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Calcium ghost:Too difficult to die
- Dr.Basavaraj. Shivayogi Hadapad (24 January 2008)
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Death By Medicine ?
- Dr. Herbert H. Nehrlich (5 February 2008)
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editorial reduces BMJ to tabloid journalism
- David Ansell (13 February 2008)
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Dr.Basavaraj. Shivayogi Hadapad, Associate Professor of Ayurveda Manipal University,Maniapl, India - 576104
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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 |
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Dr. Herbert H. Nehrlich, Private Practice Bribie Island, Australia 4507
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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 |
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David Ansell, Director, UK Renal Registry Southmead Hospital, BS10 5NB
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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 |
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