Smarter Than Nature
Excessive Calcium Causes Osteoporosis
The older you get, the higher your risk of osteoporosis.
Obviously, osteoporosis is about aging.
Osteoporosis patients originally had very strong bones, like everybody else.
Osteoporosis is not about the inability to build strong bones, but about premature degeneration of the bones.
But is there no other way to find proof?
Yes there is. Compared to other foods, only dairy products (or supplements of course) can be consumed in such large quantities on a daily basis that their consumption strongly increases calcium intake, which is proven by the fact that average BMD is highest in those countries where the most milk is consumed. There is, in fact, a tradition of consuming high amounts of milk in these countries...
And there also many scientific studies about hip-fracture incidence per country.
If extra calcium eventually has adverse effects, osteoporosis/hip-fracture incidence should be clearly higher in those countries where the most milk is consumed
In Greece the average milk consumption doubled from 1961 to 1977 (and was even higher in 1985), and during the period 1977 - 1985 the age adjusted osteoporosis incidence almost doubled too.
In Hong Kong in 1989 twice, as much dairy products were consumed as in 1966 and osteoporosis incidence tripled in the same period. Now their milk consumption level is almost "European", and so is osteoporosis incidence.
It is very simple: where the most milk is consumed, the osteoporosis incidence is highest. Compared to other countries, the most milk is consumed in Sweden, Finland, Switzerland and The Netherlands (300 to 400 kg / cap / year), and osteoporosis incidence in these countries has sky rocketed.
Like Australians and New Zealanders, Americans consume three fold more milk than the Japanese, and hip-fracture incidence in Americans is therefore 2½ fold higher. Among those within America that consume less milk, such as the Mexican-Americans and Black Americans, osteoporosis incidence is two-fold lower than in white Americans, which is not due to genetic differences.
In Venezuela and Chile, much less milk is consumed than in the US, Finland, Sweden and Switzerland, while the hip fracture incidence in Venezuela and Chile is over three fold lower.
Chinese consume very little milk (8 kg / year), and hip-fracture incidence, therefore, is among the lowest in the world; hip-fracture incidence in Chinese women is six fold lower than in the US. (The average American consumes 254 kg milk / year)
The less milk consumed, the lower is the osteoporosis rate.
In other countries where very little milk is consumed, on the average, as in Congo, Guinea and Togo (6 kg / year) osteoporosis is extremely rare too.
In the Dem. Rep. Congo, Liberia, Ghana, Laos and Cambodia even less milk is consumed (average person: 1 to 3 kg a year!!), and they have never even heard of age-related hip fracture.
Of course, 'they' will say : "that's because blacks and Asians are genetically different from whites", but that is rubbish ;
''Nature has made a mistake but fortunately we are smarter than nature, and know how to correct this; Mother's milk, by mistake, contains far too little calcium, which has to be corrected through giving to human's cow's milk which contains 4 times as much calcium.''
If calcium requirements really were four fold higher, pre-historic infants would never have been able to grow up, and ultimately, to have children. If we really need cows' milk, man could never have existed.
Because we have already been on this planet for millions of years. And we have only consumed milk for a maximum of 0.01 million years. This means that we did not drink a single drop of milk from other animals in more than 99% of human existence; in our entire development from ape to modern human being, we never drank, nor needed animals' milk.
1.6 million years ago there were already humans well over six feet tall, with apparently strong bones.
Some argue that our prehistoric diet contained more calcium, but that is not true
Human breast milk is Mother Nature's PERFECT FORMULA for baby humans. In her wisdom, Mother Nature included 33 milligrams of calcium in every 100 grams, or 3 1/2-ounce portion of human breast milk.
Of all humans, babies need the most calcium because their bones are still weak and need to be calcified much more. And mothers' milk does, of course, contain all the calcium (and other nutrients) babies need in their first two years. Babies fed on mother's milk are perfectly able to increase bone-mineral density (BMD).
What does this mean?
Adults and infants always need less calcium than babies (per kg bodyweight). Food for adults therefore does not need to contain as much calcium (in %) as mother's milk.
And because our natural foods, on the average, contain about as much calcium as mother's milk, it is absolutely impossible that these natural foods contain too little calcium.
If they did, mother's milk would contain too little calcium too, and babies would not be able to increase BMD on mother's milk.
And because many foods contain more calcium than mother's milk, the average calcium absorption rate is low, to prevent the uptake of excessive calcium. Vitamin D
The body needs broad daylight to transform cholesterol into vitamin D. The hormone that increases dietary calcium absorption (calcitriol) is composed of vitamin D.
Some say osteoporosis incidence is, therefore, higher in countries with little sunlight.
However, if you consume some fish and/or egg yolk once in a while, you will absorb all the vitamin D you need - even living in Greenland, Canada or Northern Europe.
Is osteoporosis incidence really lower in countries with more sunlight?
Not necessarily. Though Italy is much sunnier than Poland, hip-fracture incidence in Italy is much higher than in Poland (and Spain), simply because in Italy 25% more dairy products are consumed. Kuwait is extremely sunny, but, nevertheless, osteoporosis incidence in Kuwait is about as high as in Great Britain and France, because in Kuwait, also, lots of milk is consumed.
Furthermore, the effects of this vitamin D-hormone can be very different.
This hormone increases calcium absorption from food and absorption of calcium into the bones, and therefore induces death of osteoblasts. Calcitriol also stimulates deportation of calcium from the bones into the blood. (See The Calcium-hormones")
On the other hand, this hormone also inhibits secretion of PTH (excessive PTH strongly accelerates ageing of the bones). (See hyperparathyroidism) Thus, indirectly, this hormone can be protective, per saldo decreasing both uptake of calcium into the bones and deportation of calcium from the bones. (See "The Calcium-hormones")
However, since supplementary vitamin D/calcitriol increases the blood-calcium level, this extra calcium can precipitate in arteries and on the outside of the bones, causing arteriosclerosis and bone-deformities. It can also settle in joints and ligaments, and can cause muscle-cramps because the blood-calcium level needs to be low enough to deport calcium from muscle cells. It can even kill muscles cells (if the calcium cannot be deported), eventually causing fibromyalgia.
Osteoporosis is often accompanied with a very low vitamin D level.
This can have multiple causes:
In general, it is not a problem at all to have little vitamin D/calcitriol at our disposal. This even protects us against absorbing too much calcium.
Your body uses vitamin D to absorb calcium. Most people's bodies are able to make enough vitamin D if they are out in the sun for a total of 20 minutes every day. You can also get vitamin D from eggs, fatty fish, and cereal and milk fortified with vitamin D.
In 52% of examined Saudi Arabian females for example, vitamin D level was extremely low (because of clothes that block almost all sunlight), but their bones were not affected.
In alcoholics, the levels of the vitamin D-hormones were decreased by3 to 48%, but BMD was not affected.
In general, we do not need much vitamin D either to inhibit PTH secretion or to increase calcium absorption.
In fact, in countries where the people consume high amounts of fish and eggs (which are the only vitamin D containing foods), the hip fracture rates are high too; because when both the intake of calcium (due to consuming dairy products) and vitamin D is high, the vitamin D causes a high uptake ratio of the calcium - accelerating the aging of osteoblasts.
Your bones and muscles will be stronger if you are physically active. Weight-bearing exercises, done three to four times a week, are best for preventing osteoporosis.
Walking, jogging, playing tennis, and dancing are examples of weight-bearing exercises. Try some strengthening and balance exercises, too. They may help you avoid falls which could cause a broken bone.
If osteoporosis were about a lack of exercise, all healthy but physical inactive people would have osteoporosis, which is not the case. That is why bone-loss with age cannot be explained by declining physical activity levels.
Loading determines the maintenance of bone-strength. If the bones are not loaded at all (like in space), they rapidly lose calcium. If we are normally active, our bones contain sufficient calcium to cope with incidental falls.
Furthermore, a lack of exercise does not accelerate the aging of osteoblasts, so it cannot possibly be the cause osteoporosis. If one lacks exercise, one can easily increase BMD through exercise. In osteoporosis, the lack of osteoblast activity is irreversible.
Exercise causes micro fractures which stimulates the osteoblasts to increase their activity. Logically, then exercise also increases the death rate of osteoblasts. (excessive exercise is detrimental.)
But exercise can increase bone-strength in elderly, can't it?
Yes, but only as long as osteoblast reproductivity is not almost totally exhausted. Exercise increases activity and reproduction of the remaining osteoblasts, temporarily increasing bone-strength (exercise does not guarantee future bone-strength, but also accelerating aging of the bones.
If osteoblast reproductivity is almost totally exhausted, one cannot increase BMD through exercise (or extra calcium) anymore, which is often the case in osteoporosis patients. That is why the possible exercise-induced bone mass gain is far less than the disuse-induced bone loss. This is why in osteoporosis exercise only partially (20 - 40%) decreases hip-fracture risk - even in the short term. The later in life, the smaller the effects of exercise will be.
Normal activities are all the exercise you need to maintain bone health. Increased physical activity accelerates aging of the bones. On the other hand, exercising specific muscles can be effective since strong muscles can absorb the shock when falling.
Overweight & Osteoporosis
That menopause favours osteoporosis and obesity inhibits it, are well-known clinical observations.
In menopause, the estrogens level is lower, and adequate natural estrogens levels are protective because estrogens inhibits uptake of calcium in the bones and bone-formation by osteoblasts.
In obesity the leptin level is elevated and leptin also inhibits bone-formation by the osteoblasts.
Some think that obesity is protective because there is more loading on the bones, increasing their strength, but if that would be the case, osteoporosis could easily be stopped and even reversed by increasing physical activity/loading of the bones. Osteoporosis however is irreversible. Osteoporosis is not caused by a decreased bone mass, but is due to the exhaustion of osteoblasts, which is irreversible since it is about aging. The low bone mass is the result of the lack of new matrix, not the cause.
The calcium-hormones function like a fire brigade; when little calcium is being 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. The more this processed is accelerated, the more the bones erode.
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.
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 (and therefore osteoblast apoptosis 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.
PTH also stimulates secretion of calcitriol;
Calcitriol; The direct influence of calcitriol is increasing the uptake of dietary calcium into the blood, but also the uptake of calcium into the bones (Calcitriol therefore also stimulates osteoblast activity and thus increases osteoblasts apoptosis and deportation of calcium from the bones.
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. Since calcitriol also increases intestinal calcium absorption, this however also strongly increases blood-calcium level.
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, 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. (Extra calcium is the gas-pedal)
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.
Deportation of calcium from the bones by osteoclasts is a more direct process.
Structurally, estrogens do not stimulate osteoblasts, but even inhibits osteoblast activity (and number) and therefore inhibits calcium influx in the bones and also inhibits deportation of calcium from the bones. Thus estrogens protect the bones against excessive bone turnover and osteoblasts against apoptosis.
Estrogens prevent death of osteoblasts, in particular, because osteoblasts are more sensitive to aging phenomena than osteoclasts.
In general, this protective effect of estrogens is accredited to the decrease in deportation of calcium from the bones; the inhibitory effect of estrogens on calcium influx is ignored.
But a characteristic action of estrogens on the skeleton is inhibition of longitudinal bone growth.
Some claim that estrogens increases calcium influx in the bones, but this is only the case in the first six days of administration.
The reason why osteoporosis risk in women is higher than in men, regardless of menopause and milk consumption, is due to monthly estrogens and PTH fluctuations;
Estrogens levels in women strongly fluctuate monthly.
As estrogens level is at its lowest around menstruation, PTH level is at its highest, increasing deportation of calcium from the bones and uptake of calcium into the bones.
Thus lifetime bone turnover is, on the average, higher in women.
Vitamin K seems to be protective by inhibiting the death of osteoblasts, 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.
Vitamin K does not affect intestinal calcium absorption, but the intake of dietary vitamin K has a preventive effect on bone resorption caused by ovariectomie or a lack of vitamin K, and in postmenopausal women.
These foods contain much vitamin K: Especially egg yolk, kiwi and avocado, but also strawberries, plum, hazelnut, mackerel, orange, grapes and peach.
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. It also increases bone resorption and induces osteoblast apoptosis.
Other such growth factors are Fibroblast Growth Factors (FGF). FGF play a critical role in bone growth, and over expression of FGF2 increases osteoblast apoptosis.
In hyperparathyroidism the parathyroid hormone (PTH) level is elevated, the number of osteoblasts is markedly increased, and the bones become porous.
In hyperparathyroidism BMD values can differ very much per bone, and some BMD values can even be elevated due to increased osteoblast activity.
So what exact influence has PTH on the bones?
PTH stimulates uptake of calcium into the bones, osteoblast apoptosis and deportation of calcium from the bones.
This is exactly the opposite of the influence of estrogen, and since estrogen is protective, excessive PTH logically accelerates osteoporosis.
Estrogen and PTH do not just have opposite effects on bone; estrogen also prevents the PTH level from increasing too much. When estrogen level is at its lowest (around menstruation and after menopause), PTH level is at its highest.
That is why hyperparathyroidism is common in postmenopausal women and estrogen administration is an effective therapy.
If a lack of estrogen caused the hyperparathyroidism, parathyroidectomy does not result in complete bone-reparation, of course.
Besides estrogen, calcitriol also inhibits PTH secretion. Though calcitriol has similar, but less strong effects on bones, supplementary calcitriol can per saldo strongly decrease uptake of calcium into the bones and deportation from the bones, which is protective.
What is the biological purpose of PTH?
Primarily to co-regulate blood-calcium level, and secondarily to co-regulate the bone-calcium contents. These must be regulated because too much or too little calcium in the blood can be lethal, and too little or too much calcium in the bones is unwelcome too.
Our bones are constructed according to a genetic plan. Excessive calcium has eventually to be deported since holding more calcium than is the optimum amount is not beneficial. (bone-deformations)
Thus hormones that stimulate deportation of calcium from the bones are required.
PTH collaborates with calcitriol to deport calcium from the bones. PTH stimulates secretion of calcitriol, which hormone (like PTH) both increases uptake of calcium into the bones and subsequent deportation of calcium from the bones.
The difference between these two hormones is that the effects of PTH on bone are stronger. More importantly, calcitriol (which is composed of vit. D) also increases absorption of calcium from food while PTH increases the excretion of calcium into urine.
Calcitriol inhibits secretion of PTH and PTH increases secretion of calcitriol. (see "Calcium Hormones")
But the calcitriol level is low in hyperparathyroidism.
Why is the calcitriol level low in hyperparathyroidism?
The PTH level can be elevated for various reasons besides a lack of calcitriol. (due to a thyroid malfunction, a tumour or a lack of estrogen for example). The calcitriol level has to be decreased even if PTH is not elevated due to a lack of calcitriol. Otherwise the combined influence of PTH and calcitriol would cause far too much calcium deportation from the bones.
Even if in hyperparathyroidism the calcitriol level is normal, the continued uptake of dietary calcium would add up to the accelerated fractional calcium absorption and subsequent deportation, further hastening osteoporosis.
Absorption of Minerals
Minerals are elements. Animals cannot compose minerals. The only way to obtain the right amount of minerals is by adapting the absorption rate.
All animals need less minerals than their natural foods contain since the absorption rate can never be over 100%. After all, their evolution has been based on those foods.
They normally have to absorb little of the available minerals. And when the available food contains a lower level of minerals, they simply increase their mineral absorption rate.
The same goes for humans. If our food contains a high level of iron, our bodies' absorption rate is decreased. If our food contains little iron, the absorption rate is increased.
Because excessive of anything is harmful.
Excessive minerals, like iron, zinc, cobalt, manganese, copper etc. are pro-oxidative, damaging nutrients, arteries, messenger-substances, cell-DNA and enzymes.
They increase heart attack risk and can cause diabetes, colon cancer, Parkinson's disease and infertility.
In addition, too much of one mineral decreases the levels of other minerals/ race elements.
Scientific analyses showed that healthy subjects were very capable of controlling iron absorption to prevent development of iron overload, even if the diet was fortified with iron and even if meat (containing much iron) intake was high.
Not everyone, though, is be able to sufficiently decrease his/her absorption rate.
So why would the body absorb so little calcium?
Maybe because we only need very little calcium? <..... more>
The above opinionated views and information serves to educated and informed consumer . The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. .It should not replaced professional advise and consultation. A licensed physician should be consulted for diagnosis and treatment of any and all medical conditions
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