Osteoporosis is the most widely recognized
disease connected with calcium and affects over 15 million people in the USA
alone. But did you know that both too little and too much calcium can make your bones fragile? A recent study by
the Mayo clinic showed that extra calcium supplementation tripled the risk of
non-spinal fractures in women already suffering from osteoporosis.1 This
confirms findings of previous studies that calcium supplementation can increase
the risk of hip fractures.8 How can this be?
Osteoporosis can be classified into two categories: type I and type II.
Type
I Osteoporosis
Type I osteoporosis is the classical type
associated with calcium deficiency. It occurs in people with a fast metabolism.
An overactive thyroid gland causes the body to partially lose its ability to
retain calcium and magnesium. At the same time, activity of the parathyroid gland
slows down because thyroid and parathyroid glands are each other’s antagonists2.
With decreased parathyroid function, cells that normally produce hard bone
(osteoblasts) become inactive. Less calcium and magnesium are absorbed into the
bone while more is excreted through the kidneys. As a result, bones become
deficient in calcium and magnesium, grow brittle and easily break.1,2
People who suffer from this type of osteoporosis benefit from extra calcium
supplementation.
Type
II Osteoporosis
People with a slow metabolism, on the other
hand, do not benefit from calcium supplementation at all. In fact, the
opposite: it makes the problem worse. In their case, a sluggish thyroid
triggers increases activity of the parathyroid gland2,3. This leads
to more absorption and retention of calcium, while at the same time increasing
the number of cells that break down bones (osteoblasts).5,6 This
allows calcium to be drawn from the bone, weakening the bones. Since the
calcium can’t be reabsorbed into the bone due to increased osteoblast activity,
the body deposits it in soft tissue. This can result in gall stones, kidney
stones, stiffness in joints due to calcium deposits, increased arterial plaque
formation1,8 and dry skin. In those cases calcium supplementation will
not solve the problem. In fact, it will make it worse.1,2,8
Osteoporosis
due to insulin resistance
Calcium bone loss can also be the result of
an underlying metabolic problem. For instance, people with adult onset diabetes
or insulin resistance have an increased insulin production. The pancreas can
only release insulin when there is enough calcium available.4,7 To
make sure enough calcium is available, the body starts to retain calcium by
reabsorbing it in the kidneys, while at the same time the parathyroid also steps
up its activity to withdraw calcium stored in the bones. In summary, calcium is
stopped from being excreted through the kidneys, and is withdrawn from its
storage in bones, to meet the increased demand by the pancreas to produce
insulin. Any calcium that is not used for insulin production will not be
reabsorbed into the bones due to osteoblast acivity but stored elsewhere, once
again not only leading to gall stones, kidney stones etc but also to
osteoporosis.1
How
to test?
So how do you know if you should or shouldn’t
be taking extra calcium to prevent osteoporosis? A blood test is not useful,
because the body will do its utmost to keep levels in the blood the same –
either by storing excessive levels in the tissue if levels in blood become too
high or withdrawing it from the bones if levels in the blood become too low
(homeostasis). It is only when stores in bones are depleted or when the body
runs out of tissue to deposit it, that blood levels will start to fluctuate,
but by then it is far too late.
Hair Mineral Analysis is more effective way
to asses storage levels of calcium. Hair is the second most metabolically active
tissue and it provides a reliable record of metabolic activity during its
period of growth. The first 4 cm closest to the scalp can provide a good
indication of nutrient exposure over the previous 8 – 16 weeks. Mineral
deficiencies or excesses can indicate a possible deficiency, excess or
bio-unavailability of one or more minerals within the body.
If you are interested in getting a hair
mineral analysis done, please contact our clinic on 1300 133 536 or visit our website at:
https://www.massattack.com.au/contactUs.html
References:
1.
Dr D.L Watts, “Trace elements and other
essential nutrients” – 6th Writer’s B-L-O-C-K, USA 2010, p 52-58
2.
Tortora & Grabrowski, “Principles of
anatomy and physiology” 9th edition, p 581-587 – Biological Sciences
Text Books, 2000
3.
Tarrage Lopez PJ et all, “Osteoporosis in
patients with subclinical hypothyroidism” – Clin Cases Mineral Bone Metabolism,
2011 Sep;8(3):44-8
4.
Curry DL, Bennett LL,
Grodsky GM: Requirement for calcium ion in insulin secretion by the perfused
rat pancreas. Am J Physiol214 :174–178,1968
5.
Nagata Mutsuko et all, “Subclinical hypothyroidism is related to lower
heel QUS in postmenopausal women” – Endocrine Journal, 2007, vol. 54, no4,
pp. 625-630
6. Bertoli A,
Fusco A, Andreoli A, Magnani A, Tulli A, Lauro D, de Lorenzo A, “Effect of Subclinical Hypothyroidism and Obesity
on Whole-Body and Regional Bone Mineral Content” - Horm Res 2002;57:79–84
7. L. Bent-Hansen, K. Capito, C.J.
Hedeskov, “The effect of calcium on somatostatin inhibition of insulin
release and cyclic AMP production in mouse pancreatic islets”
- Biochimica et Biophysica Acta
(BBA) - General Subjects Volume 585, Issue 2, 12 June 1979, Pages 240–249
8. Reid IR,
Bolland MJ, Grey A, “Effect of calcium supplementation on hip fractures” – Osteoporosis Int (2008)
19:1119-1123
