Calcium Hormones

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Calcium Hormones

Post by nick »

After calcium is absorbed, calcitonine (or thyrocalcitonine) inhibits deportation of calcium from the bones, while the calcium automatically keeps pouring in. Calcitonine also stimulates excretion of calcium through the urine.

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.


This increased action of calcitonine is because of increased calcium levels. What exactly is the purpose of calcitonine? Obviously not to directly handle increased calcium levels, that is only an indirect reponse by the body. But since the blood-calcium is elevated, this action/hormone is our bodies first reponse?

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.

Why does it cause the secretion of 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 (23), and inhibits excretion of calcium, generally increasing a low blood-calcium level. Logically, elevated PTH level accelerates ageing of the bones

Does calcitonine induced release of PTH take place to deport the calcium from the bones due to 'too much' calcium being stored in our bones (not in accordance with our genetic plan)? However, PTH inhibits the excretion of calcium so that the blood calcium level increase. Is this due to the fact that PTH isn't the right hormone for controlling calcium levels properly? I can see where the fire brigade metaphor is starting to come into full picture.

Calcitriol however also inhibits secretion of PTH. And because PTH much stronger than calcitriol stimulates 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).

Since calcitriol increase the blood calcium leve this would then mean that calcitonine would be secreted to deal with this increase?

What happens when someone ingests 600 mg of calcium from a supplement? What are the series of events biochemically that take place in order to deal with the excess calcium?

Maybe by giving an example I'll be able to see how it works...

Thanks
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Post by nick »

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. The osteoblasts also compose the matrix upon which the calcium can precipitate.

So does excessive calcium flowing into the bone increase the number of osteoblasts in order to compose the new matrix for the cacium to precipitate?

Do the osteoblasts increase the free phospate level or is that because of the calcium coming in?

Why does the calcium-phosphate ratio need to be restored?

Structurally, estrogen does not stimulate osteoblasts, (9) but even inhibits osteoblast activity (10) (and number (11)) and therefore inhibits calcium influx in the bones (12) and also inhibits deportation of calcium from the bones.

It inhibits the deportation becuase there is no extra calcium held in the bones. That makes sense.
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Post by RRM »

I have run out of time now, but I will reply soon... :arrow:
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Re: Calcium Hormones

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This increased action of calcitonine is because of increased calcium levels. What exactly is the purpose of calcitonine?
To co-regulate (in cooperation with the other calcium hormones) the blood-calcium level, so that it is never too high (lethal) or too low.
Obviously not to directly handle increased calcium levels, that is only an indirect reponse by the body.
Most fluctuations in hormone levels are 'indirect' / in response to an 'event'; which is the essence of regulation.
But since the blood-calcium is elevated, this action/hormone is our bodies first reponse?
Yes, in response to the increase in serum calcium.
Why does it cause the secretion of PTH and calcitriol?
Because its a cooperation; the gradual / cyclic processing of ingested calcium; there are different stages in this 'production line', each involving different ratios of hormone levels.
Does calcitonine induced release of PTH take place to deport the calcium from the bones due to 'too much' calcium being stored in our bones (not in accordance with our genetic plan)?
No, calcitonine and PTH release fit in the processing of calcium, regardless of whether its too much calcium, or not.
Is this due to the fact that PTH isn't the right hormone for controlling calcium levels properly?
It is the right hormone; they all are the right hormones (not one of them is 'bad'); they are there to enable the processing of calcium. Its just that they shouldnt be over-active, just as with blood sugar levels and insulin.

... this would then mean that calcitonine would be secreted to deal with this increase?
Yes, calcitonine is essential in regulating the influx of calcium.
What happens when someone ingests 600 mg of calcium from a supplement? What are the series of events biochemically that take place in order to deal with the excess calcium?
The same, but more extreme.
Maybe by giving an example I'll be able to see how it works...
Just think of the blood sugar level; too steep increases lead to over-activity of insulin, which may exhaust the pancreas eventually (diabetes).
With osteoporosis the production of the calcium hormones seems not to be an issue. Here the temporary storage unit (our bones) is the weakest link...
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Post by RRM »

nick wrote:
So does excessive calcium flowing into the bone increase the number of osteoblasts in order to compose the new matrix for the cacium to precipitate?
Yes, and also the accelerates the speed of growth and death of these osteoblasts, eventually prematurely exhausting their production.
Do the osteoblasts increase the free phospate level or is that because of the calcium coming in?
No, yes.
Why does the calcium-phosphate ratio need to be restored?
All nutrients need to be in balance, because they all influence each other / other processes. elevated free phosphate levels will increase combining of phosphate with other minerals/metals.
It inhibits the deportation becuase there is no extra calcium held in the bones. That makes sense.
Exactly!
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Post by nick »

Thanks RRM! I beleive I have a solid understanding of your osteoporosis theory. I am taking a graphics design class where we have to make an information/explanation graphic and I want to illustrate your theory. I want to focus on the fundamentals of it so that it is simple to understand but still scientifical in nature.

I like the idea of using the "excessive sun increases aging" as a metaphor for the osteoporosis. Something that people can see the similarities and understand it.

So...

the sun would be the calcium and too much is harmful, but too little is unhealthy as well (no vit. D activation from too little sun, too little calcium causing weak bones)

The osteoblasts would be the skin cells. Having a finite replication, which is accelerated by too much sun/calcium.

The calcium hormones would like be sebum? They are activated when too much calcium is taken in. I'm not sure what the bodies response is when you get too much sun. I think I read somewhere (waitalk) that your skin increases its sebum production.


I'm trying to thing of some of the other ideas...

I think I will have something on the international statistics about the more calcium consumed the more hip fractures (adjusted for age).

I need to finish some other work, so I will report back later with more ideas. Any ideas that you have would be great too.
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Post by RRM »

nick wrote:

I like the idea of using the "excessive sun increases aging" as a metaphor for the osteoporosis. Something that people can see the similarities and understand it.
Thats a great idea!
the sun would be the calcium and too much is harmful, but too little is unhealthy as well (no vit. D activation from too little sun, too little calcium causing weak bones)
Yes, but too little is impossible if you are outdoors a lot (regarding sun
) and eating natural foods (regarding calcium).
The osteoblasts would be the skin cells. Having a finite replication, which is accelerated by too much sun/calcium.


Yes.
The calcium hormones would like be sebum? They are activated when too much calcium is taken in. I'm not sure what the bodies response is when you get too much sun. I think I read somewhere (waitalk) that your skin increases its sebum production.
Maybe estrogen is the sebum, because estrogen protects the bones against excessive calcium turnover, in as much as extra sebum is protective when your skin cells dry out due to excessive sunlight exposure (yes, then your skin increases sebum production).

Especially showing that osteoporosis incidence is greatest in those countries where bones are thickest is quite evident and confronting.
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Post by nick »

Also, in primary hyperparathyroidism, on the brink of osteoporosis, BMD levels may be significantly higher than normal.

This is a good proof that BMD isn't the truest indicator of bone health. Interesting...

So osteoblasts are stimulated by the influx of calcium (into the bone)?
Estrogen has an inhibitory influence.

So calcium is the main action agent in the 'bone cycle' much like too much sugar is in the sugar-leve/insulin system?
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Post by RRM »

nick wrote:
So osteoblasts are stimulated by the influx of calcium (into the bone)?
Yes, to prevent too much increasing serum-calcium levels; that extra calcium is temporarily stored in the bones.
Estrogen has an inhibitory influence.
Yes, estrogen 'tries to mediate', not only with the importance of not too high serum calcium levels 'in mind', but also with bone health in mind.
So calcium is the main action agent in the 'bone cycle' much like too much sugar is in the sugar-leve/insulin system?
Yes.
That is why in high-calcium consuming countries average bone density is greatest. And its also why you can increase bone mass in healthy subjects by taking calcium supplements.
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Post by nick »

And since only these osteoblasts can compose bone-matrix, too little new bone-matrix can be composed. But without the matrix, the calcium cannot precipitate, and new bone cannot be composed, while old bone is constantly being decomposed anyway, to be replaced by new bone. Since there is a lack of pre-calcified bone matrix upon which to build, replacement cannot occur, and porous holes will begin to appear.
So the osteoclasts don't slow down the decomposition/resorption rate regardless of the decreased action of osteoblasts? If the bone is absorbing less calcium, due to decreased osteoblast activity, then why do the osteoclasts keep on decomposing the bone matrix? Is that our genetic plan?
Only about 200 mg is absorbed into the blood, on the average, whether we consume 300 mg or 700 mg calcium daily, or sometimes even when we consume up to 1200 mg supplementary calcium daily. (
Is this in total of ones daily calcium intake? If you take a 600mg calcium supplement, the body is capable of decreasing the absorption rate, but in some this isn't always true(since were all different)?


The informational graohic is coming along nicely. I have 3-5 concepts that i want to emphasize and I hope to get a sketch of the design and text so that you can see it and make some suggestions.

Thanks a million RRM!
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Post by RRM »

nick wrote:
So the osteoclasts don't slow down the decomposition/resorption rate regardless of the decreased action of osteoblasts?
There is a connection between their activities, but old damaged bone cells need to be broken down any way, since they have no value anymore. So, osteoclasts will do their normal job (cleaning up the mess), even when osteoblasts cannot compose sufficient new cells.

You may compare it with our muscles; damaged muscle cells will be broken down, and you will loose muscle mass if insufficient new muscle cells are created. Its not because of a genetic plan, but the fate of old cells.


Is this in total of ones daily calcium intake?
Yes; out of the 300 or 900 mg consumed, only about 200 mg is absorbed into the blood.
If you take a 600mg calcium supplement, the body is capable of decreasing the absorption rate, but in some this isn't always true(since were all different)?
True. Actually its isnt "some", but "most", since average bone mineral density in high-calcium intake countries is significantly higher.

The informational graohic is coming along nicely. I have 3-5 concepts that i want to emphasize and I hope to get a sketch of the design and text so that you can see it and make some suggestions.
Wow, that sounds interesting. :o
Thanks a million RRM!
No, thank YOU!
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Post by nick »

In elderly, bone formation capacity has decreased, which has strong effects on bone metabolism response to dietary calcium. In elderly the ARORC (age related osteoblast replicative capacity) has diminished), and therefore less calcium can precipitate on pre-calcified matrix. High calcium intake therefore results in high serum calcium, which inhibits bone resorption, and subsequently bone formation, because of the coupling phenomenon.
What exactly is the coupling phenomenon?
Increased calcium intake is accompanied with increased bone formation rates, correlates with increased BMD, and bone formation and resorption is more or less coupled in healthy young rats (11) and mice (12).
So formation and resorption are coupled, does that mean that they are somehow balanced in terms of the amount of calcium coming in then going out?

Also, you say how our bones will resorb redundant calcium. How soon after mineralizing this calcium does this resorption take place?

Lets say I take in about 1,200 mg of calcium a day and my bones don't need that extra calcium so it goes into my bones to be stored, how soon does my body 'recognize' the fact that my bones don't need this redundant calcium. Is the storage of 'extra' calcium a temporary thing?

I have been reading some books on osteoporosis and I get the understanding that osteoclasts are always breaking down bone in order to maintain it? Since osteoclasts are needed to break bone down to enable osteoblasts to build new bone at a specific site, osteoclasts are always breaking down bone for maintenance reasons. Osteoclasts break down old bone in order for it to be replaced by new bone. Is there a osteoclast replicative capacity?

Thanks! This project is challenging but so damn fun too.
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Post by RRM »


What exactly is the coupling phenomenon?
The coupling between osteoblast and osteoclast activity (bone formation and resorption). This coupling excists as it is required to maintain healthy bone mineral density. However, when osteoblast replicative capacity is exhausted, the bones no longer can compensate for elevated blood-calcium levels (which is a safety procedure), so that, instead, bone resorption must be decreased to prevent even more calcium from entering the blood. Due to the coupling phenomenon this will also decrease bone formation. (The body still 'responds', but in a 'limp mode')
So formation and resorption are coupled, does that mean that they are somehow balanced in terms of the amount of calcium coming in then going out?
Somewhat. Only somewhat because in healthy subjects they are also separately affected.
Also, you say how our bones will resorb redundant calcium. How soon after mineralizing this calcium does this resorption take place?
that totally depends on the decrease in the blood-calcium level; only if there is a decrease, bone will be resorbed and calcium released.
Is the storage of 'extra' calcium a temporary thing?
Yes, and you can only keep the extra bone mass by maintaining a high calcium intake.
Is there a osteoclast replicative capacity?
Yes, but research has shown that osteoclasts are less vulnerable to aging phenomena. ('breaking down' must be 'easier' than 'the building up')
This project is challenging but so damn fun too.
Wow, you are the first responding this way...
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Post by nick »

The coupling between osteoblast and osteoclast activity (bone formation and resorption). This coupling excists as it is required to maintain healthy bone mineral density. However, when osteoblast replicative capacity is exhausted, the bones no longer can compensate for elevated blood-calcium levels (which is a safety procedure), so that, instead, bone resorption must be decreased to prevent even more calcium from entering the blood. Due to the coupling phenomenon this will also decrease bone formation. (The body still 'responds', but in a 'limp mode')
Is the calcitonine level increased, because it stimulates excretion of calcium through the urine? I take it your body also decreases the absorption rate as well?

And related to osteoblast, osteoclasts are still tearing down bone at a faster rate than formation anyways. So it can't be 'protective' against osteoporosis?
Somewhat. Only somewhat because in healthy subjects they are also separately affected.
Because the osteoblast capacity can keep up with the osteoclasts.
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Post by nick »


What exactly is the coupling phenomenon?
The coupling between osteoblast and osteoclast activity (bone formation and resorption). This coupling excists as it is required to maintain healthy bone mineral density. However, when osteoblast replicative capacity is exhausted, the bones no longer can compensate for elevated blood-calcium levels (which is a safety procedure), so that, instead, bone resorption must be decreased to prevent even more calcium from entering the blood. Due to the coupling phenomenon this will also decrease bone formation. (The body still 'responds', but in a 'limp mode')
So formation and resorption are coupled, does that mean that they are somehow balanced in terms of the amount of calcium coming in then going out?
Somewhat. Only somewhat because in healthy subjects they are also separately affected.
Also, you say how our bones will resorb redundant calcium. How soon after mineralizing this calcium does this resorption take place?
that totally depends on the decrease in the blood-calcium level; only if there is a decrease, bone will be resorbed and calcium released.

But with a high calcium intake, that doesn't happen, so the BMD is increased. I would think that the osteoclast activity would decrease, but for new bone to be deposited osteoclasts must break down old bone for the new bone to be deposited?
Is the storage of 'extra' calcium a temporary thing?
Yes, and you can only keep the extra bone mass by maintaining a high calcium intake.

I thought from your osteoporosis page, that redundant calcium is resorbed because there are 'too many bricks in the house' and your body would get rid of it after some period of time. But with a high calcium intake, will that calcium just stay in there longer? Is there a point in time where old bone (calcium) has reached its usefullness? How do the osteoclasts know when to tear down bone?

Is there a maximum calcium holding rate (highest BMD attainable), where your body can't keep up with excessive calcium? Thus decreasing absorption rates at all costs?

Also, I understand that young people with a low BMD still have perfectly healthy bones. Why don't they get fractures though? Their BMD is lower, perhaps weaker than a higher BMD, but you say that that isn't a concern regarding fractures?

This project is challenging but so damn fun too.
Wow, you are the first responding this way...

Your osteoporosis theory is just so technical and detailed and so interesting to see how it all fits together. I hope to make this graphic so that people can get the core concepts of understanding the details of the picture. Its like taking your technical paper and turning it into an informative t.v. show for people's eyes. :D
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