Rickets, once a public health problem of urgent importance, has largely fallen off the public’s radar. However, many prominent vitamin D researchers are calling attention to a “resurgence of rickets,” fueled in many cases by low blood levels of vitamin D. The Mayo Clinic wondered just how much rickets has increased in recent years and what is causing it.
Nutritional rickets is a disease of improper bone mineralization caused by a deficiency of vitamin D, calcium, or phosphate. Symptoms include bone pain, low blood levels of calcium, and the “bow leg” deformity classically associated with the disease.
Due to increasing concerns that rickets is on the rise, the Mayo Clinic investigated the medical records of all children on file in Olmsted County, Minnesota between 1970 and 2009 to determine how many children were diagnosed with health conditions indicative of nutritional rickets in this time period. Radiographic confirmation was required for a diagnosis of rickets. The children with rickets were then compared with healthy controls to determine risk factors for developing the bone disease.
Children whose rickets appeared to be caused by genetic or in-born errors of metabolism (non-nutritional) were excluded. Two of the seventeen cases occurred in new immigrants from the Middle East and were thus considered “imported.” Four occurred in the children of recent Somali immigrants. The median 25(OH)D level of children diagnosed with rickets was 13 ng/mL.
Compared to healthy controls, children diagnosed with rickets were more likely to be black, breast-fed, and of lower weight and height. The researchers noted that poor feeding, a low intake of milk and meat products, low amounts of sun exposure, and prematurity were noted in the medical records of the children with rickets as potential contributors to their development of the disease.
The researchers found that while the incidence of rickets remained relatively constant between 1970 and 2000, it markedly increased after 2000. While the Mayo Clinic increased its testing of vitamin D levels ten-fold after the year 2002, they note that the majority of the children with rickets first came to the attention of medical professionals based on clinical and not biochemical abnormalities. In other words, disease symptoms and not a vitamin D test were what most frequently alerted the diagnosing doctor to the presence of a problem.
Potential reasons for the increase of rickets were offered:
Recent research in the United Kingdom and Australia indicates that the increase of rickets in recent years parallels the increase of black immigrants to these countries. Darker-skinned individuals are more likely to be vitamin D deficient, and this could be causing an increase of rickets in their children. This same situation could very likely be occurring in Olmsted County, too.
Between 1994 and 2004, the number of individuals in the US with a 25(OH)D level below 30 ng/mL doubled. The increased use of sunscreen and increased avoidance of sun are cited as reasons for this trend.
Limitations of the study include a lack of radiographs for all children with diagnostic codes indicative of rickets. The authors note that had radiographs been performed on all of these children, the number of children with the diagnosis of nutritional rickets would likely be increased. Also, the study was underpowered to detect a seasonal variation in rickets diagnoses.
The researchers urge that pregnant women be tested for vitamin D deficiency and supplemented accordingly and that all breast-fed children receive vitamin D supplements. Rickets should be suspected in children that fail to grow properly, especially those that are breast-fed and of black race.
It is important to remember that while overt vitamin D deficiency can cause rickets, the low vitamin D levels present in many children are likely contributing to subclinical bone disease that manifests in unsuspected ways. Dr. Cannell has reported extensively on this phenomena.
It is critical that pregnant women not only optimize their vitamin D levels during pregnancy, but that they take steps to ensure their infants’ adequate vitamin D status after delivery. Vitamin D is not reliably transferred in the breast milk until the mother’s 25(OH)D level is 45-50 ng/mL or higher as has been previously reported.
If the breastfeeding mother’s level is not at least 45-50 ng/mL, the baby should receive oral vitamin D supplementation. Bone disease and many other tragic conditions resulting from vitamin D deficiency are largely avoidable in pregnant women and their infants after delivery when natural levels of vitamin D are maintained.