Calcium and Fructose Intake in Relation to Risk of Prostate Cancer (original) (raw)

Laboratory and clinical data indicate an antitumor effect of 1,25(OH)2 vitamin I) 11.25i()1h ,l)i on prostate cancer. High calcium intake sup presses formation of l,2>iOlli.l) from 25(OH)D, thereby decreasing the 1.25(0111.1) level. Ingestion of fructose reduces plasma phosphate tran siently, and hypophosphatemia stimulates 1,25(OH)2D production. We thus conducted a prospective study among 47,781 men of the Health Professionals Follow-Up Study free of cancer in 19X6 to examine whether calcium and fructose intake influenced risk of prostate cancer. Between 1986 and 1994,1369 non-stage Al and 423 advanced (extraprostatic) cases of prostate cancer were diagnosed. Higher consumption of calcium was related to advanced prostate cancer |multivariate relative risk (RR), 2.97; 95% confidence interval (CD, 1.61-5.50 for intakes s=2000 rng/day versus <500 mg/day; P, trend, 0.002] and metastatic prostate cancer (RR, 4.57; CI, 1.88-11.1; P, trend, <0.001). Calcium from food sources and from supplements independently increased risk. High fructose intake was re lated to a lower risk of advanced prostate cancer (multivariate RR, 0.51; CI, 0.33-0.80, for intakes >70 versus S40 g/day; P, trend, 0.007). Fruit intake was inversely associated with risk of advanced prostate cancer (RR, 0.63; 95% CI, 0.43-0.93; for >5 versus SI serving per day), and this association was accounted for by fructose intake. Non-fruit sources of fructose similarly predicted lower risk of advanced prostate cancer. A moderate positive association between energy-adjusted fat intake and advanced prostate cancer was attenuated and no longer statistically sig nificant when controlled for calcium and fructose. Our findings provide indirect evidence for a protective influence of high 1,25(OH)2D levels on prostate cancer and support increased fruit consumption and avoidance of high calcium intake to reduce the risk of advanced prostate cancer.