Failure of clonidine to stimulate feeding in healthy humans

Scott Crow, William Meller, Barbara Praus, Susan Raatz, James Mitchell

Research output: Contribution to journalArticlepeer-review

2 Scopus citations


The α2-adrenergic system is involved in the regulation of food intake in animals but its effects on feeding in humans are unknown. We hypothesized that clonidine administration would stimulate food intake in healthy human subjects. Ten men and 4 women, all physically and psychiatrically healthy, received clonidine 3 μg/kg or placebo, orally, in blinded, balanced, randomized order. Consumption of a liquid test meal was measured; also, serum growth hormone levels were used as a secondary measure of clonidine effects. Visual analog scale ratings of hunger, satiety, and sedation were obtained before, during, and after the test meal. A subset of five subjects also received 1.5 μg/kg clonidine, in addition to the two trials described above. Test meal consumption was greater following placebo than following clonidine. Sedation ratings were substantially higher at all time points after clonidine and correlated with meal consumption (correlation coefficient r = -0.584; p = 0.028). Hunger and satiety ratings did not differ. The 1.5 μg/kg dose did not provide different effects on feeding from that seen with placebo. Contrary to our hypothesis, clonidine did not stimulate food intake in humans. Sedation associated with clonidine administration may have suppressed any effects on feeding. Copyright (C) 1998 Elsevier Science Inc.

Original languageEnglish (US)
Pages (from-to)317-321
Number of pages5
JournalPharmacology Biochemistry and Behavior
Issue number3
StatePublished - Nov 1 1998


  • Clonidine
  • Feeding behavior
  • Satiety
  • α-Adrenergic system

Fingerprint Dive into the research topics of 'Failure of clonidine to stimulate feeding in healthy humans'. Together they form a unique fingerprint.

Cite this