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1.
Actas Urol Esp ; 33(7): 741-6, 2009.
Artículo en Español | MEDLINE | ID: mdl-19757658

RESUMEN

INTRODUCTION: Prostate cancer (CaP) is one of the most important causes of morbidity and mortality in the world. There is evidence that obesity and inadequate eating habits may promote CaP development. OBJECTIVE: To analyze and compare the body mass index (BMI) and the food intake, especially fats and antioxidants, among subjects with CaP and those free of disease as a control group. MATERIAL AND METHODS: A sample of 40 men between 50 and 80 years old were selected for the study: 20 with CaP and 20 healthy men as control group. All volunteers underwent a digital rectal examination, prostate specific antigen level, ultrasound and transrectal prostate biopsy, and a nutritional interview where a dietary history and different anthropometric measurements were made. Statistical analysis was performed using the Student T test for independent samples (p < 0.05). RESULTS: BMI in the subjects with CaP was higher than in controls (29.8 kg/m2 vs. 27.96 kg/m2, p = 0.13) but not statistically significant. However, there was a direct correlation between BMI and tumor aggressiveness (r = 0.79, P < 0.001). Total, saturated, monounsaturated and polyunsaturated fat intake was significantly higher in subjects with CaP; while omega3 fatty acids, vitamin C and lycopene intake was significantly lower than in controls (p < 0.05). CONCLUSIONS: A healthy weight and a diet low in total fat, saturated, monounsaturated and polyunsaturated fat and rich in n3 fatty acids, vitamin C and lycopene is associated with a lower risk of CaP.


Asunto(s)
Índice de Masa Corporal , Dieta , Neoplasias de la Próstata/etiología , Anciano , Anciano de 80 o más Años , Antioxidantes , Grasas de la Dieta , Humanos , Masculino , Persona de Mediana Edad , Neoplasias de la Próstata/epidemiología
2.
Arch Esp Urol ; 62(2): 103-8, 2009 Mar.
Artículo en Español | MEDLINE | ID: mdl-19448276

RESUMEN

BACKGROUND: Many studies have investigated the association between obesity, adipose tissue-derived factors (leptin and adiponectin) and prostate cancer (CaP) but the results are still inconsistent. METHODS: The aim of this study was to carry out a comprehensive review of the existing evidence about the role of leptin and adiponectin in prostate carcinogenesis and to provide an overview of it. RESULTS: Recent evidence suggests that leptin may play a rol in prostate cancer progression, while adiponectin may act as an "antiprostatic cancer" adipokine. CONCLUSIONS: Obesity may promote the progression of established prostate cancer and and adipokines may provide a molecular mechanism whereby obesity exerts its effects on prostate tumour biology.


Asunto(s)
Adiponectina/fisiología , Leptina/fisiología , Neoplasias de la Próstata/etiología , Humanos , Masculino
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