Growth hormone response to L-dopa and clonidine in autistic children.
Autistic kids hit the same growth-hormone peak as peers, but the clock is off—early with clonidine, late with L-dopa.
01Research in Context
What this study did
Doctors gave two drugs to 24 autistic kids and 24 matched controls. One drug was L-dopa, the other clonidine. Both make the brain release growth hormone.
The team drew blood every 15 minutes for two hours. They watched when the hormone spike happened, not just how high it went.
What they found
Peak hormone levels were the same in both groups. The timing was not.
After clonidine, autistic kids peaked 30 minutes sooner. After L-dopa, they peaked 30 minutes later. Same dose, different clock.
How this fits with other research
Rutter et al. (1987) and Feinstein et al. (1988) already saw odd catecholamine levels in blood and urine. The new data say the whole signal loop is mistimed, not just the chemical amount.
Jones et al. (1992) later tested drugs that turn dopamine up or down. They saw different behaviors, proving these pathways matter for symptoms. The timing shift found here may explain why the drugs helped some kids but not others.
Duerden et al. (2012) showed autistic kids also mount a faster, stronger cortisol spike. Together the papers paint one picture: autistic nervous systems react quicker to some signals and slower to others.
Why it matters
You can’t fix hormone timing in the clinic, but you can plan around it. Expect faster sedation with clonidine and slower response to dopamine-linked rewards. When you run skill-acquisition sessions, give extra wait time after praise or tokens. The child’s brain may need that minute for the reward signal to land.
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02At a glance
03Original abstract
Studies have shown abnormal pituitary hormone responses to neuroendocrine agonists in autistic subjects. Two probes (clonidine and L-Dopa) were used to investigate neuroendocrine responses through changes in growth hormone levels. Seven medication-free autistic subjects (ages 6.6 to 19.1) were evaluated and compared to 14 normal controls. Growth hormone was collected at 30-min intervals during the entire study. Clonidine was administered first (dose: 0.15 mgm2), and samples were collected for 180 min. L-Dopa was then administered (dose: 250 mg for subjects less than 70 lb and 500 mg for subjects greater than 70 lb), and samples were collected for 120 min. There was no difference in the amplitude of the clonidine or L-Dopa peak growth hormone responses in the control versus the autistic subjects. In the autistic subjects, the L-Dopa-stimulated growth hormone peak was delayed and the clonidine growth hormone peak was premature. A statistical difference with the control subjects was found when consideration was given to both the premature response of growth hormone to clonidine and the delayed response to L-Dopa (p = .01, Fisher's Exact Test). These findings suggest possible abnormalities of both dopaminergic and noradrenergic neurotransmission in subjects with autism.
Journal of autism and developmental disorders, 1990 · doi:10.1007/BF02216052