We have already investigated the growth axis in 50 individuals with a cytogenetically and molecularly confirmed 18q deletion by determining the height, growth velocity, insulin-like growth factor 1 (IGF1), IGF binding protein 3 (IGFBP3), bone maturation and growth hormone (GH) response to pituitary stimulants (clonidine and arginine). To summarize: children with 18q deletions are short: 64% have a height more than 2 S.D. below the mean. Affected children also grow slowly: 68% have a growth velocity more than 1 S.D. below the mean. Half of the individuals have delayed bone maturation. Growth factors are skewed downward: 72% of the IGF1 values and 83% of the IGFBP3 values are below the average for normal children. Similarly, 72% of the children failed to adequately respond to the GH stimulants. In the total group of 50 children, 20 (40%) were classically GH DEFICIENT (height <-2 S.D., velocity <-1 S.D., bone age <-2 S.D., IGF1 < -1 S.D., IGFBP3 <-1 S.D., peak GH <10 ng/ml by polyclonal GH assay) and are on GH treatment. Of the remaining 30 children, 28 have multiple abnormalities of the growth axis, primarily growth velocity <-1 S.D. (ABNORMAL GROWTH), but did not qualify for GH treatment according to criteria set by their private insurer. Almost all of these children had abnormalities suggestive of hypothalamic dysfunction involving TSH (thyroid stimulating hormone) and prolactin. None have CNS (central nervous system) abnormalities of the pituitary on MRI. Thus we suspect that many of these children have neurosecretory dysfunction. Parental heights are slightly above average (father (height standard deviation score) HTZ = 0.3 +/- 1.2, mother HTZ = 0.1 +/- 1.1) and none of the children are overweight.