Calcium and Fructose Intake in Relation to Risk of Prostate Cancer

Abstract

Laboratory and clinical data indicate an antitumor effect of 1,25(OH)₂ vitamin D (1,25(OH)₂D) on prostate cancer. High calcium intake suppresses formation of 1,25(OH)₂D from 25(OH)D, thereby decreasing the 1,25(OH)₂D level. Ingestion of fructose reduces plasma phosphate transiently, 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 1986 to examine whether calcium and fructose intake influenced risk of prostate cancer. Between 1986 and 1994, 1369 non-stage A1 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 (CI), 1.61–5.50 for intakes ≥2000 mg/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 related to a lower risk of advanced prostate cancer (multivariate RR, 0.51; CI, 0.33–0.80, for intakes >70 versus ≤40 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 ≤1 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 significant 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.