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This article has discussed the increased incidence and disproportionately increased mortality of prostate cancer among African American men.Although the exact reasons are unknown, genetics may play a role, in addition to health care practices. Morbidity from other disease states, such as diabetes, obesity, or hypertension, may influence the overall survival of patients with prostate cancer. Current research tools will continue to explore biologic differences between the races; however, socioeconomic status and access to health care must not be overlooked. Several studies have demonstrated that similar disease stages and equal access to health care will result in similar outcomes. It is recognized that screening for prostate cancer will remain a controversial topic. Several influential professional societies recommend against screening and other professional societies endorse screening. Large-scale trials are currently underway hoping to answer this critical question. Since the advent of current screening tools, however, it seems that the overall mortality for prostate cancer has decreased and this cannot be ignored. Certainly, screening programs and clinical trials have traditionally had difficulty in recruiting minority participants, although more recent trials seem to be finding success. A primary care physician who is viewed as competent by their patients can certainly have a positive impact on their African American patients' willingness to participate in studies and screening programs. Most importantly, on the individual level, primary care physicians can provide a great service to their minority patients by offering educational materials on prostate cancer and by offering screening to qualified patients. The current American Urologic Association and National Cancer Institute guidelines recommend offering screening to all men age 50 and above. African American men or men with a first-degree relative with prostate cancer should be offered screening beginning at age 40. Proper screening consists of both a digital rectal examination to assess for asymmetry or nodules of the prostate and a serum PSA. Current recommendations are that individuals with a serum PSA greater than 4 ng/mL ora prostate nodule or asymmetric prostate should be referred to an urologist,where a biopsy can be performed easily in the office setting.The PSA cutoff of 4 has recently been questioned. A study by Thompson et al [31] evaluated 2950 men with a PSA of 4 or less with prostate biopsy.They found that the risk of prostate cancer in men with a PSA between 3.1 and 4 was 26.9% and that 25% of these men with prostate cancer had high-grade disease. All men found to have cancer had T1 disease. The clinical relevance of this surprisingly high rate of prostate cancer in men with a normal PSA is yet to be determined and is pending in studies on the ultimate effect of screening on mortality from prostate cancer. This information is not intended to confuse the issue, but intended to provide the most up-to-date information and allow for the best clinical decision making by the primary care physician. What can currently be recommended is if a patient is concerned about his possibility of having prostate cancer despite a normal PSA, a referral to an urologist to at least further discuss the issue may be in order. This may be especially true if the patient is African American or has a family history of prostate cancer at an early age.
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PMID:Minority issues in prostate disease. 1592 51

Adult obesity has shown little association with prostate cancer risk, but obesity at younger ages may be associated with reduced risk. In 1997-2000, the relation between obesity before age 30 years and incident advanced prostate cancer was investigated in a population-based case-control study of African-American and White men (568 cases, 544 controls) in California. Unconditional logistic regression was used to estimate odds ratios and 95% confidence intervals, adjusted for age, race, family history of prostate cancer, and saturated fat intake. Measures of obesity for age 10 years tended to be inversely associated with prostate cancer (odds ratio (OR) = 0.79, 95% confidence interval (CI): 0.46, 1.38 for selecting the "obese" pictogram and OR = 0.76, 95% CI: 0.52, 1.11 for reporting being heavier than peers). The decreased risk was more pronounced at ages 20-29 years (OR = 0.53, 95% CI: 0.28, 1.00 for the "obese" drawing, OR = 0.59, 95% CI: 0.40, 0.88 for being heavier than peers, and OR = 0.40, 95% CI: 0.20, 0.81 for body mass index > or =30 kg/m(2)). In addition, both "obese" and small waist size at ages 20-29 years showed inverse trends. This research implicating early-life body size in prostate cancer development helps to elucidate causal mechanisms, such as altered sex hormone profiles during critical developmental periods, potentially involved in development of the disease.
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PMID:Obesity before age 30 years and risk of advanced prostate cancer. 1593 19

The role of obesity in prostate cancer etiology remains controversial. A recent report suggested that obese men younger than age 60 may have a lower risk of developing prostate cancer than men the same age who are not obese. The current study used a nested, matched case-control study design and data collected in the General Practice Research Database between January 1991 and December 2001 to assess the association between body mass index (BMI) and the risk of incident prostate cancer. Seven hundred and thirty cases of prostate cancer with adequate information on BMI were identified and matched to 2740 controls on age, sex, general practice, and index date. Obese men (BMI > or = 30.0 kilograms [kg]/square of height in meters [m(2)]) were at lower risk of developing prostate cancer (AOR=0.78, 95% CI: 0.56, 1.09) compared to normal weight men (BMI=23.0-24.9 kg/m(2)), and the data best fit an inverse quadratic model for the relation between BMI and the risk of prostate cancer. This study provides modest support for a protective association between obesity and the risk of incident prostate cancer.
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PMID:Obesity and the risk of prostate cancer (United States). 1604 1

In an era of rapidly increasing prevalence of human obesity and associated health problems, leptin gene polymorphisms have drawn much attention in biomedical research. Leptin gene polymorphisms have furthermore drawn much attention from animal scientists for their possible roles in economically important production and reproduction traits. Of the polymorphisms reported for exonic, intronic, and promoter regions of the leptin gene, 16 have been included in association studies in humans, 19 in cattle, and 6 (all exonic or intronic) in pigs. In humans, associations have been found with overweight or (early-onset) obesity, non-insulin-dependent diabetes mellitus, prostate cancer, and non-Hodgkin's lymphoma. In cattle, associations have been found with feed intake, milk yield traits, carcass traits, and reproduction-related traits, and in pigs with feed intake, average daily gain, carcass traits (backfat/leanness), and reproduction performance traits. Many of the polymorphisms were only included in a limited number of association studies, or the phenotypes studied varied largely for a given polymorphism between studies. Therefore, many of the associations found for these polymorphisms need to be confirmed in future studies before firm conclusions can be drawn.
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PMID:Leptin gene polymorphisms and their phenotypic associations. 1611 75

The 12 th Oncology Forum discussed the progress and future strategy of cancer prevention in Japan. The National Cancer Center has established a research center for screening focusing on the most common six cancer, stomach, lung, liver, colon, breast and uterus cancer. The program so far had a cumulative detection rate of 3.3%, which is high,and may reflect the selection of subjects. Screening and chemoprevention is also being investigated in prostate cancer, but the issues centre on how to make this widely available. High risk subjects can also be identified for breast cancer. Obesity and family history are especially important. In colorectal cancer studies are evaluating different diets, but general application is not yet possible and the infrastructure to implement any general screening and prevention does not exist. Development of pharmaceutical treatments for prevention is difficult because of the need for very safe treatments, and also because of the length of time needed to carry out studies. Overall, cancer prevention is still in evolution. New approaches are needed, and new infrastructure will be needed at a government level to implement this.
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PMID:[Cancer prevention]. 1622 57

Erectile dysfunction (ED) is a highly prevalent condition in aging men with significant interpersonal and psychosocial consequences. Large-scale epidemiologic studies have demonstrated a consistent age-related loss of erectile function in men from different geographic and ethnic backgrounds, with approximately half of men over 70 years of age reporting moderate to severe symptoms. ED is associated strongly with specific comor-bidities, such as cardiovascular disease and hypertension, diabetes mellitus, lower urinary tract symptoms, prostate cancer, and depression. Lifestyle factors, including obesity and exercise frequency, also have been implicated in recent studies.
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PMID:Epidemiology of erectile dysfunction: the role of medical comorbidities and lifestyle factors. 1629 Oct 33

Obesity-associated prostate cancer (PCa) remains controversial, although most studies rely on body mass index evaluation, which is an indirect measure of fatness. Studies using body fat measurement and disease stratification according to PCa stage found stronger associations between obesity and PCa. Leptin is a pleiotrophic hormone mainly synthesized by adipocytes that acts in peripheral organs such as the prostate. This article reviews obesity-associated leptin's pathophysiological role in PCa progression. PCa development results from some known risk factors. Currently, there is enough evidence suggesting that leptin is an additional factor involved in advanced PCa occurrence, and obesity association with high-grade disease. Life-long exposure to genetic and/or environmental susceptibility factors that predispose to obesity and higher leptin levels may increase the risk for advanced PCa.
Prostate Cancer Prostatic Dis 2006
PMID:The link between obesity and prostate cancer: the leptin pathway and therapeutic perspectives. 1679 46

A growing body of evidence supports or rejects preventive interventions in asymptomatic adults. Thus, counseling for smoking cessation and some immunizations have been shown to be cost-effective. Evidence supports screening for body weight (obesity), hypertension, hyperlipidemia, cervical cancer, colorectal cancer and breast cancer. Screening for lung, pancreatic and ovarian cancer has no effect on outcome and should not be performed. Controversial preventive interventions include general screening for diabetes mellitus in the young adult, thyroid disorders and prostate cancer. Physicians should be aware of a possible hidden agenda in patients presenting for a check-up.
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PMID:[Check-up-examinations in internal medicine]. 1636 64

Prostate cancer is the most common non-skin cancer among men in most western populations, and it is the second leading cause of cancer death among U.S. men. Despite its high morbidity, the etiology of prostate cancer remains largely unknown. Advancing age, race, and a family history of prostate cancer are the only established risk factors. Many putative risk factors, including androgens, diet, physical activity, sexual factors, inflammation, and obesity, have been implicated, but their roles in prostate cancer etiology remain unclear. It is estimated that as much as 42% of the risk of prostate cancer may be accounted for by genetic influences, including individual and combined effects of rare, highly penetrant genes, more common weakly penetrant genes, and genes acting in concert with each other. Numerous genetic variants in the androgen biosynthesis/metabolism, carcinogen metabolism, DNA repair, and chronic inflammation pathways, have been explored, but the results are largely inconclusive. The pathogenesis of prostate cancer likely involves interplay between environmental and genetic factors. To unravel these complex relationships, large well-designed interdisciplinary epidemiologic studies are needed. With newly available molecular tools, a new generation of large-scale multidisciplinary population-based studies is beginning to investigate gene-gene and gene-environment interactions. Results of these studies may lead to better detection, treatment, and, ultimately, prevention of prostate cancer.
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PMID:Prostate cancer epidemiology. 1636 24

Prostate cancer is associated with obesity. However, the molecular basis of this association is not well known. Adiponectin is a major adipose cytokine that decreases in circulation in obesity and ameliorates obesity. Here, we identify adiponectin as a novel inhibitor in prostate cancer cell growth. Adiponectin occurs in non-proteolytic (full-length adiponectin: f-adiponectin) and proteolytic (globular adiponectin) forms in various oligomeric states (trimer, hexamer, and high molecular weight complex). The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay demonstrates that f-adiponectin inhibits prostate cancer cell growth drastically at subphysiological concentrations. Furthermore, velocity sedimentation analysis shows that the high molecular weight complex of f-adiponectin is the inhibitory form. Moreover, f-adiponectin suppresses leptin- and/or insulin-like growth factor-I (IGF-I)-stimulated, androgen-independent DU145 cell growth, and dihydrotestosterone-stimulated, androgen-dependent LNCaP-FGC cell growth. In addition, f-adiponectin enhances doxorubicin inhibition of prostate cancer cell growth. Therefore, f-adiponectin is a molecular mediator between prostate cancer and obesity, and may be therapeutic to prostate cancer.
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PMID:Adiponectin as a growth inhibitor in prostate cancer cells. 1640 34


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