Tropical Medicine and International Health
doi:10.1111/tmi.12444
volume 00 no 00
Editorial
We are what we eat – is it time to reconsider calcium-deficiency rickets in Nigeria? (FA*) Christopher A. Sharp1, Per Magnusson1, Michael W. J. Davie2 and Lawrence M. Oginni3 1 Department of Clinical Chemistry and Department of Clinical & Experimental Medicine, Link€ oping University, SE-581 85 Link€ oping, Sweden 2 Charles Salt Centre for Human Metabolism, Robert Jones & Agnes Hunt Orthopaedic Hospital, Oswestry, UK 3 Department of Orthopaedic Surgery & Traumatology, College of Health Sciences, Obafemi Awolowo University, Ile-Ife, Nigeria
keywords nutrition, calcium deficiency, rickets, gut microbiota Rickets remains a significant health problem in West Africa (Jarrett et al. 2013). Some time ago, we (Oginni et al. 1996) and others (Thacher et al. 1997) followed up on earlier work that had described a form of rickets observed in adolescents in South Africa and in younger children in Nigeria that was refractive to vitamin D (Pettifor et al. 1981; Okonofua et al. 1991). Since then similar findings have been reported from around the world (Prentice 2013). In Nigeria, clinical studies have confirmed calcium-deficiency as the cause of this condition with radiological and biochemical healing evident after simple treatment with palatable oral calcium preparations (Oginni et al. 1999, 2003). This treatment response has since been reproduced (Thacher et al. 1999) and in a recent, more comprehensive, study the addition of vitamin D has been found to augment bone healing (Thacher et al. 2014). Calcium homoeostasis is maintained by hormonal regulation of intestinal absorption and renal reabsorption. During growth, the body’s calcium requirement increases and the calcium absorption efficiency can increase more than 60% compared with adult steady-state conditions. Fifteen to forty percent of all consumed calcium is absorbed from the intestine and in the case of low calcium intake a greater fraction is absorbed than at higher calcium intakes. However, this adaptation to nutritional calcium content is a slow process associated with complex changes in the calcium-transporting mechanisms in the gut mucosal cells (Larsson & Magnusson 2004). With this knowledge the possible causes and mechanisms of this childhood calcium-deficiency disorder were sought in wide-ranging studies of Nigerian children that included investigation of the factors associated with the condition
(Thacher et al. 2000), calcium uptake (Graff et al. 2004), mutations in the vitamin D receptor gene (Fischer et al. 2000) and knee joint angle development (Oginni et al. 2004). From India, Teotia et al. (1998) described a similar skeletal condition presenting in a cohort of patients with fluoride toxicity. However, to our knowledge, an explanation as to why a relatively small proportion of children manifest this condition in Nigeria has yet to be proposed. To put succinctly, why do some children living in similar environments develop calcium-deficiency rickets and others do not? The nutritional needs of the body are complex and change throughout life and it is now widely accepted that dietary calcium is limited (
doi:10.1111/tmi.12444
volume 00 no 00
Editorial
We are what we eat – is it time to reconsider calcium-deficiency rickets in Nigeria? (FA*) Christopher A. Sharp1, Per Magnusson1, Michael W. J. Davie2 and Lawrence M. Oginni3 1 Department of Clinical Chemistry and Department of Clinical & Experimental Medicine, Link€ oping University, SE-581 85 Link€ oping, Sweden 2 Charles Salt Centre for Human Metabolism, Robert Jones & Agnes Hunt Orthopaedic Hospital, Oswestry, UK 3 Department of Orthopaedic Surgery & Traumatology, College of Health Sciences, Obafemi Awolowo University, Ile-Ife, Nigeria
keywords nutrition, calcium deficiency, rickets, gut microbiota Rickets remains a significant health problem in West Africa (Jarrett et al. 2013). Some time ago, we (Oginni et al. 1996) and others (Thacher et al. 1997) followed up on earlier work that had described a form of rickets observed in adolescents in South Africa and in younger children in Nigeria that was refractive to vitamin D (Pettifor et al. 1981; Okonofua et al. 1991). Since then similar findings have been reported from around the world (Prentice 2013). In Nigeria, clinical studies have confirmed calcium-deficiency as the cause of this condition with radiological and biochemical healing evident after simple treatment with palatable oral calcium preparations (Oginni et al. 1999, 2003). This treatment response has since been reproduced (Thacher et al. 1999) and in a recent, more comprehensive, study the addition of vitamin D has been found to augment bone healing (Thacher et al. 2014). Calcium homoeostasis is maintained by hormonal regulation of intestinal absorption and renal reabsorption. During growth, the body’s calcium requirement increases and the calcium absorption efficiency can increase more than 60% compared with adult steady-state conditions. Fifteen to forty percent of all consumed calcium is absorbed from the intestine and in the case of low calcium intake a greater fraction is absorbed than at higher calcium intakes. However, this adaptation to nutritional calcium content is a slow process associated with complex changes in the calcium-transporting mechanisms in the gut mucosal cells (Larsson & Magnusson 2004). With this knowledge the possible causes and mechanisms of this childhood calcium-deficiency disorder were sought in wide-ranging studies of Nigerian children that included investigation of the factors associated with the condition
(Thacher et al. 2000), calcium uptake (Graff et al. 2004), mutations in the vitamin D receptor gene (Fischer et al. 2000) and knee joint angle development (Oginni et al. 2004). From India, Teotia et al. (1998) described a similar skeletal condition presenting in a cohort of patients with fluoride toxicity. However, to our knowledge, an explanation as to why a relatively small proportion of children manifest this condition in Nigeria has yet to be proposed. To put succinctly, why do some children living in similar environments develop calcium-deficiency rickets and others do not? The nutritional needs of the body are complex and change throughout life and it is now widely accepted that dietary calcium is limited (
