ecstatichamster
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An interesting study
https://www.researchgate.net/profil...ate_cancer/links/02e7e526eb8b0d1f50000000.pdf
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 suppresses formation of l,2>iOlli.l) from 25(OH)D, thereby decreasing the 1.25(0111.1) 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 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 related 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 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.
https://www.researchgate.net/profil...ate_cancer/links/02e7e526eb8b0d1f50000000.pdf
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 suppresses formation of l,2>iOlli.l) from 25(OH)D, thereby decreasing the 1.25(0111.1) 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 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 related 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 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.