The "Brittle Bone" Disease
"They" say that "Brittle Bone" disease, osteoporosis, is caused by a calcium deficiency.  "They" say that we should consume more calcium or take calcium supplements.  "They've" been saying it for more than 20 years.  Commercial interests have promoted food products with added calcium for about that long.  And osteoporosis is a bigger problem today than ever before.  Is it reasonable to keep doing what doesn't work?

What is Bone?

Sometimes you will hear or see statements that calcium is the main component in bone.  This is not true.  Bone is a composite material made of 80% collagenous protein (we'll call it cartilage) and 20% mineral, by volume.  The mineral component is dispersed in a matrix of cartilage.  The mineral component is made up of calcium, phosphorus, magnesium, potassium, boron, manganese and copper.  The cartilage is the bendy part, the minerals the stiffening agent.

One way to visualize the structure of bone is to think of it as a sponge.  The sponge corresponds to the collagen (cartilage), and the small pockets in the sponge to the places where the mineral is deposited.  A deficiency in calcium (osteomalacia) has the pockets empty of mineral.  Osteoporosis corresponds to the places where the sponge itself is missing.  Clearly, no amount of calcium can take the place of the missing sponge.

Does a Calcium Deficiency Result in Osteoporosis?

Let's apply logic to the problem.  Newborn babies have "rubber" bones.  They bend, but do not break.  As the infant grows, calcium is added to the bones and the bones become stiffer.  The child does not go through a period of brittle bones as he grows from rubber bones to strong and healthy bones.  If a lack of calcium in the bones caused the brittleness, how does the child escape?  Why don't children break their bones every time they fall?

Because lack of calcium does not make bones brittle?  If you would like to test this idea for yourself, take the drumstick from a piece of fried chicken (or baked or boiled, or even raw). After removing all the meat and cartilage, try bending the bone. You can't, right?  Put the bone in jar full of vinegar and set it aside for about a week. The vinegar will dissolve the calcium right out of the bone.  After the week has passed, remove the lid, and try bending the bone again.  This time you will be able to bend the bone in a "circle", touching the two ends without the bone breaking.  No calcium, and no brittle bone.

Bone Diseases

If a child does not get enough vitamin D, he develops a condition called Rickets, which is a condition of not enough calcium being deposited in the bones, leaving them "bendy".  If this is not corrected, the child may develop permanently bent legs, and will be bow-legged for life.

Those who suffer from alcoholic cirrhosis of the liver are prone to two bone diseases, osteoporosis and osteomalacia (sometimes called adult onset rickets).  In osteoporosis, the bones thin and become brittle.  In osteomalacia, the bones are bendy, and may be painful if the person puts strain on them.  Just as in children, this is caused by a lack of vitamin D, which caused the calcium to leach out of the bones.  How is it that there could be two diseases where calcium is deficient and one causes brittleness and the other causes bending?

Asian women are prone to "dowager's hump" as they age, but not to osteoporosis.  They do not have "brittle bones" Their traditional diet that is very low in calcium, but ample in fresh fruits and vegetables.

The Myth in Society

The preponderance of advertising about osteoporosis in the U.S. is aimed at women, who do suffer more broken bones from the problem.  However, that's not true world-wide.  In some countries, men suffer twice as many broken bones from osteoporosis as women.  In particular, menopausal women seem to be the targets of advertising, presumable because the falling production of estrogen is the precipitating cause.  Yet, only one quarter of women will ever suffer the effects of osteoporosis.  Do the rest not have declining estrogen levels?  And what about women in other cultures?  Do they not have declining estrogen levels?

Physicians will prescribe estrogen for women who suffer from loss of bone density, but it does not reverse osteoporosis. Nor do any other AMA-approved drugs.  In some cases, they appear to stop the progressive loss, but with a frequent side effect of making the bones even more brittle.  A search of the literature will show that no claim is made that increasing bone density reduces fractures.

In technical articles about osteoporosis, the discussion includes the fact that the bone becomes porous, with small holes in the bone matrix.  It is into these holes that conventional medicine tries to force calcium.  But what if the holes are holes in the cartilage?  There is evidence that homocysteine and glucocorticoid treatment (prednisone) also damage bone.  More minerals in less cartilage would make a bone more brittle, wouldn't it?

If Not Calcium, Then What?

So let's consider what makes cartilage.  Cartilage is a protein substance requiring vitamin C for its formation.  Since people take in varying amounts of vitamin C, there might be a reason for some people to get osteoporosis and not others.  Since many people eat fewer fresh fruits and vegetables in the winter, that might explain the statistical increase in fractures in the winter and early spring.

We know of no study that has attempted to make this connection.  But since most studies are funded by pharmaceutical companies, and they have no incentive to cut into the sales of prescription drugs, perhaps that's not surprising. 

Most likely osteoporosis is not a deficiency disease of only one nutrient.  Probably several elements must be missing before the symptoms develop.  But since doctors, cereal companies, and pharmaceutical companies have tried adding calcium without making a significant impact on the problem, maybe it is time to try adding the other major nutrient that goes to make bone, vitamin C.

And nobody is talking about the impact that the mind has on the body.  But there are indications that a number of emotional conditions affect bone formation.
 
If you would like a fairly technical reference to bone formation and bone conditions check this site:  http://www.rxforwellness.com/articlearchives/rx_osteoporasis.shtml
For medical abstracts about vitamin C and its impact on collagen, see the following:
  1. Chatproedprai S, Wananukul S.  Scurvy: a case report.  J Med Assoc Thai. 2001 Jun; 84 Suppl 1: S106-10. 
  2. Fain O.  Musculoskeletal manifestations of scurvy.  Joint Bone Spine. 2005 Mar; 72(2): 124-8. 
  3. Firth N, Marvan E.  Oral lesions in scurvy.  Aust Dent J. 2001 Dec; 46(4): 298-300.
  4. Libby P, Aikawa M.  Vitamin C, collagen, and cracks in the plaque.  Circulation. 2002 Mar 26; 105(12): 1396-8.
  5. Pangan AL, Robinson D.  Hemarthrosis as initial presentation of scurvy.  J Rheumatol. 2001 Aug; 28(8): 1923-5.
  6. Sakamoto Y, Takano Y.  Morphological influence of ascorbic acid deficiency on endochondral ossification in osteogenic disorder Shionogi rat.   Anat Rec. 2002 Oct 1; 268(2): 93-104. 
  7. Shamash R, Laufer D, Tulchinsky V.  Scurvy--a disease not only of historical interest.   Br J Oral Maxillofac Surg. 1988 Jun; 26(3): 258-60. 
  8. von Muhlendahl KE.  [Infantile scurvy]  Monatsschr Kinderheilkd. 1984 Apr; 132(4): 240-1.
For information on homocysteine and bone, see the following:
  1. Dhonukshe-Rutten RA, Pluijm SM, de Groot LC, et al.  Homocysteine and vitamin b(12) status relate to bone turnover markers, broadband ultrasound attenuation, and fractures in healthy elderly people.   J Bone Miner Res. 2005 Jun; 20(6): 921-9.
  2. McLean RR, Jacques PF, Selhub J, et al.  Homocysteine as a predictive factor for hip fracture in older persons.   N Engl J Med. 2004 May 13; 350(20): 2042-9. 
  3. Sato Y, Honda Y, Iwamoto J, et al.    Effect of folate and mecobalamin on hip fractures in patients with stroke: a randomized controlled trial.  JAMA. 2005 Mar 2; 293(9): 1082-8. 
  4. Tucker KL, Hannan MT, Qiao N, et al.  Low plasma vitamin B12 is associated with lower BMD: the Framingham Osteoporosis Study.   J Bone Miner Res. 2005 Jan; 20(1): 152-8.
For information on glucocorticoids and bone, see the following:
  1. Biyikli NK, Emre S, Sirin A, Bilge I.  Biochemical bone markers in nephrotic children.   Pediatr Nephrol. 2004 Aug; 19(8): 869-73. 
  2. Tanaka Y.  [Corticosteroid therapy for nephrotic syndrome]   Nippon Rinsho. 2004 Oct; 62(10): 1867-72.
  3. Ton FN, Gunawardene SC, Lee H, Neer RM.  Effects of low-dose prednisone on bone metabolism.   J Bone Miner Res. 2005 Mar; 20(3): 464-70. 
  4. van Meurs JB, Dhonukshe-Rutten RA, Pluijm SM, et al.  Homocysteine levels and the risk of osteoporotic fracture.   N Engl J Med. 2004 May 13; 350(20): 2033-41. 

For medical abstracts about the impact of emotion on osteoporosis, see the following:
 
  1. Gold PW, Gabry KE, Yasuda MR, Chrousos GP. Divergent endocrine abnormalities in melancholic and atypical depression: clinical and pathophysiologic implications.  Endocrinol Metab Clin North Am. 2002 Mar; 31(1): 37-62,
  3. Cizza G, Ravn P, Chrousos GP, Gold PW.  Depression: a major, unrecognized risk factor for osteoporosis? Trends Endocrinol Metab. 2001 Jul; 12(5): 198-203.
  5. Gold PW, Chrousos GP.  The endocrinology of melancholic and atypical depression: relation to neurocircuitry and somatic consequences.  Proc Assoc Am Physicians. 1999 Jan-Feb; 111(1): 22-34. 
 
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