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Dietary calcium deficiency & rickets.

Sir,

In the March 2008 issue of the Journal, Teotia and Teotia reviewed their extensive experience of nutritional bone disease in India gained through over 40 yr of research in the field (1). In one section, they discuss the role of dietary calcium deficiency in the pathogenesis of rickets in children and state categorically that "our observations provide scientific proof of evidence that calcium deficiency alone does not produce rickets" and then go on to suggest that the reports of dietary calcium deficiency are in fact "the syndromes of calcium deficiency and fluoride interactions". We wish to refute their arguments. In South Africa, where the first cases of rickets caused by low dietary calcium intakes were described in otherwise healthy children (2), water fluoride was measured from a number of boreholes and surface water in the community of Driefontein from which the children came and ali had levels ranging from 0.05-0.1 ppm (3). lt is unclear from where Teotia and Teotia obtained the figures of 5.5 to 14.5 ppm, which they suggest was the water fluoride content in the area of Driefontein. lt is possible they are confusing the study with another of ours where we did in fact report on the presence of rachitic like lesions in children living in another part of South Africa where endemic fluorosis was evident and water fluoride concentrations ranged from 8-12 ppm (4). A number of reports of dietary calcium deficiency causing rickets in Nigeria have also been published. Once again it is unclear where the Teotias obtained their quoted fluoride values (2.4-4.5 ppm) from, as in the Jos region where extensive work on dietary calcium deficiency rickets has been reported (5,6), water fluoride levels are undetectable or very low (S. Porter, personal communication). In Bangladesh, dietary calcium deficiency rickets has been reported from the Chakaria region (7,8). Once again the Teotias quote fluoride levels of 2.9-5.5 ppm, yet measured fluoride levels in the Chakaria region averaged 0.5 ppm with many water samples having undetectable levels (J. Arnaud, personal communication). Thus we have been unable to find elevated fluoride levels in any of the sites where we have described dietary calcium deficiency as a cause of rickets, and thus believe that endemic fluorosis has no part to play (emphasis ours) in the pathogenesis of the bone disease we have reported. However, we also believe that where high water fluoride levels are present, these combine with low dietary calcium intakes to exacerbate rachitic like bone deformities and biochemical abnormalities in children.

Teotias are correct in saying that dietary calcium deficiency probably does not act alone in most situations in the pathogenesis of nutritional rickets (1). We have suggested that genetic factors (9), other dietary constituents such as oxalates and phytates, relative boron deficiency (8) and vitamin D insufficiency (10) might all play variable roles. In contrast, the association between aluminium excess and calcium deficiency has been excluded (11). What is clear, however, is that the bone disease and biochemical perturbations respond completely to an increase in the dietary calcium content alone, indicating that whatever secondary role other factors might be playing, low dietary calcium intakes are primarily responsible (5).

John M. Pettifor *, Philip R. Fischer ** Tom D. Thacher ([dagger]), Josiane Arnaud ([double dagger]) & Craig A. Meissner ([double dagger][double dagger])

* Department of Paediatrics, Chris Hani Baragwanath Hospital & the University of the Witwatersrand Johannesburg, South Africa

** Department of Pediatric & Adolescent Medicine Mayo Clinic, Minnesota, USA

([dagger]) Department of Family Medicine Mayo Clinic, Minnesota, USA

* Department of Integrated Biology University Hospital Grenoble, France &

([double dagger])([double dagger]) Department of Crops & Soils Cornell University, Dhaka, Bangladesh

* For correspondence: John.pettifor@wits.ac.za

References

(1.) Teotia SPS, Teotia M. Nutritional bone disease in Indian population. Indian J Med Res 2008; 127 : 219-28.

(2.) Pettifor JM, Ross P, Wang J, Moodley G, Couper-Smith J. Rickets in children of rumi origin in South Africa: is low dietary calcium a factor? d Pediatr 1978; 92 : 320-4.

(3.) Pettifor JM. Dietary calcium deficiency. In: Glorieux FH, editor. Rickets. New York: Nestec, Vevey; Raven Press; 1991. p. 123-43.

(4.) Pettifor JM, Schnitzler CM, Ross FP, Moodley GP. Endemic skeletal fluorosis in children: hypocalcemia and the presence of renal resistance to parathyroid hormone. Bone Miner 1989; 7 : 275-88.

(5.) Thacher TD, Fischer PR, Pettifor JM, Lawson JO, lsichei CO, Reading JC, et al. A comparison of calcium, vitamin D, or both for nutritional rickets in Nigerian children. N Engld Med 1999; 341 : 563-8.

(6.) Thacher TD, Fischer PR, Pettifor JM, Lawson JO, lsichei C, Chan GM. Case-control study of factors associated with nutritional rickets in Nigerian children, d Pediatr 2000; 137 : 367-73.

(7.) Arnaud J, Pettifor JM, Cimma JP, Fischer PR, Craviari T, Meisner C, et al. Clinical and radiographic improvement of rickets in Bangladeshi children as a result of nutritional advice. Ann Trop Paediatr 2007; 27 : 185-91.

(8.) Fischer PR, Rahman A, Cimma JP, Kyaw-Myint TO, Kabir AR, Talukder K, et al. Nutritional rickets without vitamin D deficiency in Bangladesh. J Trop Pediatr 1999; 45 : 291-3.

(9.) Fischer PR, Thaeher TD, Pettifor JM, Jorde LB, Eccleshall TR, Feldman D. Vitamin D receptor polymorphisms and nutritional rickets in Nigerian children, d Bone Miner Res 2000; 15 : 2206-10.

(10.) Thacher TD, Fischer PR, Isichei CO, Pettifor JM. Early response to vitamin D(2) in children with calcium deficiency rickets. JPediatr 2006; 149: 840-4.

(11.) Cimma JP, Arnaud J, Labarere J, Guillard O, Nugues le; Marrauld A, et al. Effect of consumption of food cooked in aluminium or stainless-steel pots on Bangladeshi children with calcium-deficient rickets: an eight month trial. J Trace Elem Med Biol 2004; 17 : 249-53.

Authors' response

We refute Pettifor's arguments (1) based on our 40 years of systematized scientific research, observations and conclusions that provide the scientific evidence that calcium deficiency alone does not cause rickets (2-11). We are summarizing the errors in Pettifor's, studies (South Africa) and from Nigeria and Bangladesh (12-14).

(i) In 1983 Pettifor presented a paper (15) on calcium deficiency rickets in the conference "Clinical disorders of bone & mineral metabolism" at Detroit, Michigan. I opined that all his patients are of endemic skeletal fluorosis and calcium deficiency interaction syndromes and not of calcium deficiency rickets.

(ii) In 1988 at the same conference, Pettifor presented a poster (16) on ricketic skeletal deformities caused by low dietary calcium intakes and fluoride synergistic actions in South Africa in areas with water fluoride 8-12 ppm, perhaps due to my comments in 1983 as referred above.

The errors in Pettifor's, Nigerian and Bangladesh studies include:

(i) Patients reported from S. Africa and Nigeria were only hospital-based and no epidemiological surveys on calcium deficiency rickets in the representative populations to serve as controls. The emerging cross-sectional picture would have provided not only (a) the prevalence of rickets; and (b) the extent to which the rickets is likely to relate to low calcium intakes.

(ii) No study has been undertaken to measure the fluoride content of the drinking water and its aetiopathological relationship in the causation of rickets in calcium deficient and normal children.

(iii) In our experience, as little as 2 ppm fluoride in drinking water taken continuously for more than six months can produce skeletal fluorosis (9). Fluoride accumulates faster and greater in the metabolically active bones of the children, inhibits mineralization and causes rickets which is more severe and complex in calcium deficient children (9,11).

(iv) Calcium deficiency rickets in S. Africa has been reported around Johannesburg (Southern Transval, South-eastern Transval, Northern Natal, Driefontein, Piet-Retief, Kenhardt) in rural Blacks consuming drinking water from ponds and superficial wells. The concentration of fluoride in the drinking water in these areas ranged from 5.5-14.5 ppm, estimated using specific fluoride ion electrode and PHM 64 radiometer during personal surveys of the above areas (8). The concentration of fluoride in South Africa varied from 0.3-35 ppm to as high as 58 ppm (17).

(v) Similarly children reported from Nigeria with calcium deficiency rickets were drinking ground water with a fluoride content 2.4-4.5 ppm (8).

(vi) My visit to Bangladesh (Chakaria region) (8) revealed that the children living in the home for the disabled, developed vitamin D deficiency due to lack of exposure to sunlight (UVR 290-315 nm) and diets severely deficient in calcium and other nutrients. They were drinking water from the superficial uncovered wells and the hand pumps with the fluoride content of 2.9-5.6 ppm. Bone disease and rickets in these children resulted due to the combined effects of calcium deficiency, vitamin D deficiency and fluoride toxicity interactions.

(vii) We are surprised that Pettifor has mentioned the very low (0.05-0.1ppm) water fluoride values in his letter to the editor (18). The fluoride values had never been mentioned in any of his earlier publications from South Africa and from Nigeria or Bangladesh. Now only he has mentioned the water fluoride values in his letter to the editor.

(viii) Improvement reported by Pettifor in hospitalized children, only on calcium supplementations is not correct. In fact in these children improvement could have occurred due to (a) on hospitalization the exposure of children to endemic fluoride had ceased; and (b) calcium intake and diet had improved. Calcium is the most effective antagonist of fluoride toxicity and inhibits the toxic effects of fluoride on bone and bone mineral metabolism (8,10,11).

(ix) Also, Jackson from Pettifor's areas of study, reported Kenhardt bone disease (named after the village studied) in rural Blacks and subsequently attributed it to calcium deficiency and fluoride interactions (19).

(x) There is thus a strong epidemiological and scientific proof that all the children reported as calcium deficiency rickets by Pettifor (South Africa) and from Nigeria and Bangladesh (12-14) were exposed to high intakes of endemic fluoride and in fact cases of the syndromes of calcium deficiency and fluoride interactions. Jackson's research and our studies had resolved the existing "Stirred controversy on calcium deficiency rickets" to change medical practice. Each case of calcium deficiency presenting as rickets should be investigated for lack of exposure to sunlight (vitamin D deficiency) and over exposure to endemic fluoride (also fluoridated water) or some combinations (8).

S.P.S. Teotia * & M. Teotia

Sri Sathya Sai Charan

# 14-15, Hanuman Road

Sai Colony

Belthur, Kadugudi

Bangalore 560 067, India

* For correspondence:

teotia9@yahoo.com

References

(1.) Pettifor JM, Vitamin D & / or calcium deficiency tickets in infants & children: a global perspective. Indian d Med Res 2008; 127 : 245-9.

(2.) Faccini JM, Teotia SPS, Teotia M. Bone static and dynamic histomorphometry in fluorosis and calcium deficiency interaction syndromes. Calc Tiss Res 1974; 16 : 45-57.

(3.) Teotia SPS, Teotia M. Fluoride and calcium interactions: syndromes of bone disease and deformities (human studies). In: Frame B, Potts, JT Jr, editors. Clinical disorders of bone and mineral metabolism. Amsterdam: Excerpta Medica; 1983. p. 520-1.

(4.) Teotia SPS, Teotia M. Endemic skeletal fluorosis and calcium nutrition clinical and radiological variants (Review of 25 years of personal research). Fluoride 1988; 21 : 39-44.

(5.) Teotia M, Teotia SPS. An epidemiological study of dietary calcium deficiency bone disease in children living in endemic and non-endemic fluorosis villages. Indian J Environ Toxicol 1988; 31 : 172-7.

(6.) Teotia SPS, Teotia M. Endemic bone disease and deformities consequent to disorders in nutrition, bone and mineral metabolism and related hormones. New Delhi: Indian Council of Medical Research; 1992. p. l-112.

(7.) Teotia M, Teotia SPS, Singh KP. Endemic chronic fluoride toxicity and dietary calcium deficiency interaction syndromes of metabolic bone disease and deformities in India. Indian J Pediatr 1998; 65 : 371-81.

(8.) Teotia SPS, Teotia M. Calcium deficiency tickets: Scientific revelation--calcium deficiency to fluoride interactions. In: Teotia SPS, Teotia M, editors. Nutritional and metabolic bone and stone disease: An Asian perspective, 1st ed. New Delhi: CBS Publishers; 2008. p. 274-89.

(9.) Teotia SPS, Teotia M. Endemic fluorosis: A challenging national health problem. J Assoc Physician India 1984; 32 : 347-52.

(10.) Teotia M, Teotia SPS, Kunwar KB. Endemic skeletal fluorosis. Arch Dis Child 1971; 46 : 686-91.

(11.) Teotia M, Teotia SPS, Singh RK. Skeletal fluoride toxicity in children is more severe and complex in calcium deficient children. Indian J Pediatr 1979; 46: 389-96.

(12.) Pettifor JM, Ross FP, Wang J, Moodley GP, Coupersmith J. Rickets in children of rural origin in South Africa: Is low dietary calcium a factor? J Pediatr 1978; 92 : 320-4.

(13.) Oginni LM, Worsfold M, Oyelami OA, Sharp CA, Powell DE, Davie MWJ. Etiology of rickets in Nigerian children. J Pediatr 1996; 128: 692-4.

(14.) Fischer PR, Rahman A, Cimma JP, Kyaw-Myint TO, Kabir ARML, Talukder K, et al. Nutritional rickets without vitamin D deficiency in Bangladesh. J Trop Pediatr 1999; 45 : 291-3.

(15.) Pettifor JM, Sochett E, Quirk M. Ostomalacia in pseudohypoparathyroidism--the role of hypocalcemia and hyperparathyroidism. In: frame B, Potts JT Jr. editors. Clinical disorders of bone and mineral metabolism. Amsterdam: Excerpta Medica; 1983. p. 525.

(16.) Pettifor JM, Moodley GP, Quirk M, Cavalerus M. Skeletal deformities, hyperosteoidosis and elevated 1,25 dihydroxy vitamin D levels in children from an area of endemic fluorosis (poster, abstract no. 80). In: Kleerekoper M, Krane S, editors. Clinical disorders of bone and mineral metabolism (abstracts). Detroit, Michigan; 1988. p. 31.

(17.) Louw AJ, Chickte UME. Fluoride and fluorosis: The status on research in South Africa. In: Dahi E, Nielsen JM, editors. Proceedings of the 2"d International workshop on fluorosis and defluoridation of water. Nazareth, Ethiopia:The International Society for Fluoride Research; 1997. p. 15-23.

(18.) Pettifor JM, Fischer PR, Thacher TD, Arnaud J, Meissher CA. Dietary calcium deficiency & rickets. Indian J Med Res 2008; 128 : 673-4.

(19.) Jackson WPU. Further observations on the Kenhardt bone disease and its relation to fluorosis. S Afr Med J 1962; 36 : 932-6.
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Article Details
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Title Annotation:Correspondence
Author:Pettifor, John M.; Fischer, Philip R.; Thacher, Tom D.; Arnaud, Josiane; Meissner, Craig A.
Publication:Indian Journal of Medical Research
Article Type:Letter to the editor
Date:Nov 1, 2008
Words:2286
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