Bone Mineral Density

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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.

So why would the body absorb so little calcium?

Maybe because we only need very little calcium?

Scientists do not think so. They think we need more calcium (and iron etc.) because our absorption rate is low (which is because our food contains so much, remember). And because the scientists said so, we consume more, but guess what?

The absorption rate lowers even further (which is because we consume more) and they think we, therefore, have to increase mineral consumption even more to compensate for this lower absorption rate. And thus the absorption rate further decreases etc. etc. until we consume so much that the body is unable to sufficiently decrease its absorption rate, and too much is absorbed.

It never crossed our mind that there is a reason for why the body lowers its absorption rate.

And we think we are so intelligent.

Bones in Space

When extra calcium is absorbed, that calcium is temporarily stored in the bones and deported from the bones as soon as there is the opportunity to do so.

When little calcium is consumed, dietary calcium absorption rate is greater and there is less calcium to deport.

Bone cells are destroyed due to exercise, which stimulates the bones to hold on to more calcium to be better able to cope with future burdening.

The bones will deport more calcium if there is no loading of the bones since there seems to be no need to hold on to it.

Bone-mineral density (BMD) in astronauts decreased 1% to 2% each month, on the average, but the lower weight-bearing bones appeared more sensitive than the upper ones.  However, BMD of the skull, a non-weight bearing bone, does not decrease at all.

In the MIR 97- mission high calcium intake and vitamin D supplementation led to decreased bone formation and increased bone-calcium deportation.  Bone-calcium absorption is reduced during immobilization, but is increased when the body is physically active.

There 'apparently' was less need for minerals in the bones because the bones experienced no burdening in space and thus BMD decreased.

No matter how much calcium was consumed, the bones did not hold it because "there was no need to do so". Apparently not just the deportation of calcium was increased, but even calcium absorption and bone-formation were also decreased to prevent the need for subsequent calcium deportation.

The bones appear to be sensitive to this stimuli according to the need for adaptation given earthly circumstances, which is different for the legs, the arms, the head, etc.

So the bones "are not stupid". They hold the calcium they need and they deport what is not needed.

All the redundant calcium that is consumed is always deported too. The more calcium that is processed, the sooner the cells that do the processing will be worn out, eventually causing osteoporosis.

Vitamin A & Osteoporosis

They don't know how, but scientists have found out that too much Vitamin A can cause osteoporosis.

They speculate that too much vitamin A inhibits bone formation and enhances bone resorption. However, no markers of increased skeletal turnover can be detected accompanying excess Vitamin A.

Could it be that Vitamin A increases death of osteoblasts, thus accelerating the aging of osteoblast bone building activity?

It appears that vitamin A regulates apoptosis in many different cell lines.

In fact, retinoic acid also induces cell death of osteoblasts specifically..........

Also, analysis shows that, in deer antlers, significant amounts of Vitamin A (retinol) are found in tissues at all stages of differentiation.

The fact that excessive vitamin A has both differentiating and deteriorial effects on osteoblasts, and that it promotes osteoporosis, supports the theory that osteoporosis is caused by accelerating the aging of osteoblasts.

Corticosteroids & Osteoporosis - Corticosteroids kill osteoblasts

Killing osteoblasts accelerates the renewal of osteoblasts, and thus accelerates the aging of the capacity of osteoblasts to generate new bone matrix.

Cortisol is a corticosteroid produced and secreted in the body. It is a so-called 'stress hormone'.

Crohn's Disease comes with elevated cortisol levels, as this is a response to the continuous inflammatory processes in people with Crohn's Disease.

Crohn's Disease is associated with greatly increased vertebral fracture rates, even in young people.

This is not due to increased breakdown of bone tissue (urine calcium excretion is lower!), but due to suppressed bone formation.

This supports the theory that osteoporosis is caused by repeatedly inducing osteoblast cell death by any means, including a lifetime high calcium intake.

Bone Mineral Density & Osteoporosis

Bone mineral density (BMD) is mg mineral per cm2 bone.

In the old hypothesis, a high BMD is protective against osteoporosis, and therefore must be increased as much as possible.

But a low BMD due to a lifetime excessive calcium turnover is fundamentally different from a low BMD due to low calcium intake.

  • BMD is highest and about similar in those countries where the most milk is consumed and osteoporosis incidence is highest, like the USA, Australia, Switzerland, the UK and Northern Europe  Italians also drink very much milk, have a high BMD, and Italian osteoporosis incidence is very high too.

  • BMD in Polish children is lower than in US children, and so is milk consumption (22% less) and Polish osteoporosis incidence.

  • Both BMD and hip fracture risk are lower in Chinese. they even have a higher BMD decrease rate in some part of their bones.  In some part of their bones they reach peak BMD 5-10 years later than their counterparts, and the BMD decrease rate is lower.

Their lower BMD is not due to genetic differences; Chinese who immigrated to Denmark more than 12 years ago have a similar BMD to that of the Danish.

  • Hip-BMD in Taiwanese is 10 to 15% lower than in Caucasians, and hip fracture incidence is, like in mainland Chinese, far lower.  

  • Japanese osteoporosis incidence is also lower and so is their BMD.  Their BMD decrease rate is higher in some part of the bones.

This is also not due to genetic differences; America-born Japanese women have BMD values equivalent to those of whites.

  • Because fracture rates among African-American women are lower than among Caucasian women, it was thought that African Americans must, therefore, have higher BMD by nature, which is not the case.

  • In Gambia, BMD, calcium intake and osteoporosis incidence are very low. Again, this is not "genetic" since there are no significant differences in BMD and bone turnover in Gambian and Caucasian children living in the UK.

  • In Kuwait also much milk is consumed, and therefore their BMD is close to that of people in West-European countries and so is osteoporosis incidence in Kuwait.

The belief of scientists that a high BMD is protective against osteoporosis is based on a lower BMD in osteoporosis patients and in women in general.

But BMD in osteoporosis patients is lower due to excessive erosion. BMD is lower in women due to a monthly increase in bone turnover, which is caused by monthly fluctuations in estrogen level. (see "Calcium Hormones")

BMD by itself does not predict osteoporosis risk.

A natural low BMD due to a low calcium intake is protective against osteoporosis, for calcium turnover has been structurally low.

A low BMD caused by excessive calcium turnover is dangerous and accelerates osteoporosis.

Many studies have shown that calcium intake and physical activity can increase BMD, especially excessive high calcium intake (over 1200 mg) and intensive physical training.

But also many studies have shown non-significant effects of calcium intake (or normal physical activity) on BMD because the body desperately tries to limit the intake of excessive calcium.

Calcium Intake And Fracture Rate

That osteoporosis/hip fracture rates are lowest in those countries where the least calcium is consumed has bothered official institutes for quite some time.

They found a simple remedy: one shall not compare one country with another.

It has been argued in the past that certain osteoporosis fractures (e.g. hip) occur with greater frequency in countries with high calcium intakes than in countries with low intakes, and that, therefore, calcium cannot be important for bone health, at least at intakes above the levels found in the countries with the low calcium intakes, such as China

This argument was considered and rejected at several expert levels.

Briefly, it is now recognized that hip fracture is a function not just of bone density but of the way people fall, of patterns of loading the hip (e.g. squatting), and of such structural features as hip axis length, many of which vary across cultures.

For example, hip fracture risk doubles with each standard deviation increase in hip axis length, keeping bone mass constant. Adult Orientals today have shorter hip axes than adult Caucasians and thus, for the same bone mass, a lower hip fracture risk. This is just one of several reasons why cross-cultural comparisons, such as those cited above, may lead to erroneous conclusions.

So, if you lengthen the hip axis without increasing bone mass you've got a more fragile structure with its structural material spread over more area, when, to increase length, for the same sturdiness, mass needs to increase more than in proportion to hip axis. Going in the other direction, for the same bone mass on a smaller hip girdle, you get a more sturdy structure.

Instead, it is necessary to examine the relationships between the purported independent variable and the outcome variable within an ethnic, national grouping. When this is done with the Chinese, for example, the same relationship between calcium intake and bone mass or fracture emerges as has been shown in Caucasians.

It had been extensively documented a growing epidemic of hip fracture among Hong Kong Chinese, with the age specific fracture rate more than doubling between the mid 60's and the mid 80's.  The only correlates found to be associated with increased risk of fractures were decreased physical activity and low calcium intake.

Similarly, forearm bone mass in five rural Chinese countries varies directly with habitual calcium intake, just as has been shown in Europe and North America in Caucasian populations.

Finally, it must be stressed that other dietary influences (discussed elsewhere in this chapter) greatly influences the calcium requirement, and seeming ethno-culture differences in requirement cannot be evaluated without adjusting for these confounding effects.

Thus, populations with low protein, sodium, and acid ash intakes will be predicted to have a lower calcium requirement than populations with higher intakes of these dietary components.

Suppose for a second that Caucasians need 2000 mg calcium and Chinese need 500 mg daily. Then Caucasians, on the average, should consume at least four times more calcium than Chinese 'to match Chinese hip-fracture incidence'.

But in the US and Northern Europe 31 to 46 fold more milk is consumed, and hip-fracture incidence is over six fold higher than in China.

Phosphorus and Osteoporosis

Some say that osteoporosis is due to excessive dietary phosphorus, increasing deportation of calcium from the bones.

Scientific research shows that in all countries where much milk is consumed, more people have osteoporosis.

It also shows that in those countries where milk consumption has increased, osteoporosis incidence has also. But milk certainly does not contain too much phosphorus.

If this theory were correct, milk would be protective, compared to all other foods (except most fruits and vegetables).

This is obviously not the case; see Excessive Calcium Causes Osteoporosis 

Fluoride and Osteoporosis

Some claim that osteoporosis is due to high fluoride levels in drinking water.

Yes, like calcium, fluoride increases osteoblast cell proliferation.

Fluoride also causes an increase in bone mineral density (BMD).

So, basically, fluoride also has an accelerating effect on the aging process of osteoblasts. But how strong is this effect?

Cortisol, calcitriol and PTH also have such an accelerating effect. So, how strong is the influence of fluoride in our drinking water on the aging of our bones?

Very importantly, Japan only started to fluoride its water in 2000, but the hip fracture incidence in Japan was very much higher than that in other Asian countries, way before 2000. (Due to the higher milk consumption in Japan).

So, yes, extra fluoride accelerates the aging of osteoblasts, but the effect of fluoridated drinking water is low, certainly when compared to the influence of dietary/supplementary calcium.

Protein / Soy Consumption & Osteoporosis

Protein consumption has anabolic effects on cell growth in general. Protein also increases bone-formation.

Extra calcium, on the average, also increases bone-formation, so might the effects of extra protein be similar to those of extra calcium?

Like calcium intake, protein intake also positively correlates with both bone-mineral density and hip-fracture incidence; the higher the average calcium / protein consumption, the more calcium the bones will hold, on the average, but also the higher the hip-fracture incidence.

And solely because consuming more protein (in combination with high calcium) may lead to a higher bone mass, a high protein (and high calcium) diet is advised to prevent osteoporosis, simply ignoring the accelerating effect on the aging process.

No matter what the diet, the bones always contain less calcium at the age of 70 than at the age of 30. And since the bones obviously "refuse" to structurally hold on to redundant calcium, an increased bone-formation rate leads to increased bone-turnover too. More importantly, an increased bone-formation rate leads to exhaustion of osteoblast reproductivity.

Some people argue that protein even has direct catabolic effects on bone, due to increased endogenous acid production, and they point to increased urine calcium levels after animal protein consumption.  Another study however showed that there were not any correlations between extremely high protein intake (1.26 g / kg bodyweight) and calcium excretion rate.

Since osteoporosis only occurs as a lifetime effect, and since the bones try not to hold on to redundant calcium, the direct effects of protein on bone-metabolism most likely does not affect per saldo bone mineral density (BMD). That is why no correlation between BMD and protein intake was found.

So, in the same way that an increased calcium intake does not necessarily increase BMD (since the body tries to sufficiently decrease its calcium absorption rate), a higher dietary protein intake does not necessarily have any effect on calcium / bone-metabolism.

Statistically, calcium consumption strongly correlates with hip-fracture incidence.  How strong is the correlation between protein intake and hip-fracture incidence?  Less strong.  Obviously, calcium intake increases osteoblast and calcium turnover more strongly than protein does.

For example:

Protein consumption in Greece is highest, but incidence of hip fractures in Greece is not very high, and far lower than in Italy, Switzerland, Sweden,  etc.

Another example:

Swiss protein consumption is even lower than Japanese protein consumption, but osteoporosis incidence in Switzerland is far higher.

Another example:

Kuwait protein consumption is quite low, but osteoporosis incidence is comparable to osteoporosis incidence in Italy and France.

Can consuming soy-protein instead of animal protein be protective?

Animal protein consumption is believed to increase endogenous acid level due to relatively high sulphur amino acid contents (methionine and cystine). this is speculated to increase bone-resorption.

Soy protein, indeed, contains less sulphur amino acids (and the soy-protein-quality is therefore lower) and might therefore decrease bone resorption.

Some studies showed that in comparison with animal protein, soy protein decreases calcium excretion.  Other studies showed no differences in bone-turnover / calcium excretion.

Moreover, the disease osteoporosis is not due to an increased bone-resorption which decreases bone-mineral density. A low BMD is not equal to osteoporosis.

If that would be the case, osteoporosis could be easily cured by increasing BMD. But in osteoporosis the osteoblast reproductivity is irreversibly decreased with an inability to repair microfractures.

So, soy-protein can only be protective if consumption of soy-protein does not increase bone-formation (and thus not accelerate aging of osteoblasts).

Unfortunately, soy-protein (like other protein) does increase bone-formation.  More importantly, soy contains high levels of phyto-estrogens;

Lifetime adequate estrogen levels are known to be protective against osteoporosis; osteoporosis risk in women is far higher than in men because estrogen levels are decreased in women every four weeks and are permanently decreased after menopause.

These phyto-estrogens, however, are 'weak' estrogens and can replace common (powerful) estrogens.  Consuming soymilk for only three months can already decrease estradiol level 27%. Consuming phyto-estrogens can, therefore, even cause infertility.

If this decrease in estrogen level would be compensated for by an increase in phyto-estrogens that act the same as estrogens, this would be without consequence, but:

  • Estrogen inhibits activity of osteoblasts and thus inhibits uptake of calcium into the bones, slowing down the ageing process. Genisteine, however, (the main soy-phyto-estrogen) increases activity of osteoblasts and thus increases uptake of calcium into the bones, accelerating the aging process. This partly due to a genisteine-induced increased intestinal calcium absorption.

  • Estrogen, furthermore, also decreases deportation of calcium from the bones but phyto-estrogens certainly do not inhibit bone-resorption more than natural estrogens do.  In fact, where administration of estrogen decreased bone-turnover in rats, a soybean diet did not.

Soy consumption may hasten osteoporosis. The degenerative effects of calcium are, however, far greater, since osteoporosis incidence is lower in Asia than in Europe and the US.

Bio-availability of Calcium in Milk

Some say that osteoporosis is due to poor bio-availability of calcium in cow's milk, causing a lack of calcium.

All children that grow up drinking cows' milk are perfectly able to grow strong bones.

There is no doubt that one can increase the BMD by consuming cow's milk. Adults have, on the average, a higher BMD in countries where consumption of cow's milk is high.

Even if bio-availability of human milk is 100% and bio-availability of cow's milk would be 25%, still sufficient calcium would be absorbed from cows' milk.

This theory is too silly to be further discussed here.

The Magnesium-Calcium Ratio Hypothesis

In order to absorb calcium, the body needs comparable amounts of another mineral element, magnesium.

Milk and dairy products contain only small amounts of magnesium. Without the presence of magnesium, the body only absorbs 25 percent of the available dairy calcium content. The remainder of the calcium spells trouble.

Without magnesium, excess calcium is utilized by the body in injurious ways. The body uses calcium to build the mortar on arterial walls which becomes atherosclerotic plaques.

Excess calcium is converted by the kidneys into painful stones which grow in size like pearls in oysters, blocking our urinary tracts.

Excess calcium contributes to arthritis; painful calcium buildup often is manifested as gout. The  Recommended Daily Allowance (RDA) for calcium is 1500 mg. The RDA for magnesium is 750 mg.

Society stresses the importance of calcium, but rarely magnesium.  Yet, magnesium is vital to enzymatic activity.

In addition to insuring proper absorption of calcium, magnesium is critical to proper neural and muscular function and to maintaining proper pH balance in the body.  Magnesium, along with vitamin B6 (pyridoxine), helps to dissolve calcium phosphate stones which often accumulate from excesses of dairy intake.

Good sources of magnesium include beans, green leafy vegetables like kale and collards, whole grains and orange juice.

Non-dairy sources of calcium include green leafy vegetables, almonds, asparagus, broccoli, cabbage, oats, beans, parsley, sesame seeds and tofu.

Considering the above, some would say that milk causes osteoporosis because it is high in calcium and low in magnesium.

Mother's milk appears to perfectly enable the infant to grow strong bones, just as cows' milk does for the calves.

Mother's milk certainly does not enhance osteoporosis in suckling. On the contrary, mother's milk enables infants to grow stronger bones very rapidly.

A study even showed an association between a high magnesium intake and hip fracture risk.

Some say that magnesium and calcium are two competing minerals that naturally occur in a 1:2 balance. The more calcium is consumed the more magnesium is required (to deport calcium from cells).

This, of course, is utter nonsense; there is no natural magnesium-calcium balance. This ratio is different per food.

And again, mother's milk contains the least magnesium relative to calcium, and no sane person can claim that mother's milk causes osteoporosis or that pork is preventive and vegetables and oranges cause osteoporosis.

Osteoporosis is NOT a problem that should be associated with lack of calcium intake.  Osteoporosis results from calcium loss.

The massive amounts of protein in milk result in a 50 percent loss of calcium in the urine.  In other words, by doubling your protein intake there will be a loss of 1-1.5 percent in skeletal mass per year in postmenopausal women.

The calcium contained in leafy green vegetables is more easily absorbed than the calcium in milk, and plant proteins do not result in calcium loss the same way as do animal proteins. If a postmenopausal woman loses 1-1.5 percent bone mass per year, what will be the effect after 20 years?

When osteoporosis occurs levels of calcium (being excreted from the bones) in the blood are high. Milk only adds to these high levels of calcium which is excreted or used by the body to add to damaging atherosclerosis, gout, kidney stones, etc.

High-fat Diet & Osteoporosis

Some claim that osteoporosis is due to a high-fat diet.  One study shows that BMD is lower in rats fed a high-fat diet.

Their explanation:

  • "In vitro studies indicate that lipid products of oxidation promote osteoblastic differentiation of vascular cells and inhibit such differentiation in bone cells".

  • Osteoblasts are the cells that induce calcium absorption precipitation in the bones.

  • But the decrease in BMD can very well be due to a decrease in physical activity. (The bones rapidly lose calcium in space due to inactivity of the bones).

  • A high-fat diet decreases physical activity due to a lower availability of glucose relative to available fatty acids. The presence of glucose is essential to transform fatty acids into glucose (for muscle activity). If it is not sufficiently available, wastes like aceto acetic acid and beta-hydroxy buteric acid originate, which inhibit further transformation of fat into glucose. Thus, a high-fat diet inhibits physical activity. A high-sugar diet increases physical activity.

More importantly:

  • Osteoporosis incidence does not correlate with average fat consumption per country. For example:

  • Osteoporosis incidence within Europe is highest in Sweden (and Finland), significant higher than in countries like France, Italy and Greece, but fat-consumption is much lower in Sweden and Finland.

  • Also, a decreased BMD is very different from osteoporosis. They did not mention spongy holes, just a decrease in BMD, which is fundamentally different. In particular, elderly Asians can have extremely low BMD and razer-thin but very healthy and strong bones.

Prehistoric Calcium Consumption

Some claim that pre-historic man consumed more calcium than we do.

To check this, we have to compare calcium contents of foods that are consumed today, with foods in the pre-historic diet.

Before the introduction of agriculture, about 10,000 years ago, no grains and dairy products were consumed, nor beans, which need to be cooked for consumption.

So the question is:

Does a diet of only animal food and fruits and nuts contain more calcium than a diet that also includes beans, grains and dairy products?

Grains and beans, on the average, contain at least as much calcium as a diet of raw-edible plant foods and animal food, and dairy products contain even more calcium;

Vitamin D - intakes & Hip Fracture Rates

Eggs and fish are the vitamin D containing foods.

The interesting thing is, that only in countries where both much milk and fish is consumed (Iceland, Norway, Spain, Finland), or milk and eggs (The Netherlands), the hip fracture rates are very high, and not in countries where only high amounts of fish or eggs are consumed.

The differences in egg consumption are of less importance, because both the total amounts are lower AND the difference between high and low level intakes are lesser.

Athletes & Stress-fractures

The problem for athletes is that "the calcium hormones" serve two purposes:

  1. regulating blood-calcium level

  2. maintaining bone health

In athletes loading is increased and thus more micro-fractures have to be repaired and more damaged cells (due to the increased loading) have to be replaced by new ones. The damaged cells are decomposed and the calcium is deported by osteoclasts. New cells must replace damaged cells to maintain bone health.

Thus osteoblasts have to compose more pre-calcified bone-matrix. This requires increased activity of osteoblasts, and thus osteoblast apoptosis is also increased in athletes. (Exercise induces osteoblast apoptosis.

But the hormones that regulate bone formation and resorption to maintain bone-health also regulate blood-calcium level. If considerable calcium is consumed, more calcium has to be temporarily stored in the bones prior to excretion to prevent elevation of blood-calcium level (excessive calcium in the blood blocks respiration because it blocks muscle functioning)

This extra calcium can only be temporarily stored in the bones if it can precipitate on pre-calcified bone matrix which osteoblasts composed for this purpose. This calcium will subsequently be deported to be excreted because it is redundant calcium that is being temporarily absorbed for the sole purpose of preventing elevation of the blood-calcium level. Redundant calcium is deported according to the body's designed plan for the bones.

The loading on bones is so intense in athletes that maximum capacity of osteoblasts to compose new bone matrix is met.

A small percentage of the total bone cells are damaged every training session. If remaining undamaged cells must compose new matrix to absorb redundant calcium, their osteoblasts will not be able to keep up with composing new matrix the next day when the cells are damaged due to loading.

So the repairing of micro fractures will not be complete because regulating the blood-calcium level has top-priority.

You can compare it to an athlete that has to train every day but also has to do hard labour to make a living; such an athlete will never be able to increase muscle strength because he lacks time to recover.

If the bones (osteoblasts) of an athlete must recover and also must process redundant calcium to prevent excessive calcium in the blood, the osteoblasts' productivity will be insufficient to do both.

In athletes, especially, it is essential to prevent any unnecessary processing of calcium. This means that the athletes should not absorb any more calcium than they need to maintain bone-health.

It is also essential that athletes never consume large amounts of calcium in one meal (or supplement!); the more calcium consumption is spread through the day, the less redundant calcium will need to be temporarily absorbed in the bones.

Female athletes

Estrogens levels are decreased in female, because intense physical exercise makes the body produce less estrogens.

Unfortunately, estrogens maintains bone health by inhibiting both uptake of calcium into the bones and deportation of calcium (also indirectly through inhibiting PTH secretion)

Thus the lower the estrogens level, the more devastating the effect of excessive calcium intake will be. Logically, exercise can never "compensate" for the side effects of reduced estrogens levels.

If estrogens levels are low, more calcium will be actually absorbed into the bones, increasing osteoblast activity and apoptosis.

The necessity of adequate estrogens levels is less strong if less calcium is consumed.

What Can I Do for My Osteoporosis?

Treating osteoporosis means stopping the bone loss and rebuilding bone to prevent breaks. Diet and exercise can help make your bones stronger. But they may not be enough if you have lost a lot of bone density. There are also several medicines to think about. Some will slow your bone loss, and others can help rebuild bone. Talk with your doctor to see if one of these might work for you:

  • Alendronate or risedronate.

    • These medicines are bisphosphonates, drugs that slow the breakdown of bone and increase bone density. They can make it less likely that you will break a bone, most of all in your spine, hip, or wrist.

    • Side effects may include nausea, heartburn, and stomach pain. A few people have muscle, bone, or joint pain while using these medicines.

    • These drugs must be taken in a certain way :

      • when you first get up, before you have eaten, and with a full glass of water.

      • You should not lie down, eat, or drink for at least one-half hour after taking the drug.

    • Even if you follow the directions closely, these drugs can cause serious digestive problems, so be aware of any side effects.

  • Raloxifene.

    • This drug is used to prevent and treat osteoporosis. It is a SERM (selective estrogen receptor modulator).

    • It prevents bone loss and spine fractures but may cause hot flashes or increase the risk of blood clots in some women.

  • Estrogen.

    • Doctors sometimes prescribe this female hormone around the time of menopause to treat symptoms like hot flashes or vaginal dryness.

    • Estrogen also slows bone loss and increases bone mass in your spine and hip, so women can use it to prevent or treat osteoporosis.

    • But, estrogen use is thought to be risky for some women.

  • Calcitonin.

    • This hormone increases bone mass in your spine and can lessen the pain of fractures already there.

    • It comes in two form - a shot or nasal spray. The shot may cause an allergic reaction and has some side effects like nausea, diarrhea, or redness in your face, ears, hands, or feet.

    • The only side effect of the nasal spray is a runny nose in some people.

    • Calcitonin is most useful for women who are 5 years past menopause.

  • Parathyroid hormone (PTH).

    • Also called teri-paratide, this shot is given daily for up to two years to postmenopausal women and men who are at high risk for broken bones.

    • It improves bone density in the spine and hip.

    • Common side effects include nausea, dizziness, and leg cramps.

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 

Bone Testing
Smarter Than Nature
Bone Mineral Density
Osteoporosis In Woman

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