Osteoporosis is an important health issue
which is preventable through proper nutrition and exercise, especially
in childhood and as young adulthood. Later, it can be treated, again
with proper nutrition and exercise. This essay will explore the
relevant issues.

Update of 2/9/2012 — The issue of bone quality, discussed below, is becoming more accepted as being meaningful.  An article that discusses this can be accessed here.  It is interesting that the beneficial effects of the anti-resporptive drugs (foxamax, etc.), such as they are, cannot be entirely attributed to their effect on increasing bone density.

Update of 3/20/2011 — a review article has appeared in Holistic Primary Care regarding the role of bone flexibility (which is a function of healthy bone matrix (see below).  In particular the article highlights the importance of Vitamin K2 in bone health, the role of inflammation in osteoporosis, the use of Strontium in remediation, etc.


Update of 12/6/2010 — an interesting article on Calcium supplements appeared recently, and can be viewed here.  In brief, there is some evidence that supplemental calcium, while having a modest effect on diminishing fracture risk, has the unfortunate consequence of increasing the risk of heart attack.  The article points out that calcium from the diet has never been associated with any risk.

Back to the original article ….

Bone is composed of a protein and collagen (“connective tissue”)
matrix upon which calcium is deposited. In addition to providing a
solid structure for the body, bone serves as a reservoir of calcium,
which is essential not just for bone strength, but for many other vital
functions in the body, such as transmission of electrical impulses in
nerve tissue, and for muscle contraction.

There are two types of active bone cells — osteoblasts,
which take calcium from the blood stream and deposits it onto the bony
matrix, and osteoclasts, which “resorb” calcium from the bone and
release it into the bloodstream.

There are many factors which control the relative balance
of activity of these two cells. One important one (for the purposes of
this discussion) is to support the strength of bone relative to the
load it is under. Use of the body causes “strain” on bones. The more
use (exercise) the more strain. As the bone is put under strain,
electrical activity is generated in the bone, and the osteoblasts
deposit calcium into the area under strain. The greatest contrary
example to this scenario is that of the astronaut in space. Freed from
the strain of the earth’s gravity, the bone immediately starts to lose
calcium. This is a significant problem for humanity’s long-term adaptation
to extra-planetary environments. It also points out the necessity for
physical activity in human life, which serves many more purposes than
simply maintaining the calcium stores in bone.

In Osteoporosis, there is an excess of bone resorption
relative to bone formation. Literally, the term osteoporosis means
“porous bones”. Osteoporotic bone, seen under the microscope, resembles
Swiss cheese, with large holes. Another “wrinkle” in the current
situation is that osteoporotic bone, in and of itself, may not be
significantly weakened and subject to pathologic fracture (fracture
under low-strain conditions). The following quote, from the work of
Lawrence Melton of the Mayo Clinic, an osteoporosis researcher, is
taken from Better Bones, Better Body, by Susan Brown (Keats Publishing, Inc., Canaan, Ct., 1996):

“Osteoporosis alone may not be sufficient to produce such
(osteoporotic) fracture, since many individuals remain fracture-free even within the sub-groups of lowest bone density. Most women aged 65 and over and men 75 and over have lost enough bone to place them atsignificant risk of osteoporotic fracture, yet many never fracture anybones at all. By age 80 virtually all women in the United States are
osteoporotic with regard to their hip density, yet only a small
percentage of them suffer hip fractures each year.”

[Mazess, R., Personal communication, Continuing Education Course of Osteoporosis: Harvard University 1987)]

Normally, strain on bone can result in a “micro-fracture”
(one visible only under the microscope.) In health, this micro-fracture
is quickly repaired. If the healing processed is compromised (in
conditions of sub-optimal health) then another strain in the same place
deepens the crack. When this happens often and frequently enough, the
bone will finally fracture under an apparently small strain (the straw
that breaks the camel’s back).

Another aspect of bone as calcium reserve is the finding
that high-protein diets lead to obligatory calcium loss through the
kidneys. Bone, serving as a reservoir, yields it’s calcium to the
blood-stream so that the other calcium-requiring vital functions of the
body, which are more immediately necessary than bone strength, can be

For women going through menopause, there is a normal loss
of calcium from bone which takes place over a period of 5 years or so.
The body apparently senses that there will be no further need to serve
as a source of calcium for a developing baby, and lets the calcium
reservoir be drained down. Although we do not understand, as far as I
know, the rationale for this diminution of total body calcium, it is
more likely to serve a purpose than not. Recent research has, however,
has cast doubt on this scenario, and suggests that bone loss may
continue progressively into old age (Enstrud KE, et. al., in Journal of
Bone Mineral Research, 1995;10:1778-1787).

The highest incidence of osteoporotic fractures takes
place in women over the age of 75. A study reported in the Journal of
the American Medical Association reported increases in bone mineral
density in “frail elderly women” give 9 months of estrogen replacement
therapy. The study did not, however, look at the effect on the risk of
fracture in these women (Bone Mineral Density Response to Estrogen
Replacement in Frail Elderly Women, Vollaread DT, et.al., JAMA 8/15/01
vol 286, number 7, page 815-820).

Estrogen clearly stimulates the deposition of calcium into bone. This makes perfect sense. But even post-menopausal women can build bone mass (through exercise and proper nutrition) so estrogen replacement is clearly not “necessary” for bone health.

One of the strongest determinants of osteoporosis in the elderly is the bone
density achieved in childhood and early adulthood.Most adult bone mass is achieved by the age of 14 (Sabatier J-P, Guaydier-Souquieres G, Laroche D, et al. Bone mineral acquisition during adolescence and early adulthood: a study in 574 healthy females 10–24 years of age. Osteoporos Int 1996;6:141–8.)

An interesting 2001 study published in the American Journal of Clinical Nutrition looked at healthy 8 year-old boys and girls with adequate calcium intake, seeking to correlate sodium and potassium intake and excretion with bone density. Sodium intake was looked at because of evidence in adults that increased dietary sodium is associated with increased urinary calcium excretion and diminished bone mass.

In this study, the only significant positive correlation (when calcium intake was sufficient) was with potassium intake (from fruits and vegetables). (Jones, G., et al.,Association between urinarypotassium, urinary sodium, current diet, and bone density in prepubertal childrenAm J Clin Nutr 2001;73:839–44.)

The study also noted that in adults, potassium and magnesium intake are also important.

At all ages, physical activity, adequate calcium intake, sun exposure (most likely related to vitamin D levels) promote bone health.

Osteoporosis can be a sign of other diseases (such as cancer, osteomalacia (weakened and insufficiently mineralized bone matrix) , hyperparathyroidism, malabsorption or malnutrition, low sun exposure, or the side effects of steroids). Laboratory investigation can usually either suggest that one of these problems is present or, conversely, prove that they are not.

Until recently then, osteopenia was defined as a condition in which there was less bone mass, and the term osteoporosis was restricted to bone which was subject to pathologic fracture. This definition has now been changed. It seems to me that this change is roughly co-incident with the development of technology that can measure the density of bone (and therefore diagnose osteopenia) and with the use of estrogen supplementation in hormone replacement therapy (HRT.)

While common sense would dictate that osteopenic bone is more likely to
fracture than is normal bone, if the main determinant of pathologic
fracture is the health of the bone in a broader context (it’s ability
to heal micro-fractures) than simply the amount of calcium present,
then the substitution of osteopenia for osteoporosis is misplaced.

There are many factors that go into the health of bone. I will list some of the main ones here, but for a more complete discussion of this problem, I suggest you read Better Bones, Better Body by Susan Brown, Ph.D.

• Calcium deficiency or excess dietary phosphorus are
negative factors, as are excessive sugar consumption, caffeine intake, and other nutrients such as (lack of) Vitamin D. In fact, it has recently been suggested that Vitamin D levels are insufficient in a larger numbers of people than was previously recognized, and the “reference dail intake (RDI, formerly the “recommended daily allowance, or RDA) has been raised, for adults, to 800-1000 Units daily, from the previous level of 400 Units.  Higher doses are also safe, if taken in the form of Vitamin D-3 (cholecalciferol).

• Lack of exercise and sunlight are negative factors.

  • Most pathologic fractures (fractures that shouldn’t happen given the degree of trauma involved)  are the result of falls, which are all too common in the elderly. Falls can be prevented by maintaining joint range of motion, muscle strength, and coordination. Exercise, or at least ongoing use of the body, is necessary to maintain these

• Excessive acid consumption (notably the phosphoric acid
and carbonic acid present in carbonated sodas) force the bone to yield calcium into the blood stream to “buffer” the acidic load.

  • Lack of Magnesium is also an important factor. A recent article demonstrating the positive effects of magnesium intake can be found at here.

Calcium supplements are not well absorbed. The best over-the-counter supplements are Tums, Os-Call 500, and Citracal (calcium citrate). All calcium supplements should be taken with food.

Other supplements that are useful include Boron 3 mg/day.

Recently Strontium has been found useful in osteoporosis (see O’Donnell S, Cranney, A, Wells GA, Adachi J, Reginster J. Strontium ranelate for preventing and treating postmenopausal osteoporosis (Review). Cochrane Database for Syst Rev. 2006; 3:CD005326.) Strontium has the advantage of not only blocking the resorption of bone (removal of calcium) but also stimulating the formation of new bone.  It is a newer agent and has not been as extensively tested as some of the other agents.  A summary and advisory issued in England can be accessed here.  They note that strontium, being more dense than Calcium, makes the measurement of bone density “unreliable.”  I’m not sure that I agree with this statement, but in any case the issue is fracture prevention, not bone density.

In addition, Vitamin K-2 (Menatetrenone) has been found to be useful, at doses of 45 mg/day (Iwamoto, J., et. al., Effects of Combined Administration of Vitamin D3 and Vitamin K2 on bone mineral density of the lumbar spine in postmenopausal women with osteoporosis, J Orthop Sci 2000;5(6):546-51.)  An abstract of that article can be found here.

The role of conventional drug therapy is complex and
controversial. Agents such as Fossamax, which reduce the rate of
resorption of bone, have been shown to reduce the number of
pathological fractures. This seems to be equally true if Fossamax is
started early, soon after the menopause, or later in life, when the
risk of pathological fractures is elevated for other reasons. In my
opinion, the use of estrogens for the prevention or treatment of
osteoporosis is very questionable for several reasons. There are other
classes of drugs used in the conventional treatment of osteoporosis,
and for some women, there may be a valid role for one or another of
them. I do not prescribe these drugs myself, and do not consider myself
to be an expert in evaluating their advisability. When bone density is
low and/or there are other significant risk factors present (positive
family history of the disease, cigarette smoking, fair skin, past
history of pathological fracture) one should consider use of one of
these agents, and seek appropriate advise from specialists in the
evaluation and treatment of osteoporosis.

Bone density measurements are expensive, and simply
indicate the mass of bone present at any particular time. Since bone is
in a state of dynamic balance, another interesting measurement is that
of the rate of “resorption” of bone (how much of the protein matrix of
the bone is being broken down to make calcium available to the
bloodstream.) This can be accomplished through a simple, inexpensive
(approximately $70) urine test which measures collagen cross-links. The
two measurements are complementary, but the urine test is more useful
for assessing the effects of a treatment program, especially since it
is not generally useful to repeat the bone density test for at least a
year, because the changes are so small and gradual.