Prenatal Precursor: Growth Protein Deficiency Linked to Autism

Recent studies of pre and post-natal deficiency of a growth protein associated with brain cell development in mice, insulin-like growth factor (IGF), have revealed a link between IGF and both neurological and physical, development defects. Physician-researcher Gary Steinman, MD, PhD, of Touro College of Osteopathic Medicine has hypothesized an association between IGF and the onset of autism. In his article in the journal Medical Hypotheses, Steinman proposes further direct-research with human subjects. Because IGF is instrumental in human fetal growth, understanding the association between this growth protein and developmental defects could be an early detection biomarker and perhaps a path toward prevention.

IGF stimulates brain cells to produce myelin, which insulates developing nerves. Myelin is also instrumental in protecting nerve fibers, which are the means of routing functions to and from various parts of the brain. In addition to aiding in the production of myelin, IGF directs much of the growth hormone (GH) after birth. Subsequently, an IGF deficiency encompasses both neurological defects from inhibited myelin production and physical defects from the restriction of the growth hormone.

Steinman’s theory and proposed study, Insulin-like growth factor and the etiology of autism, pulls from research spanning from intrauterine environments to postpartum factors. As a fertility research specialist, Steinman asserts the need for a stronger understanding of the prenatal precursors for autism saying, “almost nothing is currently known about the predisposing molecular and histological changes that differentiate a newborn destined to be neurologically normal from an autistic one.”




Steinman G, Mankuta D. Insulin-like growth factor and the etiology of autism. Med Hypotheses. 2013 (in press). Epub 2013 January 31.

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