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The effect of coffee on lower oesophageal sphincter pressure (LOSP) and intra-oesophageal pH was assessed in 10 healthy volunteers, in the fasting state and after a standard Lundh test meal. LOSP was measured by the rapid pull-through technique. Coffee with or without milk has no significant effect on LOSP in the fasting subject. The Lundh meal alone (mean drop = 2.01 cm H₂O), or when coffee with (mean drop – 1.80 cm H₂O) or without milk (mean drop = 3.47 cm H₂O) was taken after it, produced a significant drop in LOSP. Heartburn following coffee does not appear to be due to an effect of coffee on the lower oesophageal sphincter but is more likely due to the effect of a previous meal on sphincter pressure with associated acid reflux.

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The effects of alternating ad libitum feeding and 30% restriction of the dietary intake on the development of diethylnitrosamine (DEN)-induced hepatic neoplasia were investigated. Dietary restriction retarded the growth of glucose-6-phosphatase-deficient (G6Pd) preneoplastic foci and subsequently that of hepatocellular adenomas and adenocarcinomas. The number of foci in standardized liver sections increased from 4.44 foci/cm2 at 12 weeks to 9.65 foci/cm2 at 24 weeks in ad libitum fed animals but only from 2.35 foci/cm2 to 3.29 foci/cm2 in restricted animals. In animals fed first ad libitum for 12 weeks and then for 12 weeks on a restricted diet, the number of G6Pd foci dropped from 4.44 at 12 weeks to 3.54 at 24 weeks. This reduction appeared to be the result of a regression of the small sized G6Pd foci. Dietary restriction was most efficient in inhibiting the development of G6Pd foci when started early in life. Conversely, the growth of foci was stimulated when the mice first had restricted access to food and thereafter were fed ad libitum. The plasma insulin concentrations after a glucose challenge increased with age. Insulinaemia was much higher in ad libitum fed compared to the restricted mice. It was correlated to the number of G6Pd foci in the liver. This study suggests that insulin, which is a known mitogen for hepatocytes in vitro, may contribute to the promotion of DEN-induced liver tumours in mice.