Cardiovascular risks of calcium supplements in women
BMJ 2008; 336 doi: https://doi.org/10.1136/bmj.39463.394468.80 (Published 31 January 2008) Cite this as: BMJ 2008;336:226All rapid responses
Rapid responses are electronic comments to the editor. They enable our users to debate issues raised in articles published on bmj.com. A rapid response is first posted online. If you need the URL (web address) of an individual response, simply click on the response headline and copy the URL from the browser window. A proportion of responses will, after editing, be published online and in the print journal as letters, which are indexed in PubMed. Rapid responses are not indexed in PubMed and they are not journal articles. The BMJ reserves the right to remove responses which are being wilfully misrepresented as published articles or when it is brought to our attention that a response spreads misinformation.
From March 2022, the word limit for rapid responses will be 600 words not including references and author details. We will no longer post responses that exceed this limit.
The word limit for letters selected from posted responses remains 300 words.
A very erudite and informative comment by Dr.Basavaraj. Shivayogi
Hadapad .
I am glad he has seen the disease mongers as well, they have become
as common as ambulance-chasing lawyers once were.
What puzzles me in the original paper is the apparent ignorance of
salient facts.
It is generally known that the intake of calcium will affect the body
in several ways. Take the simplistic mindset of a researcher who sees age
-related osteoporosis as a disease in need of urgent treatment, then
combine this with his/her belief that calcium is what (like Wonder Bread)
makes strong bones and you have a recipe for failure and, potentially, for
disaster.
By competing for the same transport site, excess calcium may easily
cause a magnesium deficiency. The absorption of magnesium may be severely
disrupted and be compounded in its ill effects by other factors unknown to
the treating physician or ignored.
So, the well intentioned administration of calcium may be the trigger
for cardiovascular mishaps by withholding essential magnesium.
There is probably no need to go into the many other causes of
magnesium deficiency or the many important roles magnesium must play in
the body. Suffice it to say, the administration of high doses of calcium
may well add to the list of iatrogenic casualties we really ought to
prevent.
Competing interests:
None declared
Competing interests: No competing interests
For the past few decades it is taught at medical schools that
hormonal and calcium deficiencies are the main culprit in causation of
Postmenopausal Osteoporosis.
The very definition of “normality” is flawed seriously. The
statistical mean plus/minus two standard deviations automatically brings
in five per cent of normal people into the fold of patients-the false
positives. This goes up to 25% when disease statistics are used to measure
healthy people. If we extend this definition further, almost all will come
under the umbrella of patients! Age related osteoporosis falls under this
label.
Osteoporosis is the most common metabolic bone disease which is
defined as reduction of bone mass (or density) or the presence of a
fragility fracture. The reduction in bone tissue is accompanied by
deterioration in the architecture of the skeleton, leading to markedly
increased risk of fracture. In 1994 a World Health organization study
group recommended a clinical definition of osteoporosis based on bone
mineral density (BMD) measurements expressed in standard deviation (SD)
units called T- scores which are calculated by taking the difference
between a patient’s measured BMD and the mean BMD of healthy young adults
matched for gender and ethnic group and expressing the difference relative
to the young adult population SD.
There is some space for a doubt to consider this clinical definition
of osteoporosis for postmenopausal women because decrease in bone density
is a universal feature of ageing. How could one compare the adult and
elderly bone mass density with that of young healthy adults? However these
days, irrespective of age related changes in the bone remodeling process a
patient with T- score less than – 2.5 at spine, hip or forearm is
diagnosed with postmenopausal osteoporosis.
Routine screening of apparently healthy people could seriously damage
their health says an editorial in a recent issue of the British Medical
Journal. This brings to my mind saying of Mark Twain which goes thus: “For
a man with a hammer in the hand, and wanting to use it badly, everything
in the world looks a nail needing hammering.”
High incidence of PMO could be because of “disease mongering” by the
pharmaceutical industries, disease mongering medicalises human life
turning ordinary ailments into medical problems, seeing mild symptoms as
serious, treating personal problems as medical, seeing risks as diseases ,
and framing prevalence estimates to maximize potential market (1). They
see what they want to see in their research!
Many times in these elderly women there is no deficiency of serum
calcium either. About 20% of postmenopausal women with osteoporosis have
hyper-calciurea, here hormone deficiency is not the only culprit, but
resorption rate is higher than formation, so physicians should think about
increased resorption not about formation rate by giving calcium
supplements etc. Present day management of PMO brings to my mind a saying
of Nin Anais: “We do not see things as they are; we see them as we are”
As long as women are asymptomatic it is better not to predict
unpredictable things and interfere with drug treatment. Sir William Osler
had warned years ago: “patient doing well-do not interfere.” All women,
irrespective of race and nationality, attain menopause and have deficiency
of hormones but incidence of PMO is high in western countries compared to
ours. There could be many reasons-increased salt intake in the preserved
food is a very important reason in addition to the weather, smoking,
alcohol, contraceptives, refined oils etc .
In conclusion: estrogen deficiency is not the only culprit and
calcium is not deficient in postmenopausal osteoporosis. The latter is
definitely age related.
References
1.Ray Moynihan, Richard Smith. Too much medicine? .BMJ 2002; 324:886-890
2.Vinayakumar M, Abul k. Abbas, Nelson Fausto: Robbins and Corton
Pathologic Basis of Disease, 7th edition 2005 pp 1283,
3.Janice Hopkins Tanne. Hormone trial for disease prevention stopped
early. BMJ 2002; 325:61
Competing interests:
None declared
Competing interests: No competing interests
editorial reduces BMJ to tabloid journalism
Professor Graeme Jones editorial is worthy of blatant tabloid
journalism with a headline of ‘increased risk of myocardial infarction
outweighs the reduction in fractures’ as he highlights that ‘there was
especially an increased risk of myocardial infarction 1.49, 0.86 to 2.57’,
and then quotes a non-significant p value of ‘P=0.16’. This title should
be retracted by the BMJ.
The paper by Bolland [1] actually states there was an upward trend
(ie non significant) in cardiovascular events. After adding unreported
events the relative risk of MI was non significant and the 95% confidence
intervals includes a potential 14% reduced risk of MI in the group taking
calcium supplements. The authors state that after this adjustment a
statistically significant increase in the number of women with any of the
end points in the calcium group was no longer found. ‘Thus the present
study does not unequivocally show an adverse cardiovascular effect of
calcium’.
Another highly selective quote is that ‘calcium based phosphate
binders are associated with increased vascular calcification in patients
about to undergo dialysis’ [2]. Chronic kidney disease results in high
levels of serum phosphate which is thought to be the main driver of medial
calcification which is also a very different process to that of intimal
plaque formation. A more balanced view is provided in Ketteler’s article
[3] supporting the use of calcium based binders in patients with CKD. All
current studies have shown no survival benefit of non-calcium based
binders over that of calcium based binders. An animal model of CKD seem to
show that treatment with calcium carbonate attenuated both plaque and
media calcification [4].
I note that Professor Graeme Jones is medical director of Arthritis
Australia which receives funds from corporate sponsorship (http://www.arthritisaustralia.com.au/About%20Us) and this should
have been declared as a potential conflict of interest.
References
1. Bolland MJ, Barber PA, Doughty RN, Mason B, Horne A, Ames R, et
al. Vascular events in healthy older women receiving calcium
supplementation: randomised controlled trial. BMJ 2008 doi:
10.1136/bmj.39440.525752.BE.
2. Russo D, Miranda I, Ruocco C, Battaglia Y, Buonanno E, Manzi S, et al.
The progression of coronary artery calcification in predialysis patients
on calcium carbonate or sevelamer. Kidney Int 2007;72:1255-61.
3. Ketteler M, Biggar P. After several years of witchhunting: Can calcium-
based phosphate binding be released on probation? Nephrol Dial Transplant.
2008 Jan;23(1):17-9. Epub 2007 Nov 26.
4. Phan O, IvanovskiO,Nikolov IG et al. Effect of oral calcium carbonate
on aortic calcification in apolipoprotein E deficient (apoE-/-) mice with
chronic renal failure. Nephrol Dial Transplant. 2008 Jan;23(1):82-90.
Competing interests:
None declared
Competing interests: No competing interests