AutismIntroduction

 There is mounting evidence that low serum 25-hydroxyvitamin D [25(OH)D] levels during pregnancy and early life are associated with increased risk of developing autism. 

There is mounting evidence that low serum 25-hydroxyvitamin D [25(OH)D] levels during pregnancy and early life are associated with increased risk of developing autism.

The ultraviolet-B (UVB)-vitamin D-autism hypothesis was originally proposed by John Cannell12. Evidence in support of this hypothesis includes increased prevalence of autism with increasing latitude, excess birth rate for autism in spring, low serum 25(OH)D levels for those with autism, increased risk of autism for those with darker skin, increased risk for autism born to mothers likely to have low serum 25(OH)D levels due to darker skin, increased risk of autism associated with preeclampsia, and diametrically opposed social behaviors of those with Williams syndrome.

The mechanisms whereby high serum 25(OH)D level increase the risk of autism may include protection against DNA damage of spermatocytes and ova prior to conception, impacts on fetal brain development, and reduction of oxidative stress.

To reduce the risk of autism, pregnant and nursing women should consider keeping serum 25(OH)D levels above 40-50 ng/mL, which would keep serum vitamin D levels high enough for the fetus/infant, and making sure their infants and children maintain adequate serum 25(OH)D levels. 

Autism is a disease that affects both the brain and the body. 

“Autism spectrum disorders (ASDs) are a group of developmental disabilities characterized by atypical development in socialization, communication, and behavior. ASDs typically are apparent before age 3 years, with associated impairments affecting multiple areas of a person’s life. Because no biologic marker exists for ASDs, identification is made by professionals who evaluate a child’s developmental progress to identify the presence of developmental disorders…..In 2006, on average, approximately 1% or one child in every 110 in the 11 ADDM sites was classified as having an ASD” 3

“Recent clinical studies have revealed a high prevalence of gastrointestinal symptoms, inflammation, and dysfunction in children with autism. Mild to moderate degrees of inflammation were found in both the upper and lower intestinal tract. In addition, decreased sulfation capacity of the liver, pathologic intestinal permeability, increased secretory response to intravenous secretin injection, and decreased digestive enzyme activities were reported in many children with autism. Treatment of digestive problems appears to have positive effects on autistic behavior4.” 

John Cannell’s original hypothesis12 was based on a thorough review of many lines of evidence regarding the characteristics of autism and the roles of UVB and vitamin D on neurological function. Given the importance of this hypothesis and since the reasoning involved is an excellent example of how such hypotheses can be formed from available evidence, the entire abstract is presented here:

Any theory of autism’s etiology must take into account its strong genetic basis while explaining its striking epidemiology. The apparent increase in the prevalence of autism over the last 20 years corresponds with increasing medical advice to avoid the sun, advice that has probably lowered vitamin D levels and would theoretically greatly lower activated vitamin D (calcitriol) levels in developing brains. Animal data has repeatedly shown that severe vitamin D deficiency during gestation dysregulates dozens of proteins involved in brain development and leads to rat pups with increased brain size and enlarged ventricles, abnormalities similar to those found in autistic children. Children with the Williams Syndrome, who can have greatly elevated calcitriol levels in early infancy, usually have phenotypes that are the opposite of autism. Children with vitamin D deficient rickets have several autistic markers that apparently disappear with high-dose vitamin D treatment. Estrogen and testosterone have very different effects on calcitriol’s metabolism, differences that may explain the striking male/female sex ratios in autism. Calcitriol down-regulates production of inflammatory cytokines in the brain, cytokines that have been associated with autism. Consumption of vitamin D containing fish during pregnancy reduces autistic symptoms in offspring. Autism is more common in areas of impaired UVB penetration such as poleward latitudes, urban areas, areas with high air pollution, and areas of high precipitation. Autism is more common in dark-skinned persons and severe maternal vitamin D deficiency is exceptionally common the dark-skinned. Conclusion: simple Gaussian distributions of the enzyme that activates neural calcitriol combined with widespread gestational and/or early childhood vitamin D deficiency may explain both the genetics and epidemiology of autism. If so, much of the disease is iatrogenic, brought on by medical advice to avoid the sun. Several types of studies could easily test the theory2.

Page last edited: 17 May 2011

References

  1. Cannell, J. J. Autism and vitamin D. The Vitamin D Newsletter. 2007 May;
  2. Cannell, J. J. Autism and vitamin D. Med Hypotheses. 2008; 70 (4): 750-9.
  3. Prevalence of autism spectrum disorders – Autism and Developmental Disabilities Monitoring Network, United States, 2006. MMWR Surveill Summ. 2009 Dec 18; 58 (10): 1-20.
  4. Horvath, K. Perman, J. A. Autism and gastrointestinal symptoms. Curr Gastroenterol Rep. 2002 Jun; 4 (3): 251-8.