breastprostateThe current epidemiological data suggest that the epidemic of breast and prostate cancers may be partially attributable to increased fat consumption, increased caloric intake during growth, low fiber, vegetable, and fruit consumption, and other lifestyle factors including exercise, alcohol, and smoking.

African American men are more likely to develop prostate cancer compared with Caucasian men and are nearly 2.4 times as likely to die from the disease. Although scientists do not yet understand why prostate cancer incidence and death rates are higher among African-American men, it is widely believed that it is a combination of genetic differences, lifestyle, nutritional habits and medical care may all play a role in the statistics.

Black women in the U.S. continue to die from breast cancer at a significantly higher rate than white women, a new study says. Black women were 43 percent more likely to die from breast cancer than their white counterparts, based on the most recent available data from 2014.

The study, conducted by Sinai Urban Health Institute in collaboration with the Breast Cancer Research Foundation, found that the breast cancer mortality rate for black women is 30.7 deaths per 100,000 women, compared to 21.4 deaths per 100,000 for whites. It also found that the disparity between those two rates has grown since 1990.

The study examined race-specific mortality from breast cancer in the 50 largest cities in the U.S. between 2005 and 2014. (New Orleans was not among them.) Atlanta showed the largest increase in black-white disparity, whereas Memphis, Philadelphia and Boston showed small but statistically significant decreases in the disparity.

Connie’s comments: Both prostate and breast cancers are hormone related and can be influenced by over use of plastic materials.  Both cancers are prevalent in western countries. Both organs (prostate and breasts) require gonadal steroids for their development, and tumours that arise from them are typically hormone-dependent and have remarkable underlying biological similarities.  We should consume hormone-free milk, eggs and meat. Maintain a healthy weight and avoid sugar.

Both cancers result from the accumulation of genetic lesions in a variety of oncogenes and tumor suppressor genes.

Both cancers share some genetic abnormalities that could contribute to the acquisition of the malignant phenotype by both mammary and prostatic epithelial cells.

Well known modifying risks of breast cancer related to age at first full-term pregnancy, age of menarche and menopause, number of menstrual cycles in a lifetime, oral contraceptive use, number of pregnancies, etc. However, despite the wealth of literature on steroid hormone involvement in breast cancer, we do not as yet have definitive answers to even simple questions such as:

  • Are steroid hormones carcinogens?
  • Do steroid hormones control breast cancer cell proliferation and growth rates (2)?

More recently, it has become evident that steroid hormones not only have direct actions on certain types of cells, but they can trigger additional effects through growth factors that are regulated by them; the latter act on neighboring cells in an autocrine/paracrine fashion (3). Lately, it has also been shown that steroid hormones are produced locally by cells that then use them intracellularly. Usually, the parent molecules are precursor steroids produced by the adrenals. This mode of hormone action is now referred to as ‘intracrine‘ and further expands the possible implications of steroid hormones in breast cancer pathogenesis in humans.

Major risk factors include age, ethnicity, family history, and steroid hormones. While the rate of increase of breast cancer incidence declines postmenopausally in women (1), the rate of increase of prostate cancer incidence increases continually with age. This phenomenon is likely linked to the continuation of testicular function in males throughout life and the cessation of ovarian function during the female menopause. The involvement of steroid hormones in the pathogenesis and progression of prostate cancer has been suggested for many years.

Tulinius et al. (16) in a large cohort study including 1539 Icelandic women with breast cancer, reported that the risk of prostate cancer was significantly raised for all male relatives, as well as for first-degree relatives, and second-degree relatives of breast cancer patients. It is noteworthy that in this study the information concerning which family members had cancer was obtained from the Icelandic Cancer Registry, whereas genealogical trees were constructed by using information from records of the genetics committee of the University of Iceland, thus avoiding possible bias generated by directly asking the family members about the structure and cancer cases in their families.

In addition to these genetic alterations in the first breast cancer susceptibility gene, studies of families linked to BRCA2 have revealed that prostate cancer risk is significantly increased in these families.


Dietary factors are widely believed to play an important role in determining the risk of many cancers, including those of breast and prostate. Vitamin A and carotenoids are considered anticarcinogenic in experimental systems. Fruits and vegetables seem to confer protection (23). Heterocyclic amines, consumed with charbroiled food, have carcinogenic potential (24). Plant estrogens found in soy products such as tofu have been suggested to confer protection against breast cancer in Asian populations (25, 26). Vitamin D has been proposed as an anticarcinogenic compound for breast (27) and prostate cancer (28). High circulating levels of 1,25-dihydroxyvitamin D were associated with low incidence of prostate cancer. In the United States, it was found that prostate cancer mortality rates exhibit a marked North-South gradient with higher rates observed in the North (29, 30). This gradient correlates well with ambient levels of UV radiation, giving rise to the hypothesis that low UV exposure may be a risk factor for prostate cancer. Many reports suggest that vitamin D has potent antitumor properties, and its analogs may be modifiers of the growth of various cancers including those of breast and prostate (27, 28, 31-34). A recent report suggests that the higher levels of vitamin D in men at low risk of developing prostate cancer are associated with vitamin D receptor polymorphisms (35).

Among all dietary factors, fat consumption has received the greatest attention (36). The connection between high-fat diet and increased cancer risk is supported by animal studies (37). In humans, breast cancer risk (22, 36) and prostate cancer risk (22, 38, 39) were found to increase with increased fat consumption. Although such associations are consistent between many studies, others question the validity of the data because of the presence of many confounders and the poor accuracy of obtaining food intake data (40, 41). It is expected that the role of dietary fat in the development of breast cancer will be further elucidated when a primary prevention trial among women age 50-79 is complete (1, 10). The Women’s Health Initiative is a randomized, placebo-controlled trial with three different interventions, one of which is dietary, aiming to reduce fat intake to 20% of total calories (from about 40% currently) and to increase intake of fruits and vegetables. In the same trial, another intervention includes vitamin D and calcium supplements (1). Other chemoprevention trials are underway in many countries (10). Prentice and Sheppard calculated, based on fat disappearance data, that a 50% reduction in fat consumption may reduce the relative risk of women of age 55-69 yr for breast cancer from 1.00 to 0.39 and in men for prostate cancer from 1.00 to 0.17.

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