Excessive Calcium Causes Osteoporosis

Before their bones weakened, all osteoporosis patients had very strong bones, like everybody else. All people in whatever country on whatever diet, are perfectly able to build strong bones. Everybody disposes of sufficient calcium to do so.

Osteoporosis is not about the inability to build strong bones, but about premature degeneration. 

What makes the bones degenerate prematurely?

What enhances ageing of the bones?

All our organs age. In all our organs, cells constantly reproduce themselves; they wear out and are replaced by new ones. And because the number of times cells can multiply is fixed, organs eventually age. Like the skin eventually becomes wrinkled when there are less cells available to replace the dehydrated old skin-cells.

We all know that if we expose our skin to the sun too much, that we will look old sooner. Excessive sun-exposure enhances ageing of the skin. It does so because the sun burns the outer skin cells, which have to be replaced by new cells sooner. And the sooner cells have to be replaced, the sooner the moment will be there that these cells cannot multiply anymore.

Accelerated ageing of cells is about a higher turnover of cells; new cells replacing old cells faster.

What makes old bones cells to be replaced by new ones sooner?

We know that estrogen is protective. (and androgens to a lesser extend) All bone-scientists acknowledge that if the female body disposes of sufficient estrogen all the time, osteoporosis risk is far lower.

That is why osteoporosis risk is 3-fold higher in women: In women every 4 weeks estrogen level is far lower, and are the bones less protected. And in post-menopausal women, estrogen level is structurally decreased.

If we know how exactly estrogen is protective against premature ageing of the bones, we also know how the opposite process enhances osteoporosis.

So, how exactly is bone-metabolism influenced by estrogen? 

Estrogen both inhibits uptake of calcium into the bones (1) and deportation of calcium from the bones. (see Calcium Hormones) And because estrogen is protective, both absorbing and subsequently deporting less calcium is protective against osteoporosis. And therefore accelerated ageing of the bones is obviously about both absorbing and deporting too much calcium.

But how exactly can processing more calcium cause osteoporosis?

The absorption of calcium requires the activity of specialized cells; osteoblasts. These osteoblasts also compose pre-calcified bone-matrix, upon which the calcium can precipitate. Deportation of calcium from the bones requires the activity of osteoclasts.

If more calcium is absorbed into the bones, like due to a lack of estrogen (2), production and activity of both osteoblasts and osteoclasts is increased. (3) (Like in hyperparathyroidism) If much calcium is absorbed, much calcium is deported. But with all new matrix that is composed, 50 to 70% of the composing osteoblasts die. (4) The more their activity is stimulated, the more they die (5). And because estrogen inhibits uptake of calcium, estrogen prevents death of osteoblasts (6)

If you consume much calcium all your life, reproduction of osteoblasts maybe increased all your life; many people succeed in increasing bone-mineral density by consuming more calcium. (7) That is why average BMD in people in countries where much milk is consumed, is higher.

Since the number of times cells can reproduce is fixed, reproduction capacity will be exhausted sooner if always much calcium is absorbed. And if reproduction capacity is exhausted, there will be a lack of new osteoblasts. 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 there is no new bone. Because old bone is decomposed to be replaced by new bone, porous holes will originate if there is a lack of pre-calcified bone matrix.

And this is exactly what happens in osteoporosis: In osteoporotic bone, the osteoblasts cannot sufficiently reproduce anymore, and thus less osteoblasts are available. (8) And/or activity of osteoblasts is at least impaired. (9) Like ‘exaggeratedly aged’ bones. (10) And thus in osteoporotic bones there is less matrix available that can yet be calcified, than in healthy bones. (11) In osteoporosis, dead cells cannot be replaced and micro-fractures cannot be repaired. (12)

Does that mean that dietary calcium causes osteoporosis?

Only if too much calcium is actually absorbed into the bones. 

Like with all minerals, normally, the body just absorbs as much calcium from our food as it needs. Whether we consume 300 or 700 mg in total, or sometimes even when taking 1200 mg supplementary calcium daily; averagely only about 200 mg is absorbed into the blood. (13) To absorb the right amount of calcium, absorption rate decreases as we consume more calcium. 

But if we consume too much calcium, absorption rate cannot be sufficiently decreased; about 5% of dietary calcium on top of 1500 mg a day, is yet absorbed into the blood. For example: Consuming 5-fold more calcium than before, a group of girls did in fact absorb twice as much calcium (as before) into the blood. (14)

But why is this extra calcium absorbed in the bones?

Too prevent blood-calcium level from increasing too much. 

Muscles can only function if calcium from inside the muscle cells can be deported outside the cells. And if blood-calcium level is too high, this is not possible, which would be lethal, since breathing requires muscle-action. To save your life, excessive dietary calcium is temporarily stored into the bones, prior to excretion. Normally the blood contains a total of 500mg calcium. The difference between highest and lowest blood-calcium level is only 26%, thanks to the 3 different hormones that prevent our blood from containing too much (or too little) calcium. After the calcium has been absorbed into the bones, two of these hormones stimulate deportation of calcium from the bones, and the third one stimulates excretion of calcium into urine. 

But why don’t the bones hold on to that extra calcium?

According to the old doctrine, we can prevent osteoporosis by stacking more calcium in the bones. “The more calcium your bones contain, the longer it will take before they are empty.”

This would be a simple solution if the bones indeed hold on that extra calcium, but…

Like a house, our bones are built according to a plan. And the amount of calcium in the bones has to be according to that plan. Like piling up bricks in your living room does not make your house better or stronger, stacking extra calcium in the bones is not an improvement either. To be able to watch TV and clean your house properly, you throw the bricks out. 

The redundant calcium in your bones is always deported eventually. To keep much calcium in your bones, you have to keep on consuming lots of calcium daily. But no matter how much milk you drink, or supplementary calcium you take (or not at all), your bones always contain less calcium at the age of 70, than at the age of 30.

The problem is that all this extra calcium is processed by osteoblasts and osteoclasts. If you have been absorbing 400 mg instead of 200 mg dietary calcium into the blood daily, these cells had to process 2.9 million mg calcium more during these 40 years. 

And since all this extra calcium is absorbed due to the action of osteoblasts, these osteoblasts die sooner, which leaves you with too little new bone-matrix and porous holes once you are old. Like administration of corticosteroids can cause osteoporosis for killing osteoblasts (15) ; both prematurely exhaust reproduction capacity. If little calcium is consumed, the bone-cells age slower, like a low calcium intake through adolescence has been shown to both retard and prolong longitudinal bone growth in rats. (16)

So, yes you can increase your bone mineral density (BMD) by consuming much calcium, but that will exhaust your bones sooner. That is why in those countries where average BMD is highest, hip-fracture incidence is highest too.

Does this mean that a low BMD is preventive?

If BMD is low because you consume little calcium all your life; yes. If calcium intake is very low, there will still not be a lack of calcium for calcification of bone-matrix. (17) The only difference will be that the bones do not contain redundant calcium, and do not age prematurely. 

But as the result of exhausted osteoblasts; no. Because holes do not contain calcium, in osteoporosis BMD is decreased due to the lack of new bone-matrix. 

So, BMD can be low in very strong bones and in weakened bones, which is what makes it so confusing for so many scientists.


The problem of osteoporosis, is that it is a life-time process; it takes a lifetime to study a lifetime process.

Until now, studies about the lifetime effect of calcium on osteoporosis never covered more than a few years. And because increased calcium intake increases bone-mineral density, they concluded that calcium is protective. See Bone Mineral Density and Osteoporosis

But that is like concluding that the sun is protective against ageing of the skin because you ‘look better’ with a nice tan. While sun exposure actually enhances ageing of the skin. This may not seem so when you are young, but you will definitely notice so once you get older.

Furthermore, these studies also comprised less than 1500 subjects. (18) Or the data showed that those who absorbed less calcium in the bones, had a higher bone-fracture risk (19), while this decreased capacity to incorporate calcium in the bones was very likely due to exhaustion of osteoblasts.

In many other studies, no correlation was found between calcium consumption and hip-fracture risk in men or women (20), or was concluded that “high calcium intake did not protect against hip fracture”. (21)

A recent 12-year prospective study among 77,761 women revealed that consuming milk increases bone-fracture risk. (22) Two other studies 'unexpectedly' did the same. (23)

But is there no other way to find proof?

Yes there is. 

Nobody can explain, but until now, they have not published any studies about the lifetime effects of calcium supplementation in mice or rats. Maybe they did not like the results?

Luckily, there is another way; 

Compared to other foods, only dairy products can be consumed in such large quantities on a daily base, that this strongly increases calcium intake. And there are statistics about average milk (-products) consumption per country. Like there are statistics about hip-fracture incidence per country.

If extra calcium is protective, in those countries where people are used to drinking lots of milk all their life, hip-fracture / osteoporosis incidence must be lowest.



An increase in milk consumption in whatever country (24), came with an increase in osteoporosis- / bone fracture-incidence. (25) 'Their' excuse is that this is due to the increase in average age, but the increase in osteoporosis- / bone fracture incidence often is far greater. (25) In Hong Kong for example, in 1989 twice as much dairy products were consumed as in 1966 (24), and tripled osteoporosis incidence in the same period. (26) Now their milk consumption level is almost “European”, and so is osteoporosis incidence. (27)

It is verysimple ; where most milk is consumed, osteoporosis incidence is highest. Compared to other countries, in Sweden, Finland, Switzerland and The Netherlands most milk is consumed (300 to 400 kg / cap / year), and skyrockets osteoporosis incidence. (28)

Like Australians and New Zealanders (29), Americans consume 3 fold more milk than the Japanese, and hip-fracture incidence in Americans is therefore 2½ fold higher. (30) And in those within America that consume less milk, like the Mexican-Americans and Black Americans, osteoporosis is two-fold lower than in white Americans (31), which is not due to genetic differences. (32)

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 6 fold lower than in the US. (33) (Americans averagely consume 254 kg milk / year)

The less milk is consumed, the lower osteoporosis rates are. (34)

In other countries where averagely very little milk is consumed, like in Congo (35), Guinea (36) and  Togo (37) (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've never even heard of age-related hip fracture. 


milk consumption per country in 1998

And of course, 'they' will say : "that's because blacks and Asians are genetically different from whites", but that is rubbish ; Osteoporosis incidence in female Asians is much lower than in Asian females living in the USA. (38) Like osteoporosis incidence (and calcium consumption) in African Bantu women (39) is much lower than in Bantu women living in the USA. (40) Like both calcium intake and hip-fracture rate is far lower in South African Blacks than in African Americans. (41)

Response on these findings

Alternative hypothesises about osteoporosis incidence;

Osteoporosis and protein- and soy consumption

Some think it is because of low milk-calcium bio-availability

The magnesium-calcium ratio hypothesis

The excessive-phosphorus hypothesis

Osteoporosis and a high-fat diet

Smarter Than Nature

''Nature has made a mistake but fortunately we are smarter than nature, and know how to correct this ; By mistake mother's milk contains far too little calcium, what has to be corrected through giving cow's milk to humans, containing 4 times as much calcium.''

Of course this is nonsense.

If calcium requirements really were 4 fold higher, pre-historic infants would never have been able to grow up, and have kids ultimately. If we really need cows milk, man could never have existed.

Why ? 

Because we already are on this planet for millions of years. And we only consume milk since a maximum 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 milk.

1.6 million years ago, there already were way over 6 feet tall humans (42), with apparently strong bones.

Some argue that our prehistoric diet contained more calcium, but that is not true

Babies' Food

Of all humans, babies need most calcium, because their bones are still weak and need to be calcified much more. And all the calcium babies need, mother's milk does contain of course, providing babies with everything they need in their first two years. Babies fed on mother’s milk are perfectly able to increase bone-mineral density. (BMD)

So, exactly how much calcium does mothers' milk contain ? 

Not much;

Calcium in mg / 100 g

226      Hazelnuts

140      Egg yolk

132Brazil nuts

96      Olives, green

87      Walnuts

54      Figs

44      Black berries

42      Orange

40      Raspberries

38      Kiwi

33      Mandarin

32 Human milk

20      Coconut

18      Grapes

16      Apricot

16      Pineapple

14      Plum

13      Salmon
12      Mackerel

12      Mango

11      Watermelon

10      Avocado

9      Banana

6      Muskmelon

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 averagely contain about as much calcium as mother's milk, it is absolutely impossible that these natural foods contain too little calcium. 

If they would, 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, average calcium absorption rate is low, to prevent uptake of excessive calcium. 

Vitamin D

To transform cholesterol into vitamin D, the body needs broad daylight. And 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 every once and a while, you'll 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 (43) than in Poland (and Spain) (44), simply because in Italy 50% more dairy products are consumed. (24) Kuwait is extremely sunny, but nevertheless osteoporosis incidence in Kuwait is about as high as in Great Britain and France (38), because in Kuwait also lots of milk is consumed. (24)

Furthermore, the effects of this vitamin D-hormone can be very different;

Directly, this hormone increases calcium absorption from food and absorption of calcium into the bones (45), and therefore induces death of osteoblasts (46). Calcitriolalso 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, while 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. (47) (see the “Calcium-hormones”)

However, since supplementary vitamin D / calcitriol increases blood-calcium level (48), this extra calcium can precipitate in arteries and on the outside of the bones (causing arteriosclerosis and bone-deformities (49)), joints and ligaments, and can cause muscle-cramps (since blood-calcium level needs to be low enough to deport calcium from muscle cells) and even kill muscles cells (if the calcium structurally cannot be deported), eventually causing fibromyalgia.

Mostly, osteoporosis is not accompanied with a lack of vitamin D. On the other hand, it often does (50), but this can have multiple causes;

·Consuming too much calcium causes both erosion of the bones and can strongly decrease  calcitriol level because secretion and decomposition of hormones regulating blood-calcium level, is increased when much calcium is absorbed. The body has no problem composing more of those other calcium-hormones, but calcitriol is composed of vitamin D, which availability may be limited.

·Hyperparathyroidism strongly increases both uptake of calcium into the bones and deportation from the bones, eventually causing osteoporosis. If too little calcitriol is available, secretion of PTH is not sufficiently inhibited.

·If really very little calcium is consumed (less than 300 mg / day, which is a very hard thing to achieve), a lack of vitamin D / calcitriol can cause osteoporosis for making it impossible to increase calcium absorption.

In general, it is not a problem at all to dispose of little vitamin D / calcitriol, for protecting us against absorbing too much calcium. 

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. (51)

In alcoholics levels of the vitamin D-hormones were decreased with 23 to 48%, but BMD was not affected. (52)

In general we do not need much vitamin D to either inhibit PTH secretion or increasing calcium absorption.


In osteoporosis the bones contain spongous holes. And because these holes do not contain calcium, bone mineral density (BMD) in osteoporosis patients is low. And ‘scientists’ therefore concluded that those with a low BMD therefore have an increased osteoporosis risk.

And because exercise increases BMD, couldn’t osteoporosis be due to a lack of exercise?

They simply forgot that BMD is lowest in countries where osteoporosis incidence is lowest too. And that a lack of exercise decreases BMD, but does not cause spongous holes.

Osteoporosis is quite common in female athletes for example, because intense physical exercise makes the body produce less estrogen. (53)

The reason is that by increased burdening of the bones, bone-cells are destroyed, which stimulates the bones to increase strength, to be better able to cope with future loads. To make this possible, more calcium is absorbed into the bones (increasing death of osteoblasts (54)), and less is deported. But amenorrhea is a common problem in female athletes, while estrogen is required to decrease the deportation of calcium.

This is the reason why exercise can never ‘compensate’ the side effects of reduced estrogen levels (55) ; exercise increases deportation of calcium from the bones (due to cell-damage), while increasing bone mineral density requires an decrease in calcium deportation, and that is where the estrogen is required for. 

And since the exercise itself increases deportation of calcium from the bones, exercising too intensively is detrimental. (56)

Athletes & Stress-fractures

Like muscle power can be increased through exercise, bone strength can too. And like pumping up your muscles when you are young does not make you an Arnold Schwarzenegger when you are 80, exercise at young or adult age does not guarantee future bone strength. (57)

Bone strength is determined by your current daily activities, like the volume of your muscles is. And like with your muscles, the bones can handle a fall or unusual action. That is all ‘part of the plan’. 

Most old women with osteoporosis have been working very hard all of their life, and were still normally active when they were diagnosed with osteoporosis. So the osteoporosis could never be caused by a lack of exercise.

Exercise can be effective for the treatment for osteoporosis though (58), because of the protective effect of muscle contraction (59), and it might even increase strength in the remaining intact part of the bones. 

© 2000 Copyright Artists Cooperative Groove Union U.A.


Abstracts of most sources can be found at the National Library of Medicine

(1) Bryant HU, et al, An estrogen receptor basis for raloxifene action in bone. J Steroid Biochem Mol Biol 1999 / 69 (1-6) / 37-44. , Jilka RL, et al, Loss of estrogen upregulates osteoblastogenesis in the murine bone marrow. Evidence for autonomy from factors released during bone resorption. J. Clin. Invest. 1998 / 101 (9) / 1942-1950. , Sims NA, et al, Estradiol treatment transiently increases trabecular bone volume in ovariectomized rats. Bone1996 / 19 (5) / 455-461.Smith, G.R. et al, Inhibitory action of oestrogen on calcium-induced mitosis in rat bone marrow and thymus. J. Endocrinol. 1975 / 65 (1) / 45-53.

(2)Erben RG, et al, Androgen deficiency induces high turnover osteopenia in aged male rats: a sequential histomorphometric study. J. Bone Miner. Res. 2000 / 15 (6) / 1085-1098. , Yeh JK, et al, Ovariectomy-induced high turnover in cortical bone is dependent on pituitary hormone in rats. Bone1996 / 18 (5) / 443-540. , Garnero P, et al, Increased bone turnover in late postmenopausal women is a major determinant of osteoporosis. J. Bone Miner. Res.1996 / 11 (3) / 337-349.

(3) Taguchi Y, et al, Interleukin-6-type cytokines stimulate mesenchymal progenitor differentiation toward the osteoblastic lineage. Proc. Assoc. Am. Physicians 1998 / 110 (6) / 559-574. , Jilka RL, et al, Loss of estrogen upregulates osteoblastogenesis in the murine bone marrow. Evidence for autonomy from factors released during bone resorption. J. Clin. Invest. 1998 / 101 (9) / 1942-1950. , Tau KR, et al, Estrogen regulation of a transforming growth factor-beta inducible early gene that inhibits deoxyribonucleic acid synthesis in human osteoblasts. Endocrinology1998 / 139 (3) / 1346-1353. , Hietala EL, The effect of ovariectomy on periosteal bone formation and bone resorption in adult rats. Bone Miner. 1993 / 20 (1) / 57-65. , Egrise D, et al, Bone blood flow and in vitro proliferation of bone marrow and trabecular bone osteoblast-like cells in ovariectomized rats. Calcif. Tissue Int. 1992 / 50 (4) / 336-341.

(4) Jilka RL, et al, Osteoblast programmed cell death (apoptosis): modulation by growth factors and cytokines. J. Bone Miner. Res. 1998 / 13 (5) / 793-802.

(5) Mogi M, et al, Involvement of nitric oxide and biopterin in proinflammatory cytokine-induced apoptotic cell death in mouse osteoblastic cell line MC3T3-E1.Biochem. Pharmacol. 1999 / 58 (4) / 649-654. , Kobayashi ET, et al, Force-induced rapid changes in cell fate at midpalatal suture cartilage of growing rats. J. Dent. Res.1999 / 78 (9) / 1495-1504.

(6) Vegeto E, et al, Estrogen and progesterone induction of survival of monoblastoid cells undergoing TNF-alpha-induced apoptosis. FASEB J.1999 / 13 (8) / 793-803. , Tomkinson A, et al, The role of estrogen in the control of rat osteocyte apoptosis. J. Bone Miner. Res. 1998 / 13 (8) / 1243-1250.

(7) Davis JW, et al, Ethnic, anthropometric, and lifestyle associations with regional variations in peak bone mass. Calcif Tissue Int 1999 Aug;65(2):100-5. , Ulrich CM, et al, Lifetime physical activity is associated with bone mineral density in premenopausal women. J Womens Health 1999 Apr;8(3):365-75. , Boot AM, et al, Bone mineral density in children and adolescents: relation to puberty, calcium intake, and physical activity. J Clin Endocrinol Metab 1997 Jan;82(1):57-62. , Hu JF, et al, Dietary calcium and bone density among middle-aged and elderly women in China. Am J Clin Nutr 1993 Aug;58(2):219-27.

(8) Weinstein RS, et al, Apoptosis and osteoporosis.Am. J. Med. 2000 / 108 (2) / 153-164. , Manolagas SC, Birth and death of bone cells: basic regulatory mechanisms and implications for the pathogenesis and treatment of osteoporosis. Endocr. Rev. 2000 / 21 (2) / 115-137. , Rodriguez JP, Abnormal osteogenesis in osteoporotic patients is reflected by altered mesenchymal stem cells dynamics. J. Cell. Biochem. 1999 / 75 (3) / 414-423.Gazit D, et al, Bone loss (osteopenia) in old male mice results from diminished activity and availability of TGF-beta. J. Cell. Biochem. 1998 / 70 (4) / 478-488. , Ikeda T, et al, Age-related reduction in bone matrix protein mRNA expression in rat bone tissues: application of histomorphometry to in situ hybridization. Bone1995 / 16 (1) / 17-23. , Parfitt AM, et al, Relations between histologic indices of bone formation: implications for the pathogenesis of spinal osteoporosis. J. .Bone Miner. Res.1995 / 10 (3) / 466-473. , Neidlinger-Wilke C, et al, Human osteoblasts from younger normal and osteoporotic donors show differences in proliferation and TGF beta-release in response to cyclic strain. J. Biomech. 1995 / 28 (12) / 1411-1418. , Marie PJ, Decreased DNA synthesis by cultured osteoblastic cells in eugonadal osteoporotic men with defective bone formation.J Clin Invest 1991 Oct;88(4):1167-1172.

(9) Byers RJ, et al, Differential patterns of osteoblast dysfunction in trabecular bone in patients with established osteoporosis. J. Clin. Pathol. 1997 / 50 (9) / 760-764. , Mullender MG, et al, Osteocyte density changes in aging and osteoporosis. Bone1996 / 18 (2) / 109-113. ,  Ikeda T, et al, Age-related reduction in bone matrix protein mRNA expression in rat bone tissues: application of histomorphometry to in situ hybridization. Bone1995 / 16 (1) / 17-23. , Hills E, et al, Bone histology in young adult osteoporosis. J. Clin. Pathol. 1989 / 42 (4) / 391-397. 

(10) Kassem M, et al, Demonstration of cellular aging and senescence in serially passaged long-term cultures of human trabecular osteoblasts. Osteoporos. Int. 1997 / 7 (6) / 514-524. , de Vernejoul MC, Bone remodelling in osteoporosis. Clin. Rheumatol.1989 / 8 Suppl. 2 / 13-15.

(11) Delany AM, et al, Osteopenia and decreased bone formation in osteonectin-deficient mice. J. Clin. Invest. 2000 / 105 (7) / 915-923. , Gazit D, et al, Bone loss (osteopenia) in old male mice results from diminished activity and availability of TGF-beta. J. Cell. Biochem. 1998 / 70 (4) / 478-488. , Arlot M, et al, Impaired osteoblast function in osteoporosis: comparison between calcium balance and dynamic histomorphometry. Br. Med. J. (Clin. Res. Ed.) 1984 / 289(6444) / 517-520.

(12) Dunstan CR, et al, Bone death in hip fracture in the elderly. Calcif. Tissue Int. 1990 / 47 (5) / 270-275.

(13) Kung AW, Age-related osteoporosis in Chinese: an evaluation of the response of intestinal calcium absorption and calcitropic hormones to dietary calcium deprivation. Am. J. Clin. Nutr. 1998 / 68 (6) / 1291-1297. ,  Wang MC, et al, Associations of vitamin C, calcium and protein with bone mass in postmenopausal Mexican American women. Osteoporos Int 1997 / 7(6) / 533-8.

(14) O'Brien, K.O. et al, Increased efficiency of calcium absorption from the rectum and distal colon of humans. American Journal of Clinical Nutrition 1996 / 63 (4) / 579-583.

(15) Weinstein, RS, et al, Apoptosis of osteocytes in glucocorticoid-induced osteonecrosis of the hip. J. Clin. Endocrinol. Metab. 2000 / 85 (8) / 2907-2912. , Silvestrini, G, et al, Evaluation of apoptosis and the glucocorticoid receptor in the cartilage growth plate and metaphyseal bone cells of rats after high-dose treatment with corticosterone. Bone2000 / 26 (1) / 33-42. , Gohel A, et al, Estrogen prevents glucocorticoid-induced apoptosis in osteoblasts in vivo and in vitro. Endocrinology1999 / 140 (11) / 5339-5347.

(16) Peterson CA, et al, Alterations in calcium intake on peak bone mass in the female rat. J. Bone Miner. Res. 1995 / 10 (1) / 81-95.

(17) Pazzaglia UE, Experimental osteoporosis in the rat induced by a hypocalcic diet. Ital. J. Orthop. Traumatol.1990 / 16 (2) / 257-265.

(18) Holbrook TL, et al, Dietary calcium and risk of hip fracture: 14-year prospective population study. Lancet 1988 / 2 (8619) / 1046-1049. , Lau EM, et al, Epidemiology and prevention of osteoporosis in urbanized Asian populations. Osteoporos Int 1993 / 3 (Suppl 1) / 23-26. , Ribot C, et al, Risk factors for hip fracture. MEDOS study: results of the Toulouse Centre. Bone 1993 / 14 (Suppl 1) / S77-80. , Perez Cano R, et al, Risk factors for hip fracture in Spanish and Turkish women. Bone 1993 / 14 (Suppl 1) / S69-72. , Kreiger N, et al, Dietary factors and fracture in postmenopausal women: a case-control study. Int J Epidemiol 1992 / 21 (5) / 953-958.

(19) Ensrud KE, Low fractional calcium absorption increases the risk for hip fracture in women with low calcium intake. Study of Osteoporotic Fractures Research Group. Ann Intern Med 2000 / 132 (5) / 345-353.

(20) Mussolino ME, et al, Risk factors for hip fracture in white men: the NHANES I Epidemiologic Follow-up Study. J Bone Miner Res 1998 / 13 (6) / 918-924. , Turner LW, et al, Osteoporotic fracture among older U.S. women: risk factors quantified. J Aging Health 1998 / 10 (3) / 372-391. , Owusu W, et al, Calcium intake and the incidence of forearm and hip fractures among men. J Nutr 1997 / 127 (9) / 1782-1787. , Meyer HE, et al, Dietary factors and the incidence of hip fracture in middle-aged Norwegians. A prospective study. Am J Epidemiol 1997 / 145 (2) / 117-123. , Tavani A, et al, Calcium, dairy products, and the risk of hip fracture in women in northern Italy. Epidemiology 1995 / 6 (5) / 554-557. , Meyer HE, Risk factors for hip fracture in a high incidence area: a case-control study from Oslo, Norway. Osteoporos Int 1995 / 5 (4) / 239-246. , Nieves JW, et al, A case-control study of hip fracture: evaluation of selected dietary variables and teenage physical activity. Osteoporos Int 1992 / 2 (3) / 122-127. , Wickham CA, et al, Dietary calcium, physical activity, and risk of hip fracture: a prospective study. BMJ 1989 / 299 (6704) / 889-92. , Cooper C, et al, Physical activity, muscle strength, and calcium intake in fracture of the proximal femur in Britain. BMJ 1988 / 297 (6661) / 1443-1446. 

(21) Michaelsson K, et al, Diet and hip fracture risk: a case-control study. Study Group of the Multiple Risk Survey on Swedish Women for Eating Assessment. Int J Epidemiol 1995 / 24 (4) / 771-782. 

(22) Feskanich, D. et al, Milk ,dietary calcium ,and bonefractures in women, a 12 year prospective study. Am. J. Public Health 1997 / 87 (6) / 992-997.

(23) Turner, L.W. et al, Dairy-product intake and hip fracture among older women : issues for health behaviour. Psychol. Rep. 1999 / 85 (2) / 423-430. , Cumming RG, et al, Case-control study of risk factors for hip fractures in the elderly.Am J Epidemiol 1994 / 139 (5) / 493-503.

(24) FAO database on the internet ; www.fao.org/ Statistical Database / Food Balance Sheet Reports. Hong Kong has been removed from the database since the unification with China.

(25) Paspati, I. et al, Hip fracture epidemiology in Greece during 1977-1992. Calcif. Tissue Int. 1998 / 62 (6) / 542-547. , Bonjour J.P. et al, Epidemiology of osteoporosis. Schweiz. Med. Wochenschr. 1997 / 127 (16) / 659-667. , Parkkari, J. et al, Secular trends in osteoporotic pelvic fractures in Finland : number and incidence of fractures in 1970-1991 and prediction for the future. Calcif. Tissue Int. 1996 / 59 (2) / 79-83. , Lustenberger, A. et al, Epidemiology of trochanteric femoral fractures over 2 decades (1972-1988). Unfallchirurg. 1995 / 98 (5) / 278-288. , Gullberg, B. et al, Incidence of hip fractures in Malmo, Sweden (1950-1991). Bone 1993 / 14 suppl. 1/ 23-29. 

(26) Lau, E.M. & C. Cooper, Epidemiology and prevention of osteoporosis in urbanized Asian populations. Osteoporosis 1993 / 3 / suppl. 1 : 23-26.

(27) Ho SC, et al, The prevalence of osteoporosis in the Hong Kong Chinese female population. Maturitas 1999 Aug 16;32(3):171-8.

(28) Versluis, R.G. et al, Prevalence of osteoporosis in post-menopausal women in family practise (in Dutch). Ned. Tijdschr. Geneesk. 1999 / 143 (1) / 20-24. , Oden, A. et al, Lifetime risk of hip fractures is underestimated. Osteoporosis Int. 1998 / 8 (6) / 599-603. , Smeets-Goevaars, C.G. et al, The prevalence of low bone-meineral density in dutch perimenopausal women : the Eindhoven perimenopausal osteoporosis study. Osteoporosis Int. 1998 / 8 (5) / 404-409. , Lippuner, K.o et al, Incidence and direct medical costs of hospitilizations due to osteoporotic fractures in Switzerland. Osteoporosis Int. 1997 / 7 (5) / 414-425. , Lips, P. ,Epidemiology and predictors of fractures associated with osteoporosis. Am. J. Med. 1997 / 103 (2A) / 3S-8S / discussion 8S-11S. , Parkkari, J. et al, Secular trends in osteoporotic pelvic fractures in Finland : number and incidence of fractures in 1970-1991 and prediction for the future. Calcif. Tissue Int. 1996 / 59 (2) / 79-83. , Nydegger, V. et al, Epidemiology of fractures of the proximal femur in Geneva ; incidence, clinical and social aspects. Osteoporosis Int. 1991 / 2 (1) / 42-47. , Van Hemert, A.M. et al, Prediction of osteoporotic fractures in the general population by a fracture risk score. A 9-year follow up among middle aged women. Am.J.Epidemiol. 1990 / 132 (1) / 123-135.)

(29) Lau, E.M. et al, Admission rates for hip fracture in Australia in the last decade. The New South Wales scene in a world perspective. Med.J.Aust. 1993 / 158 (9) / 604-606.

(30) Fujita, T. and M. Fukase, Comparison of osteoporosis and calcium intake between Japan and the United States. Proc.Soc.Exp.Biol.Med. 1992 / 200 (2) / 149-152.

(31) Bauer RL, Ethnic differences in hip fracture: a reduced incidence in Mexican Americans. Am J Epidemiol 1988 Jan;127(1):145-9.

(32) Kessenich CR, Osteoporosis and african-american women. Womens Health Issues 2000 / 10 (6) / 300-304.

(33) Xu. L. et al, Very low rates of hip fracture in Beijing, People's Republic of China ; The Beijing Osteoprosis Project. Am.J.Epedemiol. 1996 / 144 (9) / 901-907.

(34) Schwartz, A.V. et al, International variation in the incidence of hip fractures : cross-national project on osteoporosis for the World Health Organization Program for Research on Ageing. Osteoporosis Int. 1999 / 9 (3) / 242-253.Rowe, S.M. et al, An epidemiological study of hip fracture in Honan, Korea. Int. Orthop. 1993 / 17 (3) / 139-143.

(35) Bwanahali, K. et al, Etiological aspects of low back pain in rheumatic patients in Kinshasa (Zaire). Apropos of 169 cases. (in French) Rev. Rhum. Mal. Osteoartic. 1992 / 59 (4) / 253-257.

(36) Barss, P., Fractured hips in rural Melanesians : a nonepidemic. Trop. Geogr. 1985 / 37 (2) / 156-159.

(37) Mijiyawa, M.A. et al, Rheumatic diseases in hospital outpatients in Lome. Rev. Rhum. Mal. Osteoartic. 1991 / 58 (5) / 349-354.

(38) Memon, A. et al, Incidence of hip fracture in Kuwait. Int.J.Epidemiol.1998 / 5 / 860-865.

(39) Walker, A., Osteoporosis and Calcium Deficiency, Am. J. Clin. Nutr. 1965 / 16 / 327. 

(40) Smith, R., Epidemiologic Studies of Osteoporosis in Women of Puerto Rico and South-eastern Michigan ... Clin. Ortho. 1966 / 45 /32.

(41) Abelow BJ, et al, Cross-cultural association between dietary animal protein and hip fracture: a hypothesis. Calcif. Tissue Int.1992 / 50 (1) / 14-18.

(42) Holly Smith in  : Leakey, R. & Lewin, R., Origins Reconsidered : In Search of what Makes Us Human, London 1992 / 144-145. , Mc Henry, H.M. ,Femoral lengths and stature in Plio-Pleistocene hominids. Am. J. Phys. Anthropol. 1991 / 85 (2) / 149-158. , Brown, F. et al, Early Homo erectus skeleton from west Lake-Turkana, Kenya. Nature 1985 / 316 (6031) / 788-792.

(43) Mazzuoli, G.F. et al, Hip fracture in Italy : Epidemiology and preventive effeicacy of bone active drugs. Bone 1993 / 14 / suppl. /581-584.

(44) Lips, P., Epidemiology and predictors of fractures associated with osteoporosis. Am. J. Med. 1997 / 103 (2A) / 3S-8S / discussion 8S-11S.

(45) Erben RG, et al, Therapeutic efficacy of 1alpha,25-dihydroxyvitamin D3 and calcium in osteopenic ovariectomized rats: evidence for a direct anabolic effect of 1alpha,25-dihydroxyvitamin D3 on bone.Endocrinology1998 / 139 (10) / 4319-4328.

(46) Pascher E, et al, Effect of 1alpha,25(OH)2-vitamin D3 on TNF alpha-mediated apoptosis of human primary osteoblast-like cells in vitro. Horm. Metab. Res.1999 / 31 (12) / 653-656.

(47Sairanen S, et al, Bone mass and markers of bone and calcium metabolism in postmenopausal women treated with 1,25-dihydroxyvitamin D (Calcitriol) for four years. Calcif. Tissue Int. 2000 / 67 (2) / 122-127.

(48) Sairanen S, et al, Bone mass and markers of bone and calcium metabolism in postmenopausal women treated with 1,25-dihydroxyvitamin D (Calcitriol) for four years. Calcif. Tissue Int. 2000 / 67 (2) / 122-127. , Gurlek A, et al, Comparison of calcitriol treatment with etidronate-calcitriol and calcitonin-calcitriol combinations in Turkish women with postmenopausal osteoporosis: a prospective study. Calcif. Tissue Int. 1997 / 61 (1) / 39-43.

(49)Giunta, D.L. ,Dental changes in hypervitaminosis D. Oral. Surg. Pathol. Oral. Radiol. Endod. 1998 / 85 (4) / 410-413. , Uehlinger, P. et al, Differential diagnosis of hypercalcemia - a retrospective study of 46 dogs. (duitst.) Schweiz. Arch. Tierheilkd. 1998 / 140 (5) / 188-197. , Qin, X. et al, Altered phosphorylation of a 91-kDa protein in particulate fractions of rat kidney after protracted 1,25-dihydroxyvitamin D3 or estrogen treatment. Arch. Biochem. Biophys. 1997 / 348 (2) / 239-246. , Niederhoffer, N. et al, Calcification of medical elastic fibers and aortic elasticity. Hypertension 1997 / 29 (4) / 999-1006. , Selby, P.L. et al, Vitamin D intoxication causes hypercalcemia by increased bone resorption with responds to pamidronate. Clin. Endocrinol. (Oxf.) 1995 / 43 (5) / 531-536. , Ito, M. et al, Dietary magnesium effect on swine coronary atherosclerosis induced by hypervitaminosis D. Acta Pathol. Jpn. 1987 / 37 (6) / 955-964.

(50) Le Boff, M.S., Occult vitamin D deficiency in postmenopausal US women with acute hip fracture. J. Am. Med. Assoc. 1999 / 281 (16) / 1505-1511. , Scharla SH, et al, Prevalence of low bone mass and endocrine disorders in hip fracture patients in Southern Germany. Exp. Clin. Endocrinol. Diabetes 1999 / 107 (8) / 547-554.

(51) Ghannam NN, et al, Bone mineral density of the spine and femur in healthy Saudi females: relation to vitamin D status, pregnancy, and lactation. Calcif Tissue Int 1999 Jul;65(1):23-8

(52) Laitinen K, et al, Deranged vitamin D metabolism but normal bone mineral density in Finnish noncirrhotic male alcoholics. Alcohol Clin Exp Res 1990 Aug;14(4):551-6.

(53) attiv A, Stress fractures and bone health in track and field athletes. J. Sci. Med. Sport 2000 / 3 (3) / 268-279. , Hobart JA, et al, The female athlete triad. Am. Fam. Physician 2000 / 61 (11) / 3357-3364, 3367. , Anderson JM, The female athlete triad: disordered eating, amenorrhea, and osteoporosis. Conn. Med. 1999 / 63 (11) / 647-652. 

(54) Meyer T, et al, Identification of apoptotic cell death in distraction osteogenesis. Cell. Biol. Int.1999 / 23 (6) / 439-446. , Landry P, et al, Apoptosis is coordinately regulated with osteoblast formation during bone healing. Tissue Cell 1997 / 29 (4) / 413-419.

(55) Pettersson, U., et al, Low bone mass density at multiple skeletal sites, including the appendicular skeleton in amenorrheic runners. Calcif. Tissue Int. 1999 / 64 (2) / 117-125.

(56) Cromer B, et al, Adolescents: at increased risk for osteoporosis? Clin. Pediatr. (Phila) 2000 / 39 (10) / 565-574. , Judex S, et al, Does the mechanical milieu associated with high-speed running lead to adaptive changes in diaphyseal growing bone? Bone 2000 Feb;26(2):153-9.

(57) Rutherford OM. , Is there a role for exercise in the prevention of osteoporotic fractures?Br J Sports Med 1999 / 33 (6) / 378-386.

(58) Gregg EW, et al, Physical activity, falls, and fractures among older adults: a review of the epidemiologic evidence. J. Am. Geriatr. Soc. 2000 / 48 (8) / 883-893. , Kujala UM, et al, Physical activity and osteoporotic hip fracture risk in men. Arch Intern Med 2000 Mar 13;160(5):705-8.

(59) Kaastad TS, et al, Training increases the in vivo fracture strength in osteoporotic bone. Protection by muscle contraction examined in rat tibiae. Acta Orthop. Scand.1996 / 67 (4) / 371-376.


For the source of these documents visit: http://www.4.waisays.com/ by by Wai Genriiu