You are here

Researcher Identifies Potential Cause of Autism

Theory points to risk of IGF inhibitors in pregnant women (Jan. 31)

A physician-researcher at Touro College of Osteopathic Medicine in New York, N.Y., has reported a potential connection between autism and a growth protein that could eventually be used as a way to predict an infant's propensity to later develop the disease. The protein — insulin-like growth factor (IGF) — is involved in the normal growth and development of babies' brain cells.

Based on findings of prior published studies, researcher Gary Steinman, MD, PhD, proposes that depressed levels of this protein in the blood of newborns could potentially serve as a biomarker for the later development of autism. However, this connection has never been directly studied.

Steinman presented his theory in the Jan. 31 online edition of Medical Hypotheses.

“Insulin-like growth factor-1 directly affects the rate at which oligodendrocytes promote myelination in the central nervous system, especially in the brain,” Steinman writes. “Factors which reduce the production or availability of IGF could retard normal nerve programming in the fetus or neonate. Thus, it would be desirable to arrest the pathologic processes of autism in the early neonatal stage before irreversible nerve damage occurs.”

If corroborated, Steinman’s theory could point to potential risks to pregnant women and women of child-bearing age of drugs able to lower IGF levels, of which there are several — pegvisomant (Somavert, Pfizer), octreotide (Sandostatin, Novartis), bromocriptine (Parlodel, Novartis), and several experimental IGF receptor antagonists.

Source: Elsevier; January 31, 2013.

Recent Headlines

Despite older, sicker patients, mortality rate fell by a third in 10 years
Study finds fewer than half of trials followed the law
WHO to meet tomorrow to decide on international public heath emergency declaration
Study of posted prices finds wild variations and missing data
Potential contamination could lead to supply chain disruptions
Declining lung cancer mortality helped fuel the progress
Kinase inhibitor targets tumors with a PDGFRA exon 18 mutation
Delayed surgery reduces benefits; premature surgery raises risks
Mortality nearly doubled when patients stopped using their drugs