The calcium-hormones function like a fire brigade; when structurally little calcium is consumed, they aren't activated that much, which is good ; no fire.
When too much calcium is consumed, the calcium-hormones are very active, stimulating absorption of calcium into the bones, and subsequently deportation and excretion. And the more this processed is enhanced, the more the bones erode.
After calcium is absorbed, calcitonine (or thyrocalcitonine) inhibits deportation of calcium from the bones, whilst the calcium automatically keeps pouring in. Calcitonine also stimulates excretion of calcium through urinating.
So, calcitonine primarily lowers blood-calcium level, and absorption of calcium into the bones is one way to reach that goal. Absorbing calcium into the bones certainly is not the purpose of calcitonine, for it stimulates excretion of calcium too.
Due to the action of calcitonine, the increased blood-calcium level decreases, inhibiting calcitonine release and stimulating secretion of two other calcium-hormones; PTH and calcitriol.
Parathyroid hormone (PTH) stimulates uptake of calcium into the bones (1) (and therefore osteoblast apoptosis (2)) and deportation of calcium from the bones, and inhibits excretion of calcium, generally increasing a low blood-calcium level. Logically, elevated PTH level accelerates ageing of the bones; see hyperparathyroidism
Low levels of PTH prevent bone loss. (3)
PTH also stimulates secretion of calcitriol;
Calcitriol (1,25 dihydroxycholecalciferol = composed of vit. D); The direct influence of calcitriol is increasing the uptake of dietary calcium into the blood, but also the uptake of calcium into the bones (4) (Calcitriol therefore also increases osteoblasts apoptosis (5)) and deportation of calcium from the bones.
Calcitriol however also inhibits secretion of PTH. And since the stimulating effect of PTH on the uptake of calcium into the bones and the subsequent deportation, supplementary calcitriol can, per saldo, in fact strongly decrease uptake of calcium into the bones and subsequent deportation. (6) Since calcitriol also increases intestinal calcium absorption, this however also strongly increases blood-calcium level (7).
Too much calcium in the blood can precipitate in the arteries, joints and ligaments and kills muscle cells (since muscle cells can only contract by deporting calcium outside the muscle-cells, which is harder if the blood contains more calcium). Too much calcitriol / vitamin D can cause arteriosclerosis, bone-deformation (8), muscle cramps and fibromyalgia.
Estrogens are multi-functional hormones, and one of their functions involves the bones.
The calcium-hormones mentioned above, induce circulation of calcium; from the blood into the bones and vice versa, ‘pumping’ the calcium around. Estrogens are the brakes on this system, to minimize erosion.
Calcium is absorbed into the bones due to osteoblasts, which increase free phosphate level in the bones, which causes the ‘passive’ influx of calcium, to restore the calcium-phosphate ratio.
Deportation of calcium from the bones by osteoclasts is an active process.
Structurally, estrogen does not stimulate osteoblasts (9) , but even inhibits osteoblast activity (10) and therefore inhibits calcium influx in the bones (11) and also inhibits deportation of calcium from the bones. Thus estrogen protects the bones against excessive bone turnover, and osteoblasts against apoptosis.
Estrogen prevents death of osteoblasts in particular because osteoblasts are more sensitive to ageing phenomena than osteoclasts. (12)
In general, this protective effect of estrogen is accredited to the decrease in deportation of calcium from the bones, and is the inhibitory effect of estrogen on calcium influx ignored.
But a characteristic action of estrogens on the skeleton is inhibition of longitudinal bone growth. (13)
Some claim that estrogen increases calcium influx in the bones, but this is only the case in the first 6 days of administration. (9)
The reason why osteoporosis risk in women is higher than in men, regardless of menopause and milk consumption, is due to monthly estrogen and PTH fluctuations;
Estrogen levels in women strongly fluctuate monthly.
As estrogen level is at its lowest (around menstruation), PTH level is at its highest, increasing deportation of calcium from the bones. (14) (and uptake of calcium into the bones)
Thus lifetime bone turnover averagely is higher in women.
Vitamin K seems to be protective for inhibiting death of osteoblasts. (15) But how exactly this happens, remains unclear; vitamin K may inhibit fractional calcium absorption and therefore prevent osteoblast apoptosis. Or vitamin K may reduce ‘unnecessary’ apoptosis of osteoblasts even without excessive calcium turnover. Vitamin K can however also increase osteoblast apoptosis. (16)
Vitamin K does not affect intestinal calcium absorption (17), but the intake of dietary vitamin K2 has a preventive effect on bone resorption caused by ovariectomie or a lack of vitamin K, and in postmenopausal women. (18)
The hormones mentioned above influence bone-metabolism through different mediators, like growth factors.
One such a growth factor is Insulin-Like Growth Factor-1 (IGF-1). That an increased uptake of calcium increases osteoblast apoptosis, is also shown by IGF-1 influence; IGF-1 is a potent growth factor for osteoblasts (and also increases bone resorption) and induces osteoblast apoptosis. (19)
Other such growth factors are Fibroblast Growth Factors (FGF). FGF play a critical role in bone growth, and overexpression of FGF2 increases osteoblast apoptosis. (20)
Abstracts of most sources can be found at The National Library of Medicine
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