August 22, 2005

Terbutaline's Contribution to Autism

Terbutaline is a new piece of the autism puzzle, and I am learning how exactly it fits into the picture in Chandler’s autism. Duke University says that it has a causal link to the disorder, and it does so by making the brain more vulnerable to toxins. In the case of the Duke Study, the toxin that they identified was a pesticide. I don’t know if they looked at increased risk of mercury toxicity, although it seems logical that if the brain has been made vulnerable to one kind of toxin, increased vulnerability to all is possible/probable.

I had not heard about the Hopkins twin study.

If you are a terbutaline mom, you might want to take a listen:

- Terbutaline and autism connection? Listen to Dr. Larry Kaplan on AutismOne Radio, Tuesday, August 23rd at 10:30 am ET. (http://autismone.org/radio/)

- Is there a connection between the pre-term labor drug Terbutaline and autism? To
find out additional information about this controversial issue, listen to AutismOne radio at http://autismone.org/radio/ this Tuesday, August 23rd at 10:30 am Eastern Time. Teri Small interviews Dr. Larry Kaplan to discuss this off-label drug prescribed for pre-term labor. Hear the facts about maternal, fetal, and neonatal side effects, the Johns Hopkins study of fraternal twin pairs, and the Duke University study.

9 comments:

samfredpat said...

I was given turbutaline for my 2nd pregnancy at 27 weeks. My second son was born at 37 weeks. He was diagnosed with autism just prior to his 2nd birthday. I have two other boys ages 4 and 18 months who are typical both of which I did not have to take turbutaline. If anyone knows anything more about this connection or how I can help the research, please email me at masderf3@hotmail.com
THanks

Anonymous said...

I was given terbutaline in the third trimester of my pregnancy with my first son, and took it for a few weeks until he reached 37 weeks. He was born a few days after I came off the medication and bedrest. He was diagnosed with infantile torticollis (head-tilt caused by inutero positioning or birth injury) at four months, and though we have not had him officially diagnosed for autism, he exhibits many of the symptoms and his Early Intervention Therapists believe he has it. I had a second son less than two months ago, did not take terbutaline with that pregnancy, and his behavior is already noticeably different than my first son's. If I can be of help with research, feel free to contact me at jreig@swwnet.com

Anonymous said...

Take your research and your OB info and see an attorney

cindy said...

I was given terbutaline for my identical twins both diagnosed with Autism. This is scary.

See my blog:
autismpreventiondiet.blogspot.com
howtostartgfcf.com

Tracy Hoogenboom said...

We support hundreds of high-risk moms every year and while there seems to be so many unanswered questions about autism, it might be a far stretch to relate it to terbutaline use in pregnancy. Here is a good link to information:
http://www.sidelines.org/frequent-questions/index.cfm#autism

Tracy
Sidelines National Support Network

Tracy Hoogenboom said...

By the way, I had triplets plus one, all exposed to terbutaline, procardia, mag sulphate, and no child with autism.

Ginger Taylor said...

There is more evidence than that Tracy:

J Child Neurol. 2005 Nov;20(11):876-84.
beta2-adrenergic receptor activation and genetic polymorphisms in autism: data from dizygotic twins.

Connors SL, Crowell DE, Eberhart CG, Copeland J, Newschaffer CJ, Spence SJ, Zimmerman AW.

Department of Neurology and Developmental Medicine, Kennedy Krieger Institute, Baltimore, MD 21205, USA.

Gestational and genetic factors can contribute to autism during infancy and early childhood through their effects on fetal brain development. Previous twin studies have shown strong genetic components for the development of autism, a disorder that can have multiple causes. We investigated the effects of prenatal overstimulation of the beta2-adrenergic receptor in dizygotic twins who were exposed to terbutaline, a selective beta2-adrenergic receptor agonist used to treat premature labor, as a gestational factor. As a possible genetic mechanism, we studied two beta2-adrenergic receptor polymorphisms in twins from whom DNA was available: glycine substitution at codon 16 (16G) and glutamic acid substitution at codon 27 (27E), which show diminished desensitization in vivo compared with the wild-type receptor. Continuous terbutaline exposure for 2 weeks or longer was associated with increased concordance for autism spectrum disorders in dizygotic twins (relative risk = 2.0), with a further increase in the risk for male twins with no other affected siblings (relative risk = 4.4). A significant association was found between the presence of 16G and 27E polymorphisms in autistic patients compared with population controls (P = .006). Prenatal overstimulation of the beta2-adrenergic receptor by terbutaline or by increased signaling of genetic polymorphisms of the beta2-adrenergic receptor that have diminished desensitization can affect cellular responses and developmental programs in the fetal brain, leading to autism.

PMID: 16417856 [PubMed - indexed for MEDLINE]

Ginger Taylor said...

J Pharmacol Exp Ther. 2007 Jul;322(1):16-22. Epub 2007 Mar 30.
Neuroinflammation and behavioral abnormalities after neonatal terbutaline treatment in rats: implications for autism.

Zerrate MC, Pletnikov M, Connors SL, Vargas DL, Seidler FJ, Zimmerman AW, Slotkin TA, Pardo CA.

Department of Neurology, Pathology 627, 600 N. Wolfe St., Baltimore, MD 21287, USA.

Autism is a neurodevelopmental disorder presenting before 3 years of age with deficits in communication and social skills and repetitive behaviors. In addition to genetic influences, recent studies suggest that prenatal drug or chemical exposures are risk factors for autism. Terbutaline, a beta2-adrenoceptor agonist used to arrest preterm labor, has been associated with increased concordance for autism in dizygotic twins. We studied the effects of terbutaline on microglial activation in different brain regions and behavioral outcomes in developing rats. Newborn rats were given terbutaline (10 mg/kg) daily on postnatal days (PN) 2 to 5 or PN 11 to 14 and examined 24 h after the last dose and at PN 30. Immunohistochemical studies showed that administration of terbutaline on PN 2 to 5 produced a robust increase in microglial activation on PN 30 in the cerebral cortex, as well as in cerebellar and cerebrocortical white matter. None of these effects occurred in animals given terbutaline on PN 11 to 14. In behavioral tests, animals treated with terbutaline on PN 2 to 5 showed consistent patterns of hyper-reactivity to novelty and aversive stimuli when assessed in a novel open field, as well as in the acoustic startle response test. Our findings indicate that beta2-adrenoceptor overstimulation during an early critical period results in microglial activation associated with innate neuroinflammatory pathways and behavioral abnormalities, similar to those described in autism. This study provides a useful animal model for understanding the neuropathological processes underlying autism spectrum disorders.

PMID: 17400887 [PubMed - indexed for MEDLINE]

Ginger Taylor said...

Do terbutaline- and mold-associated impairments of the brain and lung relate to autism?

Kilburn KH, Thrasher JD, Immers NB.

Neuro-Test Inc., Pasadena, California, USA. khkilburn@sbcglobal.net

Increased prevalence of the autism spectrum disorders (ASD) and the failure to find genetic explanations has pushed the hunt for environmental causes. These disorders are defined clinically but lack objective characterization. To meet this need, we measured neurobehavioral and pulmonary functions in eight ASD boys aged 8 to 19 years diagnosed clinically and compared them to 145 unaffected children from a community with no known chemical exposures. As 6 of 35 consecutive mold/mycotoxin (mold)-exposed children aged 5 to 13 years had ASD, we compared them to the 29 non-ASD mold-exposed children, and to the eight ASD boys. Comparisons were adjusted for age, height, weight, and grade attained in school. The eight ASD boys averaged 6.8 abnormalities compared to 1.0 in community control boys. The six mold-exposed ASD children averaged 12.2 abnormalities. The most frequent abnormality in both groups was balance, followed by visual field quadrants, and then prolonged blink reflex latency. Neuropsychological abnormalities were more frequent in mold-exposed than in terbutaline-exposed children and included digit symbol substitution, peg placement, fingertip number writing errors, and picture completion. Profile of mood status scores averaged 26.8 in terbutaline-exposed, 52 in mold exposed, and 26 in unexposed. The mean frequencies of 35 symptoms were 4.7 in terbutaline, 5.4 in mold/mycotoxins exposed and 1.7 in community controls.