1, MSH2, MSH6, and PMS2 genes. Other genes, however, have an unclear cancer risk and unknown clinical importance. |
[4,20,21,22,23,24,25,26] |
Obesity, overweight and physical inactivity |
Obesity is implicated in the dysregulation of various hormonal pathways, leading to higher levels of insulin and IGF, oxidative stress, and inflammatory cytokines, and lower levels of adiponectin, testosterone, and sex hormone-binding globulin. Obesity is associated with an increased risk of PCa mortality and recurrence, worsened treatment-related adverse effects, development of obesity-related comorbidities, and the earlier progression and development of metastatic disease. Nevertheless, the physiological mechanisms associated between obesity and poor PCa outcomes remain unknown. |
[3,27,28,29,30,31,32,33] |
Tobacco use |
Smoking increases the risk of death from PCa, which increases with obesity, specifically for advanced PCa. Moreover, tobacco smoking increases the risk of biochemical recurrence and metastasis. Nevertheless, the association between tobacco smoking and PCa prognosis needs to be explored. |
[3,32,34,35,36,37,38] |
Lycopene and tomato-based products |
Epidemiologic studies have focused on tomatoes as a specific source of lycopene, with more consistent findings supporting the protective effect of a higher intake of tomatoes on PCa risk. Furthermore, studies have shown a reduced risk of advanced PCa with the consumption of cooked tomatoes, since these products have more available lycopene. Current epidemiologic evidence is not definitive but suggests that a higher intake of tomato-based products is associated with a reduced risk of PCa and a potentially lower risk of progression. Further studies are required to determine whether the effect is because of lycopene or other components of tomatoes. |
[3,32,39,40,41,42,43,44] |
Calcium, dairy products, and vitamin D |
An intake of dairy products above the daily recommended dose has been positively associated with PCa risk. A potential mechanism underlying the association with calcium is through suppressing circulating levels of dihydroxyvitamin D, which seems to have a protective effect against PCa. The mechanisms behind this association are not yet fully understood, but researchers suggest reducing dairy intake while increasing the consumption of fish and tomato products for PCa prevention. |
[3,32,45,46,47,48] |
Cruciferous, soy, and green tea |
Cruciferous, soy, and green tea seem to have a role in decreasing the risk of PCa due to compounds with anticarcinogenic properties in their composition. Asian populations consume soy foods as a part of their regular diet, which might contribute to the lower PCa incidence found in these countries. However, the preventive action of these compounds needs to be further explored. |
[32,43,49,50,51,52,53,54] |