Postmenopausal bone loss has long been recognized as a major problem.
It always amused me that women were told to take calcium when their bones were leaching calcium. When osteopenia or osteoporosis occurs following the menopause shouldn't one suspect a hormonal issue?
A 1988 paper [1] reported that:
"Long-term studies confirm that postmenopausal women who regularly use estrogen have greater bone mass and fewer osteoporotic fractures."
"Timely restoration of E2 levels can prevent estrogen-dependent bone loss and can reduce significantly the risk of fracture."
"High calcium intake without estrogen is not effective in preventing the accelerated loss of bone that occurs in the years immediately after menopause."
I suspect that many women don't want to hear that estradiol [E2] may be the solution, but a low-dose E2 patch is not going to reverse the menopause or promote cancer.
These days, doctors know that calcium may not be effective if the patient is deficient in vitamin D. & so calcium + vitamin D is now the mantra. Most have not yet learned about vitamin K - or any on the other essential nutrients for bone health.
Sometimes one sees a comment that men too can suffer bone loss - but at a much older age, as though it isn't really a serious problem.
The French MINOS study was a "Cross-sectional assessment of age-related bone loss in men". The first of many papers appeared in 2000. In 2001 [2] we discover that:
"Low 17betaE(2) {total estradiol} levels may be an important risk factor for osteoporosis in men."
In 1999, a Swedish study of idiopathic (unknown cause) osteoporosis in men, reported that "The patient group compared with the controls had significantly lower serum levels of estradiol ..." [3]
...
Natto is a good source of vitamin K2. In a 2012 Japanese study [4]:
"Habitual intake of natto was associated with a beneficial effect on bone health in elderly men, and this association is primarily due to vitamin K content of natto ..."
The pathogenesis of osteoporosis is multifactorial, but it isn't really that complicated.
It's amazing that people swallow a gram or two of calcium daily in the hope that osteopenia or worse can be prevented. When one takes a mega-dose of one mineral, it is usually to the detriment of another. The calcium:magnesium ratio is particularly important. From 1990 [5]:
"Prophylactic treatment of postmenopausal osteoporosis with oestrogen and calcium, often in combination, disregards the likelihood that an excess of each agent may increase magnesium requirements and decrease serum Mg levels."
"If the commonly recommended dietary Ca/Mg ratio of 2/1 is exceeded (and it can reach as much as 4/1 in countries with low to marginal Mg intakes), relative or absolute Mg deficiency may result, and this may increase the risk of intravascular coagulation, since blood clotting is enhanced by high Ca/Mg ratios."
We know from the PCa literature that calcium intake is associated with progression. This is likely due to inhibition of the conversion of calcidiol to calcitriol - starving PCa cells of hormonal active vitamin D.
Incidentally, in the recent vitamin D study that was the subject of a thread [6], there was a drop in parathyroid hormone [PTH] in the high-dose D group. It was suggested that D itself caused this. Unmentioned was that the intervention included calcium citrate to a maximum of 600 mg. 76% of participants received supplements.
Vitamin D (cholecalciferol) is converted to inactive calcidiol. Neither cholecalciferol nor calcidiol affect PTH. PTH is produced when serum calcium levels fall. PTH tells the kidneys to convert some calcidiol to calcitriol. Calcitriol causes a number of things to occur. Calcium is taken from bone, there is increased calcium uptake from the gut, & calcium is returned to bone. Supplemental calcium in the blood inhibits PTH.
-Patrick
[1] ncbi.nlm.nih.gov/pubmed/317...
[2] ncbi.nlm.nih.gov/pubmed/112...
[3] ncbi.nlm.nih.gov/pubmed/100...
[4] ncbi.nlm.nih.gov/pubmed/213...
[5] ncbi.nlm.nih.gov/pubmed/213...
