The Effect of Autism on Bone Metabolism in Peripubertal Boys

Saturday, May 19, 2012: 10:15 AM
Osgoode Ballroom East (Sheraton Centre Toronto)
10:15 AM
A. M. Neumeyer1, A. Gates2, C. Ferrone2 and M. Misra3, (1)Lurie Center for Autism, Massachusetts General Hospital/ Harvard Medical School, Lexington, MA, (2)Lurie Center for Autism, Massachusetts General Hospital, Lexington, MA, (3)Pediatric Endocrine Unit, Massachusetts General Hospital/ Harvard Medical School, Boston, MA
Background:  

Little is known about bone metabolism in children with autism spectrum disorders (ASD).  There are many factors that may impact bone mineral density (BMD) in children with ASD including impaired calcium and vitamin D intake subsequent to unusual diets, alterations in hormones such as cortisol, gonadal steroids, growth hormone (GH) and insulin like growth factor-1 (IGF-1), and use of medications such as anticonvulsants. Cortisol levels increase in conditions of stress with possible deleterious effects on bone. GH peaks during puberty and leads to increase IGF-1 secretion; both GH and IGF-1 increase pubertal bone formation. Additionally, the gonadal steroids increase with increasing pubertal stage and reduce bone loss. Changes in these hormones could potentially impact bone. 

Objectives:  

Our objective was to determine whether BMD is lower in peripubertal boys with autism compared to controls and assess determinants of BMD in this population.  

Methods:  

In 18 peripubertal boys (mean age 10.5±0.4 years) with ASD and 19 age matched controls (11.2±0.3 years) (p=0.23) 8-14 years old we measured BMD at the spine and hip using dual energy x-ray absorptiometry (DEXA). We also assessed caloric, vitamin D and calcium intake using food records, fasting serum levels of calcium, phosphorus, 25(OH) vitamin D [25(OH)D], testosterone, IGF-1 and  salivary cortisol (AM and PM).

Results:  

Boys with autism had lower BMD Z-scores compared with healthy boys at the spine (-1.13±0.28 vs. -0.21±0.25, p=0.02), total hip (-0.71±0.03 vs. 0.14±0.29, p=0.04) and femoral neck (-1.64±0.21 vs. -0.52±0.24, p=0.001). Total caloric intake did not differ between groups.  However, dietary vitamin D intake was lower in boys with autism compared with controls (5.0±0.6 vs. 8.5±1.4 mcg/d, p=0.03) while calcium intake trended lower (878±92 vs. 1184±121 mg/d, p=0.05). These differences may reflect lower intake of milk and dairy products in ASD. Total calcium (878±92 vs. 1184±121 mg/d, p=0.05) and vitamin D (7.9±1.6, vs. 12.2±2.1 mcg/d, p=0.07) intake from diet and supplements also trended lower in boys with autism. 25(OH)D levels were lower in boys with autism (26.7±1.9 vs. 31.7±1.6 ng/ml, p=0.05), and a larger proportion of boys with autism (76.5%) than controls (36.8%) had levels <32 ng/ml. IGF-1 and testosterone levels did not differ. PM cortisol was higher in autistic boys (1.44±0.37 vs. 0.47±0.16 nmol/L, p=0.004), but did not correlate with BMD. Importantly, lower dietary vitamin D intake was a very strong predictor of lower BMD measures at all sites.  Differences between the groups at the femoral neck (p=0.02) persisted   even after controlling for dietary vitamin D.

Conclusions:

This is the first study to describe low BMD in peripubertal boys with ASD compared to controls, associated with lower dietary vitamin D intake. Further studies are necessary to investigate both the rate of bone accrual in children with ASD as well as the effect of optimizing vitamin D intake through dietary intervention.

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