A B S T R A C T Growth hormone (GH) release was studied in adults of normal stature, ages 21-86 yr. The subjects were 85-115% of ideal body weight, between the 5th and 95th percentiles in height, and free ofactive or progressive disease. 9 to 12 individuals in each decade from third to ninth were evaluated. The following criteria of GH status were measured: serum GH concentration, analyzed by radioimmunoassay at halfhour intervals for 4 h after onset of sleep, and at 1-h intervals from 8 a.m. to 4 p.m. in 52 subjects; daily retention of N, P, and K in response to 0.168 U human (h)GH/kg body wt314/day in 18 subjects; and plasma somatomedin C (SmC) level before and during exogenous hGH treatment in 18 subjects.All 10 individuals, 20-29 yr old, released substantial amounts of endogenous GH during both day and night (average peak serum GH obtained during day and night was 7.3 and 20.3 ng/ml, respectively); average plasma SmC was 1.43 U/ml (95% tolerance limits, 0.64-2.22 U/ ml). There was no significant effect of exogenous hGH on elemental balances or on plasma SmC. In contrast, 6 of 12 individuals 60-79 yr old showed the following evidences of impaired GH release: peak waking and sleeping seruim GH < 4 nglml; plasma SmC < 0.38 U/ ml; a significant retention in N, P, and K; and a significant rise in plasma SmC, in response to exogenous hGH.Plasma SmC, serum GH during sleep, serum GH during the day, retentions of N, P, and K in response to exogenous hGH, and rise in plasma SmC in response to hGH were all intercorrelated (P < 0.05). Plasma SmC < 0.38 U/ml corresponded to peak nocturnal serum GH < 4 ng/ml. The prevalence of plasma SmC < 0.38 U/ml

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Our objective was to study the relationship between dispensed aspirin, nonaspirin nonsteroidal antiinflammatory drugs (NSAIDs), steroidal antiinflammatory drugs (SAIDs), acetaminophen, calcium, psyllium, and multivitamin preparations and the risk for subsequent colorectal adenoma and adenocarcinoma. The design was a case-control study. The patient population was from a large municipal teaching hospital in Atlanta, Georgia. In logistic regression models, the risk of colorectal adenoma or adenocarcinoma decreased in the first two years of continuous NSAID use in a linear, time-dependent manner. The risk of colorectal neoplasia after two years of continuous NSAID use was reduced significantly (P < 0.01) as compared to nonusers. Risk reduction appeared greater for adenocarcinoma than adenoma. The use of SAIDs, calcium, multivitamins, and psyllium, as prescribed to our patient population during the mean six-year study period, conferred no measurable risk reduction. These results suggest that in prospective chemoprevention trials, a significant risk reduction can be expected after only two years of aspirin use, in doses similar to those recommended for the prevention of cardiovascular disease, or nonaspirin NSAIDs [correction of nonaspirin. NSAIDs], in doses commonly prescribed for the management of musculoskeletal pain. The results also imply that any short-term reduction in the incidence of colorectal adenoma detected in a phase II trial would underestimate the chemopreventive effect of NSAIDs on the risk of adenocarcinoma.