New French study below.
There are "convincing" studies going back at least 20 years that associate excess calcium intake with aggressive PCa. "Convincing" in the sense that avoidance of high levels of calcium from dairy &/or supplements has become common PCa advice.
Perhaps less known is the mechanism by which excess calcium might increase risk.
25-D, the inactive form of vitamin D, is converted to the active form, as needed, by various tissues in the body, including those of the prostate. In that context, the active (hormonal) form, 1,25-D, is subject to autocrine control - the conversion of 25,D to 1,25-D by one enzyme, triggers the production of a second enzyme that will clear 1,25-D from the cell. There is thus a window of opportunity for the hormone to do its stuff.
PCa down-regulates the first enzyme & upregulates the second, so that cancer cells make less (or no) 1,25-D & clear it faster.
Fortunately, the kidneys create 1,25-D & put it into the circulation where PCa cells have access to it. The kidneys do this in response to a dip in serum calcium. They do not do this when calcium levels are elevated.
From the new paper: "the results of a preclinical study from our own group demonstrate that a diet high in calcium dose-dependently accelerated the progression of early-stage prostate tumours and that dietary vitamin D prevented this effect."
1,25-D has several roles in calcium homeostastis, with the basic sequence being (a) osteoclastic activity releases calcium from bone, (b) calcium uptake from the gut is increased, & (c) calcium is drawn from the blood as osteoblastic activity rebuilds bone.
The French study suggests that chronic elevation of blood calcium only happens with 25-D insufficiency coupled with high calcium intake.
{Not mentioned is the importance of vitamin K to calcium transport to bone.}
The term "dietary calcium" is a little vague. What is an unsafe level with poor 25-D status? What is the upper safe level with good 25-D status?
How much "dietary vitamin D" was required to negate risk?
I have often wondered why a high intake of calcium would lead to high blood levels? Blood calcium is otherwise highly regulated. Might more calcium be taken up when there is osteopenia or osteoporosis? Perhaps low 25-D levels can be sufficient to get calcium into the blood in those conditions, but not into bone?
-Patrick
ncbi.nlm.nih.gov/pubmed/297...
Nat Rev Urol. 2018 May 15. doi: 10.1038/s41585-018-0015-z. [Epub ahead of print]
Do dietary calcium and vitamin D matter in men with prostate cancer?
Capiod T1, Barry Delongchamps N1,2, Pigat N1, Souberbielle JC1,3, Goffin V4.
Author information
1
Inserm Unit 1151, Institut Necker-Enfants Malades (INEM), Université Paris Descartes, Paris, France.
2
Urology Department, Hôpital Cochin, Assistance Publique Hôpitaux de Paris, Paris, France.
3
Physiology Department, Hôpital Necker-Enfants Malades, Assistance Publique Hôpitaux de Paris, Paris, France.
4
Inserm Unit 1151, Institut Necker-Enfants Malades (INEM), Université Paris Descartes, Paris, France. vincent.goffin@inserm.fr.
Abstract
Active surveillance (AS) is an attractive alternative to immediate treatment for men with low-risk prostate cancer. Thus, the identification of environmental factors that promote the progression of indolent disease towards aggressive stages is critical to optimize clinical management. Epidemiological studies suggest that calcium-rich diets contribute to an increased risk of developing prostate cancer and that vitamin D reduces this risk. However, the potential effect of these nutrients on the progression of early-stage prostate tumours is uncertain, as studies in this setting are scarce and have not provided unambiguous conclusions. By contrast, the results of a preclinical study from our own group demonstrate that a diet high in calcium dose-dependently accelerated the progression of early-stage prostate tumours and that dietary vitamin D prevented this effect. The extent to which the conclusions of preclinical and epidemiological studies support a role for calcium and vitamin D and the relevance of monitoring and adjustment of calcium and/or vitamin D intake in patients on AS require further investigation.
PMID: 29765146 DOI: 10.1038/s41585-018-0015-z