Beth Cowell is a mother of triplets who all have been diagnosed with autism. She was given terbutaline beginning in the 20th week of her pregnancy with triplets, and believes this to be the major causative factor in the abnormal neurological development. In addition to the use of terbutaline she was given beta-methasone and magnesium sulfate causing her blood sugar levels to drop far enough to put her in a coma for about an hour. Hundreds of ultrasounds were done within the last few weeks of pregnancy and a MRI was performed 3 days before the birth. The birth was done by a cesarean section. With these multiple interventions, and all of their possible negative effects on fetal development, one might ask why point the finger at terbutaline? With a background in chemistry and the need to find some answers, Beth has researched the subject for many years. The following are some of her findings.
Terbutaline, also known as brethine, is a beta-adrenergic stimulant used to treat asthma. Using the drug to stop premature labor is an off label procedure not even approved by the drug's manufacturer or the FDA. This drug has been shown to cross the placenta and have an equal chemical concentration in the fetus as in the mother. In addition to the harmful effects to the fetus, there is a long list of side effects to the mother including chest pains and high blood pressure and can mimic toxemia.
The neurological effects, as well as the outward behavioral expression, can be identical to autism. The receptor cells in the brain that are affected by this drug are normally activated during neural migration to stop cell division and allow these cells to differentiate. This is the process necessary for development of specific parts of the brain controlling certain organs and physiological coordination. When this is activated prematurely a number of results can occur including a low nerve cell count in the brain and overproduction of neuropeptides and hormones such as dopamine, norepinephrine, vasopressin and ADH (antidiuretic hormone). Synapses between nerves develop abnormally, thus changing the ability of the nervous system to fire in a timely and coordinated fashion. The total picture becomes one of disorganization in the central nervous system and concurrent physiological and behavioral dysfunction. These neurological findings are similar to those found in the brains of children with autism. Premature stimulation of these receptors can occur from events other than terbutaline exposure and may play a causal role in the etiology of autism.
One research study shows an early shift in the autonomic nervous system from sympathetic to parasympathetic, thus causing abnormal neurovisceral control such as heart function. This may be a key factor in the chiropractic care of these children. The balancing of the autonomic nervous system is an integral part of many chiropractic techniques and may be a necessary element in the correction of the subluxation. In an animal study, the researchers found that the uptake of norepinephrine in the cerebellum was negatively affected. Again sympathetic influence of the brain is involved and this study shows a direct pathway for this drug to effect behavioral components of development.
Beth is continuing to research the subject. She is also writing to inform others as well as helping create new research models for further studies. Beth has found 45 other families who have had the same experience with their children. Please let women know the possible dangers! Also, please ask about this in the history of any of your patients with autism and let us know with a case study. The triplets have been under chiropractic care and there will hopefully be results to report in the future.
- Crowell B, "Does Premature beta-adrenergic stimulation play a causal role in the etiology of autism?"
- Hou QC; Slotkin TA. Effects of prenatal dexamethasone or terbutaline exposure on development of neural and intrinsic control of heart rate. Pediatr Res 1989; 26(6):554-7
- Slotkin TA, et al, Prenatal terbutaline exposure in the rat: selective effects on development of noradrenergic projections to cerebellum. Brain Res Bull 1989; 23(4-5):263-5