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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Measurement of obesity is not as simple as its definition. Currently, several methods of measuring obesity are used in clinical studies. Skinfold thickness, crude weight, lean body mass (LBM), body mass index (BMI), and waist-to-hip ratio (WHR) are some of the more popular methods, but each contains its inherent strengths and flaws. In general, the results of the largest studies on prostate cancer and obesity have not been conclusive. One of the largest studies found an inverse relation to prostate cancer in the youngest age groups. The age and duration of obesity or any rapid changes in weight gain, along with other unhealthy exposures, may have some relation to prostate cancer incidence and mortality. Early intrinsic or extrinsic exposure to estrogen or estrogenlike compounds may provide a protective effect. The timing and duration of a higher estrogen and/or lower testosterone exposure may have a beneficial or detrimental impact on the prognosis of an established prostate tumor. Negative exposures over time such as low levels of sex hormone-binding globulin (SHBG), a greater exposure to growth factors, elevated insulin levels, greater sympathetic activity, higher cholesterol levels, immune system dysfunction, inadequate diets, smoking status, and other factors may be associated with an increased risk of prostate cancer and other diseases. Obesity may also be associated with other cancers for similar and different reasons. For example, morbidity and mortality from postmenopausal breast cancer, colon, kidney, and other cancers are potentially associated with obesity. Other comorbidities such as cataracts, coronary heart disease, diabetes, erectile dysfunction, hypertension, and others are also associated with obesity. The 2 largest prospective studies on BMI and overall mortality have also demonstrated the substantial negative impact of excess weight on society. Prostate cancer risk and obesity need further research to establish if a true association exists, but at this time, does it really matter? Overall, the profound adverse effect of being obese on general health is dramatic, and this is what clinicians and patients need to remember.
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PMID:Is obesity a risk factor for prostate cancer, and does it even matter? A hypothesis and different perspective. 1193 35

Breast and prostate cancer share similar intrinsic and extrinsic risk factors. Based on laboratory, ecologic/international comparison, and case-control studies, the impact of dietary fat or other fat subtypes has been suggested as a potential route to reduce risk. Recent large-scale prospective studies have failed to find an association between fat and breast cancer risk. These studies may provide some insight for researchers examining the relation between fat and prostate cancer. Prospective studies to date have also failed to find a consistent association between prostate cancer and fat intake. Some fat subtypes (eg, saturated fat) or other lifestyle changes (eg, obesity, physical activity) may affect risk and progression of these cancers when examining the sum total of the research, but more precise and specific investigations in humans are needed to address these issues. Other concerns, such as the impact of excess energy or overall caloric consumption on carcinogenesis, still need to be addressed, as well as other methodologic limitations of past investigations. Large gaps exist in environmental (eg, diet, lifestyle) and heritable causes of these diseases. Regardless, until more extensive research is completed, lifestyle changes should be recommended based on reducing morbidity and mortality from cardiovascular disease-the number 1 cause of death in the United States. Additionally, cardiovascular disease remains the number 1 or 2 cause of death in patients diagnosed with breast or prostate cancer. Practical and simple dietary changes should be encouraged by health professionals because they could improve the overall longevity and quality of patients' lives. Numerous ongoing prospective studies of diet and cancer should provide researchers and the public with much-needed answers in this area.
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PMID:Dietary fat reduction to reduce prostate cancer risk: controlled enthusiasm, learning a lesson from breast or other cancers, and the big picture. 1193 36

Prevention of cancer through interventions based on sound scientific research remains an important strategy of oncology research at the National Cancer Institute (NCI). Reducing the burden of cancer in the United States is focused on clinical investigations in medical settings and public health intervention research on cancer risk factors regarding lifestyle and diet. Chemoprevention research at the NCI has progressed systematically to identify potential agents that reduce cancer risk and to develop public health strategies that take advantage of basic research results. In addition, advances in our understanding of molecular targets and pathways and our use of new and emerging technologies have become important tools for oncology research. Priority areas for chemoprevention research, identified from experimental and clinical research, are investigated in clinical trials to determine their ability to reduce cancer risk in selected populations or in the general population. Priority areas discussed in this review are the relationship of the arachidonic acid pathway to carcinogenesis, lung cancer prevention in former smokers, breast cancer prevention, and prostate cancer prevention. In addition, two lifestyle factors that have potential to influence cancer risk-obesity and functionally enhanced foods-are discussed in the context of their link between clinical and public health-related research.
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PMID:Cancer prevention clinical trials. 1472 55

Serum testosterone concentration appears to be higher in black men than white men, particularly at younger ages. The higher incidence of prostate cancer in blacks has been attributed, at least in part, to this difference. Other factors associated with androgen levels in men include age and obesity. However, most of the studies of adult androgen levels are limited by their cross-sectional design. We conducted longitudinal analyses (Generalized Estimating Equation) of the associations of age, body mass index (BMI), and waist circumference with total and free testosterone and sex hormone-binding globulin (SHBG) concentrations during an 8-year period and compared these hormonal factors between black (n = 483) and white (n = 695) male participants of the Coronary Artery Risk Development in Young Adults (CARDIA) Study. For men ages 24 years and older at the time of the first hormone measurement, increasing age was associated with a statistically significant decrease in serum total and free testosterone and an increase in SHBG (P < 0.05). BMI and waist circumference were inversely associated with total testosterone and SHBG, but only BMI was inversely associated with free testosterone. After adjustment for age and BMI, total testosterone was higher in blacks (0.21 ng/ml; P = 0.028) than whites, an approximately 3% difference. However, after further adjustment for waist circumference, there was no black-white difference (0.05 ng/ml; P = 0.62). These results indicate that the age-associated decrease in circulating testosterone and increase in SHBG begin during the 3rd decade of life, and that increasing obesity, particularly central obesity, is associated with decreasing total testosterone and SHBG. Results also suggest that the previously observed difference in total testosterone between black and white men could be attributed, for the most part, to racial differences in abdominal obesity.
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PMID:Serum androgen concentrations in young men: a longitudinal analysis of associations with age, obesity, and race. The CARDIA male hormone study. 1237 5

Scientific evidence is accumulating on physical activity as a means for the primary prevention of cancer. Nearly 170 observational epidemiologic studies of physical activity and cancer risk at a number of specific cancer sites have been conducted. The evidence for decreased risk with increased physical activity is classified as convincing for breast and colon cancers, probable for prostate cancer, possible for lung and endometrial cancers and insufficient for cancers at all other sites. Despite the large number of studies conducted on physical activity and cancer, most have been hampered by incomplete assessment of physical activity and a lack of full examination of effect modification and confounding. Several plausible hypothesized biological mechanisms exist for the association between physical activity and cancer, including changes in endogenous sexual and metabolic hormone levels and growth factors, decreased obesity and central adiposity and possibly changes in immune function. Weight control may play a particularly important role because links between excess weight and increased cancer risk have been established for several sites, and central adiposity has been particularly implicated in promoting metabolic conditions amenable to carcinogenesis. Based on existing evidence, some public health organizations have issued physical activity guidelines for cancer prevention, generally recommending at least 30 min of moderate-to-vigorous intensity physical activity on > or =5 d/wk. Although most research has focused on the efficacy of physical activity in cancer prevention, evidence is increasing that exercise also influences other aspects of the cancer experience, including cancer detection, coping, rehabilitation and survival after diagnosis.
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PMID:Physical activity and cancer prevention: etiologic evidence and biological mechanisms. 1242 70

A growing body of evidence supports preventive interventions in asymptomatic adults. Primary prevention, which includes counselling (in particular for smoking cessation) and review of immunisation status, has been shown to be more cost-effective than secondary prevention. Evidence supports screening for hypertension, hyperlipidaemia, cervical cancer, colorectal cancer, breast cancer and obesity. 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, thyroid disorders and prostate cancer. Physicians should be aware of a possible hidden agenda in patients presenting for a checkup.
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PMID:Evidence for prevention and screening: recommendations in adults. 1242 90

The purpose of the present study was to perform a BPH risk factor analysis in men, relating the prostate gland volume to components of the metabolic syndrome and to identify clues to the etiology of BPH. Our material comprised a consecutive series of 158 patients with lower urinary tract symptoms with or without manifestations of the metabolic syndrome. In this group, the measured volume of the prostate was related consecutively to potential risk factors. The diagnoses atherosclerosis, non-insulin-dependent diabetes mellitus (NIDDM) and treated hypertension were obtained from the patient's medical history. Data on blood pressure, waist and hip measure, body height and weight were collected and body mass index (BMI) and waist/hip ratio (WHR) were calculated. Blood samples were drawn from fasting patients to determine insulin, cholesterol, triglycerides, HDL and LDL-cholesterol, uric acid and ALAT. The prostate gland volume was determined using ultrasound. Our results show that there was a larger prostate gland in men with NIDDM (P=0.0058), treated hypertension (P=0.0317), obesity (P<0.0001), low HDL-cholesterol levels (P=0.0132) and high insulin levels (P<0.0001) than in men without these conditions. The prostate gland volume correlated positively with the systolic blood pressure (r(s)=0.17; P=0.03), obesity (r(s)=0.34; P<0.0001) and fasting insulin (r(s)=0.38; P<0.0001) and negatively with HDL-cholesterol (r(s)=-0.22; P=0.009). On the basis of our findings, we concluded that NIDDM, treated hypertension, obesity, low HDL-cholesterol levels and high insulin levels constitute risk factors for the development of BPH. The results suggest that BPH is a facet of the metabolic syndrome and that BPH patients may share the same metabolic abnormality of a defective insulin-mediated glucose uptake and secondary hyperinsulinemia as patients with the metabolic syndrome. The findings generate a hypothesis of a causal relationship between high insulin levels and the development of BPH. In a clinical setting, the findings of the present report suggest that, in any patient presenting with BPH, the possible presence of NIDDM, hypertension, obesity, high insulin and low HDL-cholesterol levels should be considered. Conversely, in patients suffering from these conditions, the possibility of a clinically important BPH should be kept in mind.
Prostate Cancer Prostatic Dis 1998 Mar
PMID:Components of the metabolic syndrome-risk factors for the development of benign prostatic hyperplasia. 1249 10

Androgens, diet, race and obesity are thought to play some roles in the pathogenesis of prostate cancer. We wanted to evaluate if there were any inter-relationships between prostate specific antigen (PSA), serum testosterone, serum cholesterol, HDL, triglycerides, body mass index (BMI) and race, in older patients with and without prostate cancer (CaP). We evaluated 308 patients referred to urologists in private practice offices and clinics with and without prostate cancer with regard to race, serum PSA, age, serum testosterone, full lipid profile, height and weight, and stage of cancer. We used multivariate analysis, Fisher's exact test and t-tests as well as logistic regression analysis. Data was analyzed using SPSS computer software, and P-values<0.05 were considered statistically significant. Significantly higher levels of serum testosterone were found in black men with CaP than black men without CaP (526+/-28 vs 404+/-19, respectively.) We also found significantly higher levels of serum testosterone in white men with CaP than white men without CaP (409+/-20 vs 302+/-14, respectively, P<0.05). HDL was higher in black men than white men, and triglycerides were higher in white men than black men. Cholesterol was similar across all groups, but BMI was highest in white men with CaP. We also found a significant association between BMI and pathological stage of prostate cancer patients among both black and white men (P<0.05). Our study demonstrated that black men who developed CaP had higher serum testosterone levels, on average, than white men who developed CaP. Furthermore, BMI was highest in white men developing CaP compared to black men, but we found a significant association between pathological stage and BMI in both black and white patients. Although it is controversial whether obesity is considered to be a risk factor for prostate cancer, this small pilot study suggests that BMI may play a role in the progression of the disease once it is established.Prostate Cancer and Prostatic Diseases (2001) 4, 101-105
Prostate Cancer Prostatic Dis 2001
PMID:A pilot study analyzing PSA, serum testosterone, lipid profile, body mass index and race in a small sample of patients with and without carcinoma of the prostate. 1249 46

We present a review of the epidemiological evidence for relations of prostate cancer risk to circulating total and bioavailable androgens, to alterations in the metabolism of insulin-like growth factor-1 (IGF-1), and to anthropometric indices of longitudinal growth (body stature) and overweight. In addition, we review the physiological inter-relationships between insulin, growth hormone/IGF-1 axis, and sex steroid metabolism, as well as the associations of bioavailable sex steroid levels with overweight and obesity. A first conclusion of this review is that, taken together, epidemiological studies have provided little support for the hypothesis that prostate cancer risk is increased in men with elevated total or biovailable testosterone (T). Although one prospective study showed an increased risk in men with low plasma sex hormone-binding globulin (SHBG) and with elevated plasma T for given levels of SHBG, this was not confirmed by results from other cohort studies. A second conclusion is that overweight, which is generally associated with moderate reductions in both total and bioavailable plasma T, appears to be unrelated to any significant increase or decrease in prostate cancer risk. However, significant increases in risk have been observed for men with a taller body stature, or with elevated plasma IGF-1. IGF-1 may directly enhance prostate tumorigenesis by inhibiting apoptosis and by stimulating cell proliferation. In addition, IGF-1 downregulates the synthesis of SHBG, and enhances sex steroid synthesis. Therefore, we do not entirely rule out that due to an elevation of plasma IGF-1 levels, men at increased risk of prostate cancer also have mildly elevated plasma bioavailable T, which epidemiological studies may have failed to demonstrate because of methodological problems. Prostate Cancer and Prostatic Diseases (2000) 3, 157-172
Prostate Cancer Prostatic Dis 2000 Nov
PMID:Plasma androgens, IGF-1, body size, and prostate cancer risk: a synthetic review. 1249 92

We conducted a review of previous cohort studies on the association between a history of diabetes mellitus (DM) and the occurrence of cancer. We limited the papers to those concerning cohort studies on 9 cancer sites, i.e. the kidney, liver, biliary tract, pancreas, colon or rectum, prostate, breast, endometrium, and ovary, in addition to all cancers. With regard to kidney, liver, biliary tract, pancreatic, colorectal, breast, and endometrial cancers, the risk of cancer development has been consistently reported to be positively associated with DM by two or more cohort studies. In contrast, DM was shown to relate negatively to the risk of prostate cancer by two cohort studies. However, there were no cohort studies which showed an either significantly positive or negative association of DM with ovarian cancer. Elevated levels of insulin or IGFs among DM patients have been proposed as a causal mechanism of increased risk for most of the reviewed cancers. In addition, increased estrogen levels in DM patients have been suggested to explain the casual mechanism of increased risk for kidney, breast and endometrial cancers, and decreased risk for prostate cancer. On the other hand, the possibility of detection bias has been suggested in the association of DM with the risk of most of these cancers. Obesity and heavy consumption of alcohol have been indicated as confounding factors in the relationship of DM to the risk for some of them. Thus, further studies are necessary for firm conclusions regarding the association of DM with cancer risk.
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PMID:A Review of Cohort Studies on the Association Between History of Diabetes Mellitus and Occurrence of Cancer. 1271 99


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