Adult dietary intake and prostate cancer risk in Utah: a case-control study with special emphasis on aggressive tumors

Abstract

A population-based case-control study in Utah of 358 cases diagnosed with prostate cancer between 1984 and 1985, and 679 controls categorically matched by age and county of residence, were interviewed to investigate the association between dietary intake of energy (kcal), fat, protein, vitamin A, beta-carotene, vitamin C, zinc, cadmium, selenium, and prostate cancer. Dietary data were ascertained using a quantitative food-frequency questionnaire. Data were analyzed separately by age (45-67, 68-74) and by tumor aggressiveness. The most significant associations were seen for older males and aggressive tumors. Dietary fat was the strongest risk factor for these males, with an odds ratio (OR) of 2.9 (95 percent confidence interval [CI] 1.0-8.4) for total fat; OR = 2.2 (CI = 0.7-6.6) for saturated fat; OR = 3.6 (CI = 1.3-9.7) for monounsaturated fat; and OR = 2.7 (CI = 1.1-6.8) for polyunsaturated fat. Protein and carbohydrates had positive but nonsignificant associations. Energy intake had an OR of 2.5 (CI = 1.0-6.5). In these older men, no effects were seen for dietary cholesterol, body mass, or physical activity. There was little association between prostate cancer and dietary intake of zinc, cadmium, selenium, vitamin C, and beta-carotene. Total vitamin A had a slight positive association with all prostate cancer (OR = 1.6, CI = 0.9-2.4), but not with aggressive tumors. No associations were found in younger males, with the exception of physical activity which showed active males to be at an increased but nonsignificant risk for aggressive tumors (OR = 2.0, CI = 0.8-5.2) and beta-carotene which showed a nonsignificant protective effect (OR = 0.6, CI = 0.3-1.6). The findings suggest that dietary intake, especially fats, may increase risk of aggressive prostate tumors in older males.

Foods, nutrients and prostate cancer: a case–control study in Uruguay

“…These chemicals have proved to be associated with cancers at other sites (De Stefani et al, 1997) and further studies on prostate cancer and heterocyclic amine intake are needed. Total fat intake was associated with risk in our study as in previous studies (West et al, 1991;Giovannucci et al, 1993;Whittemore et al, 1995).…”

“…The risk associated with fat intake was more evident among obese patients, and also after controlling for dietary fibre and vitamin E intakes (results not shown). As in previous studies (West et al, 1991;Rohan et al, 1995;Whittemore et al, 1995;Meyer et al, 1997), total energy intake was a risk factor for prostate cancer.…”

Hypertriglyceridemia as a possible risk factor for prostate cancer

“…[13][14][15] Whereas increased intraprostatic cholesterol levels have been associated with malignancy, 29 cholesterol increases in tumor tissue likely occur by complex mechanisms that are inadequately mirrored by serum cholesterol. Furthermore, we found no association between BMI and the development of PC.…”

“…11 The Norwegian study found a positive association between a-linolenic acid and PC risk and an inverse association between the ratio of linoleic (from non-animal fat) to a-linolenic acid and PC. 12 Cholesterol has also been examined in dietary studies, and a positive association with PC was reported in two case-control studies that did not adjust for energy intake, 13,14 whereas no such correlation was found in a Swedish study that did adjust for energy intake. 15 Overall, there is a high degree of consistency with regard to consumption of animal fat, particularly red meat, and PC.…”

Exercise therapy across the prostate cancer continuum

“…More than half the studies in this area show an inverse relationship between physical activity and PC, [15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30] other studies show no association [31][32][33][34][35][36][37][38][39][40][41][42] and four studies even found exercise increased PC risk. [43][44][45][46] Perhaps this uncertainty in the literature can be attributed to the epidemiological nature of the research designs utilized in these studies, which relied upon survey or patient self-reporting to elicit physical activity and/or exercise exposure. In addition, many of these studies made no distinctions about the type of physical activity that respondents were performing and few validated physical activity exposure with objective measurements of fitness (that is, cardiorespiratory fitness testing).…”