Overgrowth, Autism, and Vitamin A and Vitamin D
Excessive infant supplementation of vitamin A and vitamin D: a risk factor for early overgrowth and autism?
Mr. Seth S. Bittker1*, Dr. Thomas E. Bittker, M.D.2
*Corresponding author: Seth S. Bittker
117 Edmond Street, Darien, Connecticut 06820
2Reno Psychiatric Associates, 80 Continental Drive, Reno, Nevada 89509
We commend the article by Campbell, et al. on “Early Generalized Overgrowth in Autism Spectrum Disorders” appearing in the October issue of the Journal of the American Academy of Child & Adolescent Psychiatry and appreciate their work showing that it is not just neurological overgrowth that is a risk factor for autism but also non-neurological overgrowth as well. We also applaud Campbell, et al.’s suggestion that factors which may upregulate such growth in infants warrant examination.
With respect to such factors, while genetics and known environmental toxins should be considered, a policy of universal vitamin A and D supplementation among infants is a risk factor that compels closer examination. Zhou et al. has suggested previously an association between excessive vitamin consumption in infancy and autism.i
Vitamin A and vitamin D in particular are fundamental to growth in infancy and deficiency can cause stunted growth.ii This suggests excessive consumption of these vitamins among infants could plausibly be a risk factor for the generalized overgrowth that Campbell, et al. describe. In addition Tekes, et al. found when baby rats are given a single large dose of a combination of vitamin A and vitamin D, there are life-long effects in the brain including monoamine neurotransmitter dysregulation.iii Zhou, et al. has observed that such neurotransmitter dysregulation is also characteristic of autism.i
But what happens when one takes human infants and gives them large doses of vitamin A and vitamin D? Such experimentation would seem to be unethical. However, as Tekes observed significant supplementation of these vitamins in infancy is common in most developed countries.iii So it may be revealing to examine autism prevalence in years in which supplementation regimes were first implemented. For example, in 1978 in an effort to combat rickets, Sweden’s National Board of Health and Welfare began recommending daily supplements of 3300 IU of vitamins A and 400 IU of vitamin D for all infants from ages 6 weeks to 6 years.iv And what was the effect of this policy in Sweden? Gillberg, et al. in their careful study of registered prevalence of autism in Goteborg, Sweden tracked autism by birth year. For birth year 1978 there were 10 cases of autism in Goteborg. For birth year 1979 there were 21 cases of autism in Goteborg. This represents a 110% increase. While there were variations in the number of cases of autism in nearby birth years, it is worth noting that in no future years did the number of cases ever approach the lower levels associated with birth years 1977 and 1978 and the percentage increase in cases was by far the greatest between 1978 and 1979.v We find this evidence is troubling, and we believe that additional research in this area is warranted.
Conflicts of Interest
The authors declare they have no conflict of interest regarding publication of this letter.
i Zhou SS, Zhou YM, Li D, Ma Q. Early infant exposure to excess multivitamin: a risk factor for autism? Autism Res Treat. 2013:963697.
ii Rolfes SR, Pinna K, Whitney E. Understanding Normal and Clinical Nutrition. 2011: 358,364.
iii Tekes K, Gyenge M, Folyovich A, Csaba G. Influence of neonatal vitamin A or vitamin D treatment on the concentration of biogenic amines and their metabolites in the adult rat brain. Horm Metab Res. 2009;41: 277-280.
iv Blomquist HK, Frangsmyr A, Hernell O, Stenberg B, Back O. Dietary intake of vitamin D during the second half of infancy in Swedish infants. Scandinavian Journal of Nutrition. 2004;48:173-177.
v Gillberg C, Cederlund M, Lamberg K, Zeijlon L. Brief Report: “The Autism Epidemic”. The Registered Prevalence of Autism in a Swedish Urban Area. Journal of Autism and Dev Disorders. 2006;36:429-435.