Prostate cancer is the commonest malignant disease in men in some Western countries. Although Asia has not been found, in the last ten years there was significant increase in cases.
The risk of prostate cancer is determined by two things: genetic factors and environmental factors. The role of the environment is evident from studies which found an increase of migration in prostate cancer incidence in first-generation immigrants from Japan and China in the United States.
From the results of these studies made the hypothesis that diet plays as one of the risk of the occurrence or spread of prostate cancer.
Fat
Research on animals proved that fat-free diet can reduce the growth of malignant prostate tumors. Conversely, high-fat diet causes the growth of prostate cancer cells more quickly. The role of fats in increasing the risk of prostate cancer occur by several mechanisms. First, it proved that the fat may affect levels of testosterone, a hormone that is needed for the growth of prostate cells, both benign or malignant. Men who ate less fat would have testosterone levels that are relatively low.
Second, fat is a source of free radicals, and the third is the result of fatty acid metabolism is thought to be carcinogenic. Examples are unsaturated fatty acids omega-6 that can spur the growth of prostate cancer cells.
The correlation between fat consumption and prostate cancer risk is also evidenced in several epidemiological studies. Giovannucci and colleagues conduct a prospective study of the relationship between diet and prostate cancer. This study proved that high-fat diets increase risk of advanced prostate cancer development.
In addition, there are still some other studies that support such a cohort study in Hawaii. Unfortunately, few other epidemiological studies failed to prove a similar thing among others is a prospective study in Norway.
Thus, although many epidemiological studies and biological studies that prove the relationship between high dietary fat and risk of prostate cancer, still needed additional epidemiological studies to prove this with certainty.
The risk of prostate cancer is determined by two things: genetic factors and environmental factors. The role of the environment is evident from studies which found an increase of migration in prostate cancer incidence in first-generation immigrants from Japan and China in the United States.
From the results of these studies made the hypothesis that diet plays as one of the risk of the occurrence or spread of prostate cancer.
Fat
Research on animals proved that fat-free diet can reduce the growth of malignant prostate tumors. Conversely, high-fat diet causes the growth of prostate cancer cells more quickly. The role of fats in increasing the risk of prostate cancer occur by several mechanisms. First, it proved that the fat may affect levels of testosterone, a hormone that is needed for the growth of prostate cells, both benign or malignant. Men who ate less fat would have testosterone levels that are relatively low.
Second, fat is a source of free radicals, and the third is the result of fatty acid metabolism is thought to be carcinogenic. Examples are unsaturated fatty acids omega-6 that can spur the growth of prostate cancer cells.
The correlation between fat consumption and prostate cancer risk is also evidenced in several epidemiological studies. Giovannucci and colleagues conduct a prospective study of the relationship between diet and prostate cancer. This study proved that high-fat diets increase risk of advanced prostate cancer development.
In addition, there are still some other studies that support such a cohort study in Hawaii. Unfortunately, few other epidemiological studies failed to prove a similar thing among others is a prospective study in Norway.
Thus, although many epidemiological studies and biological studies that prove the relationship between high dietary fat and risk of prostate cancer, still needed additional epidemiological studies to prove this with certainty.
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